The most recent information on EGR1 is here. Click here for the function of EGR1. Edit this page in Wiki Genes - EGR1 or see Wiki Gene. Evaluation of EGR1 as a candidate gene for high myopia. Paper-12933735. Co-factors p300 and CBP catch Egr1 in their network. Paper-10743129. In contrast, depletion of EGR1 significantly decreases T-bet induction. Paper-13774591. Early growth response-1-dependent apoptosis is mediated by p53. Paper-1124820. EGR-1 binds to the ATF3 promoter as assessed by gel shift assay. Paper-11320612. Both growth arrest and EGR-1 are induced via the type I receptor of IL-1. Paper-152270. Mader is a transcriptional regulator shown to negatively regulate EGR-1. Paper-1601812. EGR1 is a novel target for AhR agonists in human lung epithelial cells. Paper-10622369. EGR1 predicts PTEN and survival in patients with non-small-cell lung cancer. Paper-10744151. The transcription factor Egr1 regulates the HIF-1alpha gene during hypoxia. Paper-13076447. During the initial phase EGR-1 is rapidly induced and NAB2 levels are down-regulated. Paper-9870750. Conversely, EGF, which stimulates Na/H exchange poorly, strongly activated EGR1 expression. Paper-6307061. T-bet expression is regulated by EGR1-mediated signaling in activated T cells. Paper-13774591. 12-O-tetradecanoylphorbol-13-acetate activation of the MDR1 promoter is mediated by EGR1. Paper-382784. Knockdown of E2F-4 or Egr-1 inhibited CSE- induced LC3B expression. Paper-13018935. EGFR Mutation Up-regulates EGR1 Expression through the ERK Pathway. Paper-13751761. Nab1 does not act by blocking DNA binding or nuclear localization of NGFI-A. Paper-1274604. Early growth response-1 mediates up-regulation of telomerase in placenta. Paper-13432688. HCV-core protein induced the binding of Sp1 and Egr1 on its binding sites on IGF-II P4. Paper-8806515. RAGE-mediated increased expression of Egr-1 upregulates a central downstream gene, MIP2. Paper-13729113. Our results show that Egr-1 is induced dramatically by TGZ but not by other PPAR gamma ligands. Paper-9857077. These data suggest a role for EGR1 in modulating MDR1 promoter activity in hematopoietic cells. Paper-382784. EGR1 induction by various types of stress is markedly augmented in cells expressing mutant p53. Paper-10561252. MAPK, CREB and zif268 are all required for the consolidation of recognition memory. Paper-9701806. In contrast, other DNA repair-associated genes, such as GADD45A, EGR1 MDM2 and p53, were not affected. Paper-10707204. Egr-1 mRNA expression rose approximately 9-fold within 2 hours of Ang-1 exposure and declined thereafter. Paper-13585488. Ionizing radiation-inducible apoptosis in the absence of p53 linked to transcription factor EGR-1. Paper-1277330. Overexpression studies revealed that NAB1 is able to completely block transcription mediated by Egr-1. Paper-8520088. WT1 binds preferentially to DNA sequences that are closely related to the EGR-1 consensus site. Paper-12557224. Early growth response gene 1 ( EGR1) is deleted in estrogen receptor-negative human breast carcinoma. Paper-10746577. CONCLUSIONS: The EGR1 gene appeared to be deleted in ER-negative human breast carcinomas. Paper-10746577. EGR1 bound to two binding sites on the LHB promoter and this binding was increased by GNRH1. Paper-13603591. Regulatory mechanism of TNFalpha autoregulation in HaCaT cells: the role of the transcription factor EGR-1. Paper-12916816. Inhibition of p53 function with dominant-negative p53 mutants abrogates EGR-1-dependent apoptosis. Paper-1124820. The concomitant MT1-MMP expression and MMP-2 activation by CSE are inhibited by EGR-1 siRNA. Paper-13155789. Functionally, par-4 inhibited transcription activated by WT1, but not by the related protein EGR1. Paper-837264. The regulation of NAG-1 is complex, but these agents act through either p53 or EGR-1 related pathways. Paper-12334249. PAX3- FOXO1 controls expression of the p57Kip2 cell-cycle regulator through degradation of EGR1. Paper-12605575. BDNF also induces expression of the immediate-early genes c-FOS and NGFI-A but not NGFI-B or NGFI-C. Paper-107344. PLD- induced suppression of Egr-1 was reversed by inhibition of phosphatidylinositol 3-kinase ( PI3K). Paper-12644692. The promoter of human transforming growth factor beta 1 ( TGF-beta 1) contains two GC-rich EGR-1 binding sites. Paper-732827. Sp1 and Egr1 both bind to IGF-II P4 and functionally cooperate in mediating the maximal activity of IGF-II P4. Paper-8806515. Part of the VEGF- triggered gene induction depends on a cooperation of the transcription factors NFAT and EGR-1. Paper-13346844. Detailed analysis of the TopBP1 promoter revealed that the early growth response protein-1 (Egr-1) induces this promoter. Paper-12231772. Serum and epidermal growth factor ( EGF) were each found to strongly stimulate EGR1 expression in both cell types. Paper-6307061. In addition, EGR1 protein was increased by TCDD and PAHs that have binding affinity to the aryl hydrocarbon receptor. Paper-10622369. The M-CSF gene was expressed in 6 cases and the FMS and the EGR-1 genes were expressed in 2 of the latter cases. Paper-165355. Egr1 regulates the coordinated expression of numerous EGF receptor target genes as identified by ChIP-on-chip. Paper-13545444. Transcription of PRDM1, the master regulator for plasma cell differentiation, depends on an SP1/ SP3/ EGR-1 GC-box. Paper-12943737. Early growth response gene 1 ( EGR1) regulates heparanase gene transcription in tumor cells. Paper-10974272. We found a time-dependent induction of Egr-1 and VEGF mRNA expression and phosphorylation of ERK1/2 by SDF-1alpha. Paper-9879794. The gene is located between the IL9 and the EGR1 genes, bordering the smallest commonly deleted region of chromosome 5. Paper-1431906. The OM treatment further enhances this interaction, resulting in a large increase in the Egr1 transactivating activity. Paper-10043986. However, several putative binding sites for transcription factors SP1, AP2, Krox 24, IgHC.4, and Zeste are present. Paper-989208. EGR-1 forms a complex with YAP-1 and upregulates Bax expression in irradiated prostate carcinoma cells. Paper-13632715. Moreover, E2F1 directly induced the transcription of the Egr1 gene using the kappaB site located in its proximal promoter. Paper-13669979. Two Egr-1 binding sites are present within the SOCS-1 promoter as shown by EMSA and supershift analysis. Paper-10737355. Cotransfection of either an EGR-1 or Sp1 expression vector had no significant effect on the activity of the c-myb promoter. Paper-377121. Both GM-CSF and TPA also elicited rapid, transient expression of TIS8 and TIS11 mRNA in postmitotic human neutrophils. Paper-6235822. CB1 stimulation with HU210 activated ERK and induced the transcription factor Krox-24. Paper-12242684. These results indicate that EGR-1 suppresses growth of human HT-1080 fibrosarcoma cells by induction of TGF-beta 1. Paper-732827. The MEK1/2 signaling cascade participates in H. pylori- mediated Egr-1 expression, but the p38 pathway does not. Paper-10264745. Results also suggest that Egr-1 is an important mediator of IL-1 beta and TNF-alpha action in normal human osteoblastic cells. Paper-619170. These findings support the involvement of an MAP kinase/pp90rsk/ EGR-1 cascade in the response of myeloid leukemia cells to TNF. Paper-196414. Moreover, chromatin immunoprecipitation analysis indicates that mutant p53 is physically associated with the EGR1 promoter. Paper-10561252. These studies are the first demonstration that the HIF-1alpha transcription factor is targeted directly by Egr1 in hypoxia. Paper-13076447. However, at 24 h following 5 min of ischemia NGFI-A continued to be expressed in the CA1 region and dentate gyrus. Paper-760133. These data suggest that inhibition of EGR-1 function confers radio resistance despite the induction of wild-type nuclear p53. Paper-795962. The results demonstrate that treatment of HL-60 cells with TNF is associated with the transient induction of the EGR-1 gene. Paper-196414. We conclude that PGE(2)inhibits induced TNF-alpha expression in target cells through an Egr-1/ Krox-24 mediated signaling process. Paper-1963764. Inhibition of the JNK and p38 MAP kinase signals inhibited Egr-1- mediated p21Waf1/ Cip1 promoter activity. Paper-13193894. The important question of the role of EGR1 in regulating heparanase transcription in tumor cells was then assessed. Paper-10974272. We have recently identified a common group of genes induced in human epileptic foci, including EGR1, EGR2, c-fos, and MKP-3. Paper-12486828. Furthermore, activation of pp90RSK, CREB and egr-1 in GM-CSF-treated cells was inhibited by the presence of the inhibitor, PD98059. Paper-2188803. In transient transfection assays, the WT1 protein functioned as a repressor of transcription when bound to the EGR-1 site. Paper-7143882. These observations also support the view that EGR-1 regulates PTEN expression in the initial steps of the apoptotic pathway. Paper-10806061. Both TFs known to function in this stimulation response such as EGR1 and AP1 and new TFs such as HSF1 were identified. Paper-12869505. Phorbol myristate acetate-induced Egr-1 expression is suppressed by phospholipase D isozymes in human glioma cells. Paper-12644692. Our study of mRNA expression profile of Egr1, WT1 and MDR1 in fresh AML samples demonstrated that there are disease-specific patterns. Paper-9344763. SR146131 partially activated mitogen-activated protein kinase and enhanced the expression of the immediate early gene krox 24. Paper-1832132. The minor groove binder chromomycin A3 inhibited EGR1 complex formation but resulted in a smaller increase of the TBP complex. Paper-709475. Furthermore, differential expression of selected marker genes, cyclin E2, EGR1, and DDIT3, was dose dependent for Chk1 inhibition. Paper-12266768. MAPK and SRC-kinases control EGR-1 and NF-kappa B inductions by changes in mechanical environment in osteoblasts. Paper-8844294. These results indicate that EGR1 may promote prostate cancer development by modulating the androgen receptor signaling pathway. Paper-10043975. Furthermore, MEK1 was phosphorylated by TGF-beta, which was sufficient to drive Egr-1 transactivation. Paper-12952450. Egr-1 binding to a recognition sequence in the TIMP-1 promoter was demonstrated in gel retardation and reporter gene assays. Paper-9759771. Early growth response-1 regulates angiopoietin-1-induced endothelial cell proliferation, migration, and differentiation. Paper-13585488. WT1 encodes a transcription factor which binds to the EGR1 consensus sequence, mediating transcriptional repression. Paper-7864627. In contrast, RAGE-stimulated Egr-1-independent pathways regulate TNF-alpha production and apoptosis in response to I/R. Paper-13729113. The TAM-induced p21Waf1/ Cip1 promoter activity was blocked by the expression of small interfering RNA (siRNA) targeted to Egr-1 mRNA. Paper-13193894. Oxidized phospholipids stimulate tissue factor expression in human endothelial cells via activation of ERK/ EGR-1 and Ca(++)/NFAT. Paper-9188461. In addition, the MEK inhibitor U0126 inhibited EGR1 expression, while the phosphatidylinositol 3-kinase inhibitor LY294002 did not. Paper-13751761. Neuregulin-1 induces expression of Egr-1 and activates acetylcholine receptor transcription through an Egr-1-binding site. Paper-10273189. Thus, the biological function of the inhibitory domain of Egr-1 is solely to provide a docking site for NAB1 via protein-protein interaction. Paper-8520088. In addition, fibroblasts expressing Egr-1 at high levels were found to express increased levels of TIMP-2 and TIMP-3 messenger RNA. Paper-9759771. Moreover, the half-life of GM-CSF- induced EGR-1 transcripts was prolonged from 33 to 70 min following inhibition of protein synthesis. Paper-7043144. The Egr-1-binding region contains overlapping Egr-1, SP1, and nuclear factor of activated T-cells ( NFAT) sites and a CpG island. Paper-13616207. As has been described elsewhere, EGR1 induction was dependent on activation of p42/44 MAP kinase, as it was blocked by the MEK inhibitor U0126. Paper-9513726. Through inhibitor assays, we have further shown that MEK-ERK1/2 is required for FGF1-induced neurite outgrowth, pSTAT3(S727) and Egr1 expression. Paper-13735014. This defect is caused by reduced levels of the EGR1 transcriptional activator resulting from a direct, destabilizing interaction with PAX3- FOXO1. Paper-12605575. The TNF-alpha-initiated MEK/ ERK cascade connected to EGR-1 and TF expression is clearly less sensitive to PKC inhibition. Paper-8728745. In this study, the region within + P5 to which both WT1 -- KTS and WT1 + KTS bind was defined as 5'-GGAGAGGGAGGATC-3'. EGR1 did not bind + P5. Paper-747124. Our data suggest that EGR-1 acts as a mediator in LY294002- induced ATF3 expression via a PI3K-independent pathway. Paper-11320612. CONCLUSIONS: Our data demonstrate that IL-1beta-induced Id2 expression in VSMC is mediated by the transcription factor Egr-1 in VSMC. Paper-13428818. Delayed activation of insulin-like growth factor-1 receptor/Src/MAPK/ Egr-1 signaling regulates clusterin expression, a pro-survival factor. Paper-10791607. Gel shift analysis and chloramphenicol acetyl transferase (CAT) reporter assays indicate that EGR-1 transactivates the promoter of the Bax gene. Paper-13632715. The EGR-1- stimulated transactivation was inhibited by expression of the Wilms tumor suppressor, a known specific DNA-binding competitor. Paper-732827. To explore the role of EGR1 in prostate tumorigenesis, we examined the impact of EGR1 expression on the androgen receptor ( AR) signaling pathway. Paper-10043975. Treatment of astrocytes with a NO donor enhanced expression of early growth response 1, with an ensuing reduction in ASCT1 expression (p < 0.05). Paper-13330602. Dominant-negative EGR-1 mutant (dnEGR-1) or repressor of EGR-1, NGFIA binding protein 1 ( NAB1), increased radioresistance of these cells. Paper-13632715. RESULTS: TIMP-1 and Egr-1 were coexpressed in synovial fibroblasts of inflamed joints, and Egr-1 activated the expression of TIMP-1. Paper-9759771. Activation of mitogen-activated protein kinase couples neurotensin receptor stimulation to induction of the primary response gene Krox-24. Paper-792851. Accordingly, we showed that rearing conditions did not affect GR mRNA or NGFI-A expression in the hippocampus of offspring or cross-fostered offspring. Paper-13627311. Furthermore, we show that a mutation of the phosphorylation motif of c/EBPbeta diminished the OM- stimulated interaction of Egr1 and c/EBPbeta. Paper-10043986. This appears to be related to the heavily phosphorylated state of EGR-1 in PC-3 cells which is correlated with increased levels of CKII found in these cells. Paper-10766775. The clearest evidence for a factor that works in this way relates to c-Jun, while other factors may include Notch, Sox-2, Pax-3, Id2, Krox-24, and Egr-3. Paper-13014864. The extracellular signal-regulated protein kinases Erk1/ Erk2 stimulate expression and biological activity of the transcriptional regulator Egr-1. Paper-8890515. E2F1 Induces tumor cell survival via nuclear factor-kappaB-dependent induction of EGR1 transcription in prostate cancer cells. Paper-13669979. Zta not only binds to the Egr-1 promoter but also activates the ERK signaling pathway to trigger binding of Elk-1 to the Egr-1 promoter. Paper-12063895. Here, we characterize the essential human T-bet promoter elements and show that binding of EGR1 to this promoter induces T-bet transcription. Paper-13774591. Reduction in the expression of endogenous EGR-1 with antisense oligonucleotide to EGR-1 inhibited PMA-induced Galphaq transcription. Paper-12314600. Furthermore, this activation of PI3K/ ERK signaling by the EP(4) receptors induces the functional expression of early growth response factor-1 ( EGR-1). Paper-9663242. Utilizing wild-type and mutant FN promoter/luciferase reporter genes, we demonstrated that EGR-1 positively regulated the activity of the FN gene. Paper-8360417. E2F1 physically interacted with the RelA subunit of nuclear factor-kappaB and modulated its transactivity to fully activate EGR1 transcription. Paper-13669979. Serum-stimulated cells also showed increased expression of TCF4 and p300, while inhibition of Egr1 by specific siRNAs resulted in decreased expression. Paper-13092792. The functional role of Egr1 in LDLR transcription was assessed by cotransfection of an Egr1 expression vector with an LDLR promoter reporter construct. Paper-9626639. Induction of the TNF-alpha gene by ionizing radiation and EGR-1 was mediated via a GC-rich EGR-1- binding motif in the TNF-alpha promoter. Paper-1277330. However, knockdown of Egr1 did not affect CCAAT/ enhancer binding protein (C/EBP)beta protein expression or phosphorylation of CREB Ser133. Paper-13718618. Taken together, we provide strong evidence that Egr1 regulates LDLR transcription via a novel mechanism of protein-protein interaction with c/EBPbeta. Paper-10043986. In the absence of p53, WT1 acts as a potent transcriptional activator of the early growth response gene 1 ( EGR1) site, rather than a transcriptional repressor. Paper-7864627. In this study using chromatin immunoprecipitation, we demonstrate for the first time that EGR1 binds to the heparanase gene promoter in vivo. Paper-10974272. The translation inhibitor anisomycin induces Elk-1-mediated transcriptional activation of egr-1 through multiple mitogen-activated protein kinase pathways. Paper-12391470. In addition, DNA binding by EGR-1, a transcription factor structurally related to WT1, increased during differentiation of P19 EC and embryonic stem cells. Paper-972750. The differential expression of 4 genes ( EGR-1, elastin, osteoprotegerin, and IGFBP3) was confirmed via real-time polymerase chain reaction ( PCR). Paper-13253474. These results suggest that physiological action of WT1 is mediated by binding sites of significantly higher affinity than the 9-bp EGR-1 binding motif. Paper-167903. Sp1 and early growth response protein 1 play pivotal roles in GnRH- stimulated LHbeta gene expression in synergism with steroidogenic factor-1 and Ptx1. Paper-8986417. Using prostate tumor-derived cell lines, we showed here that E2F1 activated the expression of transcription factor EGR1 for promoting cell survival. Paper-13669979. Taken all, DON-activated MAPK sentinel signals of the epithelial cells which promoted interleukin-8 production and its positive modulator EGR-1. Paper-13419401. This leads (i) via Ca(++) to the activation of calcineurin and NFAT and (ii) via PKC and the MEK/ ERK MAPK pathway to the upregulation of EGR-1. Paper-13346844. The ability of TGF-beta to stimulate Egr-1 was preserved in Smad3-null mice and in explanted Smad3-null fibroblasts. Paper-12952450. The early growth response protein ( EGR-1) regulates interleukin-2 transcription by synergistic interaction with the nuclear factor of activated T cells. Paper-1597810. Inhibition was not rescued by overexpression of two key transcription factors for LHbeta, early growth response-1 ( Egr-1) and steroidogenic factor-1 ( SF-1). Paper-13590439. CONCLUSION: Mutant EGFR constitutively up-regulates EGR1 through the ERK pathway, and its expression is correlated with EGFR signal activation. Paper-13751761. NRG-1 induces expression of Egr-1 in myotubes, which presumably is responsible for the ability of NRG-1 to stimulate protein binding to the NRE. Paper-10273189. Here we show that transcription factor early growth response 1 ( Egr1) acts as an initial mediator through up-regulating the expression of TCF4 and p300. Paper-13092792. Chromatin immunoprecipitation experiments confirm LPS- induced binding of Egr-1 to the SOCS-1 promoter in vivo. Paper-10737355. As signaling mediators in mPGES-1 induction by EGCG, active ERK1/2 MAP kinases and early growth response gene 1 ( EGR-1) were increased after exposure to EGCG. Paper-12373229. We show that A beta-induced expression of TNF-alpha, IL-1 beta, MCP-1, IL-8, and MIP-1 beta was abrogated in Egr-1 small inhibitory RNA-transfected cells. Paper-9790556. In MCF-7 cells, EGR1 is present at lower levels and the basal PCYT2 promoter activity is maintained by proximal CAAT and GC regions and by elevated nuclear NFkappaB activity. Paper-12947108. NO-treated ECs resulted in a reduction of binding of nuclear proteins to the Egr-1 binding sequences in the platelet-derived growth factor-A promoter region. Paper-1955966. Functional analysis of the SOCS-1 promoter demonstrates that early growth response-1 ( Egr-1) is an important transcriptional regulator of SOCS-1. Paper-10737355. Mammalian two-hybrid assays demonstrate that the N-terminal transactivation domain of Egr1 specifically interacts with c/EBPbeta but not with c/EBPalpha or CREB. Paper-10043986. As a result of further computer analysis, we discovered a site postulated to be an EGR-1 consensus binding site at -273 to -281 in the hTERT promoter region. Paper-13432688. Differences in activation of the SREs in Egr-1 and c-fos were related to promoter sequence, which defines the affinities of Elk-1 and SRF to their respective binding sites. Paper-10661932. The results of nuclear run-on assays demonstrate that EGR-1 mRNA levels are increased in part by transcriptional activation of this gene in M-CSF-stimulated monocytes. Paper-7061561. Smad-independent transforming growth factor-beta regulation of early growth response-1 and sustained expression in fibrosis: implications for scleroderma. Paper-12952450. Inhibition of the ERK or JNK pathway suppressed TNFalpha- induced EGR-1 expression, resulting in the inhibition of TNFalpha-induced TNFalpha promoter activation. Paper-12916816. Recently, the Egr1 transcription factor was shown to up- or down-regulate p300 and CBP transcription based on the nature of its post-translational modification. Paper-10743129. Two were identical to known transcription factors, EGR1 and EGR2, and the other clone, named DB1, encoded a novel protein of 516 amino acids with six zinc finger motifs. Paper-8012833. Early growth response proteins (EGR) and nuclear factors of activated T cells ( NFAT) form heterodimers and regulate proinflammatory cytokine gene expression. Paper-9741776. These results demonstrate an important role for Egr-1 in regulating both the basal and LPS- induced activity of the SOCS-1 promoter. Paper-10737355. EGR1 expression has been linked to tumor suppression as a result of cell cycle arrest and apoptosis through regulation of tumor suppressor pathways including PTEN. Paper-10744151. These results show that transcription factors AP-1, AP-2alpha, and NGFI-A are involved in activated NPY transcription during the onset of neuronal differentiation. Paper-1407518. CONCLUSIONS: Ang-1 triggers significant and transient induction of Egr-1, and Egr-1 contributes to Ang-1-induced endothelial cell migration and proliferation. Paper-13585488. Changes in expression of EGR1, EGR3, ATF3, MKP-1, FOSB, CTGF and CYR61 were verified in separate experiments and in a variety of oesophageal cell lines. Paper-10824898. Transforming growth factor-alpha enhances cyclin D1 transcription through the binding of early growth response protein to a cis-regulatory element in the cyclin D1 promoter. Paper-1277344. Further, mutation of the Egr-1 binding sites significantly reduces both the basal and LPS-induced transcriptional activity of the promoter. Paper-10737355. Consequently, Med23 knockout (KO) nearly eliminates Egr1 (early growth response factor 1) transcription in embryonic stem (ES) cells, leaving a paused polymerase at the promoter. Paper-13755371. OBJECTIVE: To investigate the regulatory potential of early growth response 1 ( Egr-1) on tissue inhibitor of metalloproteinases 1 ( TIMP-1) expression in synovial fibroblasts. Paper-9759771. The early growth response gene EGR-1 behaves as a suppressor gene that is down-regulated independent of ARF/ Mdm2 but not p53 alterations in fresh human gliomas. Paper-8856147. The fact that TGZ-induced NAG-1 expression was accompanied by the biosynthesis of EGR-1 also suggests that EGR-1 plays a pivotal role in TGZ- induced NAG-1 expression. Paper-10205397. Total RNA extracted from prostate tissues was probed with EGR-1, EGR-2, and EGR-alpha cDNA for Northern blots and digoxigenin-labeled cRNA for in situ hybridization. Paper-1465662. Signaling pathway associated with stimulation of CB2 peripheral cannabinoid receptor. Involvement of both mitogen-activated protein kinase and induction of Krox-24 expression. Paper-564596. Mutational analysis in the -136 to -96 bp region provided evidence that a Sp1/ early growth response protein (Egr) motif was responsible for cyclin D1 promoter activation by Ang II. Paper-9047336. Thus, activation of the CXCR3 receptor in proximal tubular cells might disturb natriuresis during inflammatory and ischemic kidney disease via EGR-1-mediated imbalance of ROS. Paper-9659652. Our findings suggest that high levels of EGR1 coupled with low levels of NAB2 can result in high, unrestrained EGR1 transcriptional activity in human prostate cancers. Paper-8856593. Overexpression of EGR1 enhanced AR-mediated transactivation, whereas EGR1 knockdown by small interfering RNA inhibited AR signaling pathway activity. Paper-10043975. WT1 activated the murine E-cadherin promoter through a conserved GC-rich sequence similar to an EGR-1 binding site as well as through a CAAT box sequence. Paper-2188856. Our studies further suggested that the defect of early growth response-1 in T cells might be responsible for the impaired CD40L up-regulation in K14-IL-4-Tg/SKH1 mice. Paper-12920375. Amyloid peptide- induced cytokine and chemokine expression in THP-1 monocytes is blocked by small inhibitory RNA duplexes for early growth response-1 messenger RNA. Paper-9790556. Intraplaque endoglin, pSmad (indicative for TGFbeta signaling), EGR-1, and TGFbeta levels were analyzed using Western blots and enzyme-linked immunosorbent assays, respectively. Paper-13591708. In INS-1 cells, activation of 44-kDa MAP kinase was partially correlated with the induction of early response genes junB, nur77, and zif268 but not with stimulation of DNA synthesis. Paper-199362. These studies show that EGR1 regulates heparanase transcription in tumor cells and importantly, can have a repressive or activating role depending on the tumor type. Paper-10974272. Post-ischemic expression of c-FOS, FOS B, c-JUN, JUN B, JUN D and KROX-24 was investigated by in situ hybridization and immunocytochemistry up to 48 h of recirculation. Paper-353069. Here we demonstrate that binding of early growth response protein 1 (Egr-1) to the distal part of the -92/-62 site is also required for gastrin-dependent CgA transactivation. Paper-9647642. Abstract Changes in limbic brain activity in response to novel configurations of visual stimuli were assessed by quantifying two immediate-early genes, c-fos and zif268. Paper-12313950. TPA induced EGR1 binding to the -69/+20 promoter sequences over a time course which correlated with increased MDR1 promoter activity and increased steady-state MDR1 RNA levels. Paper-382784. CSE-induced MMP-2 mRNA and protein expression and activity were significantly inhibited using EGR-1 small interfering RNA (siRNA) or in Egr-1-null(-/-) mouse fibroblasts. Paper-13155789. Differential expression for EGR1 (an immediate early gene) and RCN2 (coding for the calcium-binding protein Reticulocalbin 2) were reconfirmed by qRT-PCR in the independent sample. Paper-12931110. Taken all, EGCG was strong inducer of EGR-1 expression and mediated EGR-1 nuclear translocation via ERK signaling pathway in A549 pulmonary epithelial cells. Paper-12373229. Transfection of EGR1 siRNA with T24 bladder cancer cell line significantly downregulated heparanase expression compared to the control siRNA transfection. Paper-11206301. Consistent with these findings, phospho- p44/42 and phospho- JNK MAPK and c-Jun were strikingly suppressed in RAGE(-/-) versus WT mice, but not in Egr-1(-/-) mice. Paper-13729113. RESULTS: The mRNA levels of 8 ( EGR1, p21, KRT17, PIM1, S100P, TNFRSF, WFDC2, and TRIM29) of 91 genes changed significantly with time of surgery in normal and tumor tissue. Paper-12668554. The genes most overexpressed in Tff1-/- mice included claudin-7 ( CLDN7), early growth response-1 ( EGR1), and epithelial membrane protein-1 ( EMP1). Paper-10757695. Furthermore, Western blot and immunocytochemical analyses showed that constitutive overexpression of EGR1 promotes the translocation of AR from the cytoplasm to the nucleus. Paper-10043975. By using Affymetrix microarrays to detect cellular genes whose expression is regulated by Smad3, we identified early growth response factor-1 ( EGR-1) as a novel Smad3-inducible gene. Paper-12071186. CONCLUSION: The enhanced expression of Egr-1 may regulate the activity of matrix metalloproteinases in synovial fibroblasts by enhancing the expression of the TIMP-1, -2, and -3 genes. Paper-9759771. Electrophoretic mobility shift assay, with specific antibodies, showed that DB1 constitutively binds to this region whereas EGR1 binds in a T-cell activation-dependent manner. Paper-8012833. Fluorescence in situ hybridization with probes for two tumor suppressor genes on chromosome 5q also showed deletion ( CSF1R [at 5(q33.2-q33.4) and EGR-1 [5(q31-q32)]). Paper-2183172. In terms of signaling pathway, ERK1/2 MAP kinases and its substrate Elk-1 transcription factor were involved in the sulindac sulfide- induced EGR-1 gene expression. Paper-13427028. Overexpression of two dominant negative Egr-1/ Krox-24 constructs in THP-1 cells considerably diminished the inhibitory effects of PGE(2)on rhIL-17- induced TNF-alpha mRNA expression. Paper-1963764. In addition, FGF23 activated the MAPK pathway in the parathyroid through ERK1/2 phosphorylation and increased early growth response 1 mRNA levels. Paper-13435656. When DB1 was cotransfected with a Tax expression vector, transcription activity of the IL-3 promoter induced by Tax was significantly increased, while EGR1 and EGR2 were without effect. Paper-8012833. For comparative purposes and validation of the protocol, the complex between the DBD of EGR1 and its DNA target site within the proximal mdr1 promoter was simulated under the same conditions. Paper-9879798. Cotransfection of a WT1 expression vector repressed the activity of the c-myb promoter in both cell lines, and this repression was relieved when the EGR-1/ WT1 sites were removed. Paper-377121. A significant positive correlation between nuclear beta-catenin and TCF4 was observed, but no such link was evident for Egr1, probably due to the existence of negative feedback regulation. Paper-13092792. G-protein- mediated ERK activation enhanced the transcription of early growth response 1, whereas beta-arrestin 2-dependent ERK activation did not. Paper-10561246. Moreover, adhesion was greatly enhanced in EGR-1- regulated cells and was reversed by treatment with Arg-Gly-Asp (RGD) or PAI-1 antibody indicating that the secreted proteins are functional. Paper-1748903. RESULTS: The mean EGR1/ chromosome 5 ratio for the ER-negative group was significantly lower compared with the same ratio for the ER-positive group (P < 0.001). Paper-10746577. Three Egrs, Egr1, -2, and -3, are induced within the first hour of NRG treatment, with Egr1 and -3 RNA levels showing the most significant increases of approximately 9- and 16-fold, respectively. Paper-10536848. An inverse relation was noticed for the level of DON induced expression of transcription factors ( JUN, FOS, EGR1 and ATF3) and the susceptibility of the cell lines towards the mycotoxin. Paper-13716171. Using a real-time polymerase chain reaction, we determined the messenger RNA expression of TGFbeta-1, VEGF, FGF-2, EGR-1, ATF-3, CTGF, MMP-1, MMP-2, and decorin. Paper-12298313. These results suggest that the inhibition of hepatic gluconeogenesis by AMPK may, in part, be mediated by an immediate early gene response involving EGR1 and its target, DUSP4. Paper-12217860. Induction of Krox-24 by Endogenous Cannabinoid Type 1 Receptors in Neuro2A Cells Is Mediated by the MEK- ERK MAPK Pathway and Is Suppressed by the Phosphatidylinositol 3-Kinase Pathway. Paper-12242684. EGR-1 overexpression or treatment with monokine induced by IFN-gamma resulted in a ROS-dependent inhibition of basolateral Na(+)/K(+)-ATPase activity, compromising sodium transport in these cells. Paper-9659652. A potential binding site for either the EGR-1 or WT1 protein was identified by in vivo footprinting in the 5'-flanking region of c-myb in a region of negative regulatory activity in T cells. Paper-377121. Genes consistently induced ( ATF3, CCNG2, CDKN1A, EGR1, INSIG1, and MAF) or repressed ( CCND1 and VGF) in both cell lines, were also found after gemcitabine treatment. Paper-12464314. In Fao cells, small interfering RNA targeted EGR1 also depletes DUSP4 expression following treatment with AICAR, further supporting a direct link between EGR1 and DUSP4 activation. Paper-12217860. Furthermore, phosphorylated EGR-1 was highly increased in LY294002-treated cells, indicating that EGR-1 phosphorylation induced by LY294002 may facilitate ATF3 transactivation. Paper-11320612. Inhibition of protein synthesis with cycloheximide also had no detectable effect on EGR-1 gene transcription but was associated with superinduction of EGR-1 mRNA levels in GM-CSF-treated cells. Paper-7043144. Furthermore, we observed an uncoupling of EGR1, JUNB, and WNT signaling in response to SS18-SSX2 expression, suggesting that the SWI/SNF-associated coactivation functions of the SS18 moiety are impaired. Paper-12254294. We used transfection assays to study how the abundantly and constitutively expressed Sp1 protein and the immediate early EGR-1 zinc finger protein regulate IL-2 gene expression. Paper-1597810. CORT containing saline partially normalized basal and restraint- induced ACTH secretion and restraint- induced AVP hnRNA, c-fos mRNA, and zif268 mRNA in the PVN in ADX rats. Paper-13524932. One consisted of EGR1, EGR2, EGR3 and EGR4, whereas the only known paralogue of the other is WT1, which controls the developmental fate of the entire nephric system, and therefore of gonads. Paper-1933555. However, serum removal or blockade of PI3K signaling by LY294002 transiently stimulated basal Krox-24 expression and increased CB1- mediated induction of Krox-24. Paper-12242684. PATIENTS AND METHODS: Patients who underwent surgical resection for NSCLC had RNA extracted from tumor tissue and EGR1 gene expression was quantified by real-time quantitative polymerase chain reaction. Paper-10744151. Conversely, depletion of EGR1 or DUSP4 using siRNA not only partially abrogates the inhibition of Pepck expression by AICAR, but also importantly affects glucose production by Fao cells. Paper-12217860. In addition, induction of Egr-1 expression by TAM occurred at the transcriptional level via Ets-domain transcription factor Elk-1 through the JNK and p38 mitogen-activated protein (MAP) kinase pathways. Paper-13193894. Intra-species comparative genomics revealed that TRIP8- EGR2 locus at human chromosome 10q21.3 and 5qNCA- EGR1 locus at human chromosome 5q31 are paralogous regions within human genome. Paper-10183444. DNA binding studies revealed that the EGR-4 protein binds to the EGR consensus motif GCGTGGGCG, but not to the G-rich regulatory ZIP-element of the human IL-2 gene, that is a binding site for EGR-1. Paper-1255110. The WTE motif is similar to the consensus binding sequence 5'GCG(G/T)GGGCG3' recognized by EGR-1 and is also suggested to function as a binding site for WT1, setting up a competitive regulatory loop. Paper-167903. To explore this possibility, a structure-based design strategy was used to construct a fusion protein, TBP/ZF, in which the three zinc fingers of Zif268 were linked to the COOH terminus of yeast TBP. Paper-993994. Recent studies are reviewed indicating that the transcription factor early growth response-1 ( Egr1) is a direct regulator of multiple tumor suppressors including TGFbeta1, PTEN, p53, and fibronectin. Paper-11321166. The proximal breakpoint is localized between EGR1 and FGFA in one patient and between FGFA and ADRB2 in the other, and the distal breakpoint is localized between GLUH1 and NKSF1 in both patients. Paper-120828. Treatment of resting peripheral blood monocytes with the macrophage colony-stimulating factor ( M-CSF) was also associated with rapid (within 15 min) increases in expression of the EGR-1 and EGR-2 genes. Paper-7061561. Brain-derived Neurotrophic Factor (BDNF)- induced Synthesis of Early Growth Response Factor 3 ( Egr3) Controls the Levels of Type A GABA Receptor{alpha}4 Subunits in Hippocampal Neurons. Paper-12248795. Cholinergic stimulation of early growth response-1 DNA binding activity requires protein kinase C and mitogen-activated protein kinase kinase activation and is inhibited by sodium valproate in SH-SY5Y cells. Paper-2009624. In this report, we show that the expression of the antitumorigenic and/or pro-apoptotic gene NAG-1 (nonsteroidal anti-inflammatory drug- activated gene-1) is induced by TGZ and correlates with EGR-1 induction. Paper-10205397. GRObeta enhances transcription of EGR-1, via the extracellular signal-regulated kinase 1/2 ( ERK1/2) pathway, which can be blocked by a specific antagonist of CXCR2 (SB 225002) or specific antibody to GRObeta. Paper-11312059. To elucidate the mechanism of the transcriptional upregulation of the HIF-1alpha gene, we have shown that Egr1 is able to directly bind to the HIF-1alpha promoter using chromatin immunoprecipitation. Paper-13076447. CONCLUSIONS/INTERPRETATION: These findings suggest that exendin-4 activates Ccnd1 transcription through induction of EGR1 binding to a cis-regulatory element between -153 and -134 on the rat Ccnd1 promoter. Paper-11824179. Early growth response (EGR) transactivators act as critical regulators of several physiological processes, including peripheral nerve myelination and progression of prostate cancer. Paper-12020576. Posttranscriptional regulation of the zinc finger-encoding EGR-1 gene by granulocyte-macrophage colony-stimulating factor in human U-937 monocytic leukemia cells: involvement of a pertussis toxin-sensitive G protein. Paper-7043144. We show here that EGR1 binds to the AR in prostate carcinoma cells, and an EGR1- AR complex can be detected by chromatin immunoprecipitation at the enhancer of an endogenous AR target gene. Paper-10043975. RESULTS: Seven genes, CYR61, UCHL1, FOS, FOS B, EGR1, VIP, and KRT24, were consistently up-regulated in the mucosa of all six patients compared with the mucosa from four healthy controls. Paper-13123810. The identification that induction of MMP-2 and MT1-MMP by CSE from lung fibroblasts is EGR-1-dependent reveals a molecular mechanism for matrix remodeling in cigarette smoke-related emphysema. Paper-13155789. TNF-alpha- mediated activation of MEK/ ERK and EGR-1 can be blocked by adenoviral expression of a dominant negative mutant of IKK2, whereas the VEGF signaling pathway is unaffected. Paper-8728745. Induced EGR-1 then stimulated the induction of mPGES-1 gene expression and this effect mechanistically can be linked to the pharmacological or toxicological actions after human exposure to green tea catechins. Paper-12373229. Up-regulation of Egr1 by 1,25-dihydroxyvitamin D3 contributes to increased expression of p35 activator of cyclin-dependent kinase 5 and consequent onset of the terminal phase of HL60 cell differentiation. Paper-10489512. This zinc-finger region, which is thought to bind DNA in a sequence-specific manner, is similar (greater than 80% on the amino acid level) to two previously described transcription factors pAT 225/ EGR1 and pAT 591/ EGR2. Paper-7169753. Curcumin inhibits human colon cancer cell growth by suppressing gene expression of epidermal growth factor receptor through reducing the activity of the transcription factor Egr-1. Paper-10809958. The Cys2His2 zinc finger proteins EGR1, WT1, and NIL2A, the basic leucine-zipper protein wbJun/wbFos, and the minor groove binding protein hTBP were chosen as representative transcription factors. Paper-141548. Transcription factors E2F5 and early growth response 1 ( EGR1), Ca(2+) signaling molecules S100A8 and S100A9, and two oxidative stress-induced genes were identified as immediate-early genes of KC. Paper-12265286. In cells rendered deficient in PK-C, serum and EGF were each still capable of inducing high levels of EGR1 mRNA, demonstrating that additional non-protein kinase C pathways are capable of stimulating EGR1 expression. Paper-6307061. The repression function was mapped to the glutamine- and proline-rich NH2-terminus of WT1; fusion of this domain to the zinc finger region of EGR-1 converted EGR-1 into a transcriptional repressor. Paper-7143882. Tamoxifen-induced activation of p21Waf1/ Cip1 gene transcription is mediated by Early Growth Response-1 protein through the JNK and p38 MAP kinase/Elk-1 cascades in MDA-MB-361 breast carcinoma cells. Paper-13193894. Induction of urokinase-type plasminogen activator, interleukin-8 and early growth response-1 by STI571 through activating mitogen activated protein kinase in human small cell lung cancer cells. Paper-13309807. Sustained EGR-1 expression consistently leads to an antiangiogenic state characterized by an altered responsiveness to VEGF and bFGF and a striking inhibition of sprouting and tubule formation in vitro. Paper-12057370. Using tagged NFATc and NFATp in glutathione S-transferase pull down assays showed interaction and physical complex formation of each NFAT protein with recombinant, as well as native, EGR-1 and EGR-4 proteins. Paper-9741776. GNRH1 induces expression of early growth response 1 ( EGR1), which interacts with steroidogenic factor 1 ( SF1) and paired-like homeodomain transcription factor 1 ( PITX1) to regulate Lhb promoter activity. Paper-13603591. CSE decreased HDAC activity, resulting in increased binding of early growth response-1 ( Egr-1) and E2F factors to the autophagy gene LC3B promoter, and increased LC3B expression. Paper-13018935. We conclude that TAM stimulation of p21Waf1/ Cip1 gene transcription in MDA-MB-361 cells depends largely on Elk-1- mediated Egr-1 expression induced by activation of the JNK and p38 MAP kinase pathways. Paper-13193894. In cotransfection and gel shift assays, we show that EGR-1- binding sites are located within region -73 to -51 of the NAG-1 promoter and have an important role in the transactivation of TGZ-induced NAG-1 expression. Paper-10205397. Transcriptional activity of the heparanase promoter is stimulated by demethylation, early growth response 1 ( EGR1) transcription factor, estrogen, inflammatory cytokines and inactivation of p53. Paper-12242592. Of three protein kinase C-coupled transcription factors examined by gel retardation assay, ( AP1, NF kappa B, EgrK/ Krox24) only NF kappa B and, to a lesser extent, AP1 was stimulated in response to irradiation. Paper-7634142. Significant changes included genes involved in inflammatory response ( LTA, SELPLG, and IL8), repair and wound-healing activity ( MMP10), and growth activity ( GREB1, EGR1), suggesting repair in this period. Paper-13030576. Cotransfection with pCMV- Egr1 potentiates the inhibition of COL2A1 promoter activity by IL-1beta, whereas overexpression of dominant-negative Egr-1 mutant, Wilm's tumor-1 (WT1)/Egr1, Sp1, or Sp3 reverses the inhibition by IL-1beta. Paper-9708340. Aprotinin inhibited intracellular signaling through p42/44 mitogen-activated protein kinase (P < .05) and early growth response 1 transcription factor (P < .05), as well as interleukin 6 secretion caused by thrombin (P < .005). Paper-10822712. CONCLUSION: Glucose induces proinflammatory changes, including increases in AP-1, Egr-1, MMPs, and TF, the factors that regulate processes that are potentially relevant to atherosclerotic plaque rupture and thrombosis. Paper-10292722. Increasing the DNA binding activity of the phosphorylated form of Sp1 and Egr1 might be an important mechanism for regulating IGF-II gene expression and for promoting cell division during hepatic carcinogenesis. Paper-8806515. Additionally, Egr-1(-/-) macrophages show reduced levels of LPS- induced SOCS-1 expression in comparison with macrophages derived from Egr-1(+/+) littermate controls. Paper-10737355. This experiment was designed to investigate the role of egr-1 in the cancerous process of hepatocellular carcinoma ( HCC) and esophageal carcinoma (EC), and then to appraise the effects of EGR-1 on the growth of these tumor cells. Paper-9566595. We show here that a constitutive active mutant of mitogen-activated kinase kinase-1 ( MAPKK-1) strongly stimulates the activity of the Egr-1 promoter, thus explaining the effects of mitogens upon Egr-1 mRNA and protein levels. Paper-8890515. We review a strategy whereby ligating TNF-alpha to segments of the chemo-inducible EGR1 or MDR1 promoters activates expression of TNF-alpha cDNA and enhances effectiveness of gene therapy and chemotherapy. Paper-10426682. There was no observed effect on the kinetics of expression as judged by TIS 8 induction by beta NGF and protein kinase C (PKC) downregulation did not change the levels of inhibition by orthovanadate seen in control cells. Paper-87713. The present findings suggest that EGR-1 plays an important role in activating the transcription of hTERT, showing that activation of the transcription of hTERT by EGR-1 is involved in the trophoblast growth mechanism. Paper-13432688. Among them, only five are known to regulate angiogenesis: cyclooxygenase 2 ( COX2), heparin-binding epidermal growth factor-like growth factor, early growth response 1 ( EGR 1), CYR61, and angiopoietin 2. Paper-10715770. Expression profiling of stably transfected HEK293 cells revealed specific up-regulation of the immediate early response genes EGR1/ EGR2/ EGR3 and FOS/ FOSB, mediated by activation of the MEK/ ERK5/ Nur77 pathway. Paper-12365580. Phospholipase D prevents etoposide- induced apoptosis by inhibiting the expression of early growth response-1 and phosphatase and tensin homologue deleted on chromosome 10. Paper-10829040. Significant activation of caspases 3 and 9 and Bcl2-associated X ( Bax) with increased poly(ADP-ribose) polymerase (PARP) cleavage and cytochrome c release was observed in radiation-exposed EGR-1 overexpressing cells. Paper-13632715. Furthermore, we observed expression alterations in genes encoding early-immediate genes (ARC, EGR1, EGR2, FOS, DUSP1, DUSP6) and critical cellular signaling systems (CDKN1c, CCND2, CAMK1g, RGS4). Paper-12132671. ANX induced the phosphorylation of the ERK1/2, JNK, and p38 MAPKs in a time-dependent manner and also induced transactivation of Gal4-Elk-1, suggesting that Elk-1 is involved in SRE-mediated egr-1 transcription. Paper-12391470. RESULTS AND LIMITATIONS: We identified five genes ( FOS, EGR1, MYC, TFRC, and FOLH1), which displayed significant differential expression between morphologically normal prostate tissues from men of each of the three risk groups. Paper-13076044. Together, these data demonstrate that EGR1 is an important transcriptional stimulator of the human PCYT2 and that conditions that modify EGR1 also affect the function of ECT and consequently PE synthesis. Paper-12947108. The corresponding trans-regulatory proteins ( SP1, ERG1, GATA1, SREBP1, USF1, and CREBP1) were identified, and in vivo binding of EGR1 and SREBP1 was shown by chromatin immunoprecipitation. Paper-9723891. Secondly, using the tissue factor gene as a readout for VEGF- induced and EGR-1- regulated gene expression we demonstrate that NAB2 can completely block VEGF-induced tissue factor reporter gene activity. Paper-9870750. HGF-induced expression of Egr-1, PDGFA, and VEGF was suppressed by pharmacologic and siRNA inhibitors of mitogen- activated protein kinase kinase 1/2 (MEK1/2) and protein kinase C ( PKC) pathways. Paper-10804544. The transcription factor early growth response-1 ( Egr-1) mediates the stimulation of collagen transcription elicited by TGF-beta and is necessary for the development of pulmonary fibrosis in mice. Paper-12952450. The requirement for EGR-1 in TNFalpha autoregulation was confirmed using a construct harboring a point mutation in the EGR-1 binding site within the TNFalpha promoter and the introduction of EGR-1 siRNA. Paper-12916816. ECs cotransfected with a dominant negative mutant of Ras (RasN17), Raf-1 (Raf301), or a catalytically inactive mutant of extracellular signal-regulated kinase (ERK)-2 (mERK) inhibited shear stress- induced Egr-1 promoter activity. Paper-1955966. Two different AS-ODNs -- both down-regulated the expression of hTERT -- changed the expression of different genes mainly involved in stress response (including EGR1, ATF3 and GDF15), but without an association to telomerase function. Paper-12085650. Three genes, early growth response factor 1 ( EGR-1), dual specificity phosphatase 2, and CD69 (early T-cell activation antigen), showed a 2.0-fold or greater increase in mRNA transcription at four or more of six time points in two studies. Paper-10024344. Here, we report that LY294002 alters early growth response 1 ( EGR-1) phosphorylation and subsequently enhances activating transcription factor 3 ( ATF3) expression independently of PI3K inhibition. Paper-11320612. These findings establish a direct functional link between EGR-1 and the p53- mediated cell death pathway and suggest that mutant forms of p53 in tumor cells may provide resistance to the anti-proliferative effects of EGR-1. Paper-1124820. These data demonstrate that CB1- mediated activation of the Krox-24 transcription factor is negatively regulated through the PI3K-Akt pathway and reveals several points of signaling cross-talk between these two important kinase pathways. Paper-12242684. Taken together, our results demonstrated that curcumin inhibited human colon cancer cell growth by suppressing gene expression of EGFR through reducing the trans-activation activity of Egr-1. Paper-10809958. A functional MEK- ERK pathway is an important requirement for CB1- mediated Krox-24 induction as blockade of MEK signaling by UO126 reduces both basal and CB1- mediated activation of Krox-24. Paper-12242684. Deletion analysis of the Egr-1 promoter identified a minimal E2-responsive region of the promoter that contained serum response element (SRE)3 (-376 to -350) which bound Elk-1 and serum response factor ( SRF) in gel mobility shift assays. Paper-10661932. Among the 41 statistically significant named overexpressed genes at the 1-hour time point were early growth response 1 ( EGR1), jun B proto-oncogene (jun B), jun D proto-oncogene (jun D), and activating transcription factor 3 ( ATF3). Paper-9545040. Using peptide combinatorial libraries expressed in yeast, we have screened for novel zinc finger proteins that selectively bind to an overlapping EGR1/ SP1/ WT1 regulatory site in the promoter of the MDR1 multidrug resistance gene. Paper-8411212. DON-activated ERK1/2 also mediated the production of early growth response gene 1 ( EGR-1) in the epithelial cell line and EGR-1 had the positive regulatory effect on the interleukin-8 production in the human epithelial cells. Paper-13419401. AMPK also induces the immediate early transcription factor Egr1 ( early growth response 1), a known transcriptional activator of Dusp4, and it directly binds the Dusp4 promoter at its known binding site. Paper-12217860. Several genes were uniquely up-regulated by MF treatment, including multiple IFN-related genes ( STAT1, G1P2, OAS1, OAS3, G1P3, IFITM1) and TGF-beta-associated genes ( EGR1, VEGF, THBS1, and TGFB2). Paper-13191334. Twenty upregulated genes, including early stress response and transcription factor genes, were identified, most of which, e.g., EGR1, EGR3, SNAI1, RASD1 and GADD45B, were also induced by hypertonicity, indicating common regulatory mechanisms. Paper-11071328. One day post infection, in three cell-culture models of persistence, namely treatment with penicillin or IFN-gamma, or iron-depletion, infection induced the genes of CTGF, IL-6, IL-8, IL-11, LIF, EGR-1 and ETV4 in a similar fashion. Paper-11045251. Interaction of EGR-1 and Yes kinase- associated protein 1 ( YAP-1) through the WW domain of YAP-1 enhances the transcriptional activity of EGR-1 on the Bax promoter as shown by chromatin immunoprecipitation and reporter assays. Paper-13632715. Ethylation interference footprinting localized binding of Puralpha to a region between nucleotides -91 and -77 within the NHE element, which contains binding sites for the double-stranded DNA-binding transcription factors Sp1, EGR-1 and WT1. Paper-10775714. Because the pulses of released GnRH vary greatly in amplitude, we studied the biosynthetic response of the gonadotrope to varying GnRH concentrations, focusing on extracellular-regulated kinase ( ERK) phosphorylation and egr1 mRNA and protein production. Paper-12260949. Our data show that PSP-induced apoptosis in HL-60 cells might be mediated by up-regulation of early transcription factors such as AP-1, EGR1, IER2 and IER5, and down-regulation of NF-kappaB transcription pathways. Paper-11083800. Curcumin, the active constituent of turmeric, inhibits amyloid peptide- induced cytochemokine gene expression and CCR5- mediated chemotaxis of THP-1 monocytes by modulating early growth response-1 transcription factor. Paper-10561261. In this study, we investigated the functional role of early growth response-1 ( Egr1 gene) in the regulation of radiation- induced clonogenic inhibition and apoptosis in p53 wild-type and mutant prostate cancer cells 22Rv1 and DU145, respectively. Paper-13632715. Furthermore, TAM-induced p21Waf1/ Cip1 promoter activity was enhanced by transient expression of the gene encoding Early Growth Response-1 ( Egr-1) protein, a transcription factor that plays an important role in cell growth and differentiation. Paper-13193894. The expression of the early response genes c-fos, egr1, and cytokine-inducible SH2 protein ( CIS) in response to SCF or Epo stimulation demonstrated that the transient expression of p42/44 correlated with the transient expression of c-fos and egr1. Paper-8406308. RESULTS: Among the genes that showed altered expression patterns, some were already known to be regulated by irradiation, for instance ODC, EGR1, FGF2, PCNA, PKC, and several p53-target genes, including p53DINP1, BTG2, GADD45, and MDM2. Paper-10833431. We find that the IEG c-fos is unaffected by suppression of calcineurin activity, the plasticity-related genes Egr1/ Zif268 and Egr2/ Krox-20 are up-regulated, and genes encoding the orphan nuclear hormone receptors Nor1 and Nur77 are down-regulated. Paper-13736051. The expression profile of growth factors/cytokines showed the up-regulation of many growth-enhancing factors such as EGR1, tumor-derived growth factor 1, platelet-derived growth factor A chain etc. as well as Th1-type cytokines e.g. interleukin-1beta and interferons. Paper-8360627. To determine EGR-1 functions, we re-expressed EGR-1 in human glioblastoma U251 cells and found that the secretion of transforming growth factor-beta1 ( TGF-beta1), plasminogen activator inhibitor-1 ( PAI-1), and fibronectin ( FN) was greatly enhanced. Paper-8360417. The analysis of promoter sequences showed putative Egr-1 binding sites in the PDGFA or VEGF but not in the IL-8 promoter, and HGF-induced Egr-1-binding activity was confirmed by chromatin immunoprecipitation (ChIP) assay. Paper-10804544. Electrophoretic mobility shift assays reveal that recombinant EGR-1 and NFATc bind independently to their target sites within the IL-2 promoter, and the presence of both sites on the same DNA molecule is required for EGR-1.NFATc.DNA complex formation. Paper-1597810. Furthermore, Egr-1-deficient embryonic mouse fibroblasts showed attenuated TGF-beta responses despite intact Smad activation, and forced expression of ectopic EGR-1 in these cells could restore COL1A2 stimulation in a dose-dependent manner. Paper-12071186. The over expressed genes included surfactant protein A1, two members of the MAPK- EGR-1- HSP70 pathway that regulate cigarette-smoke induced inflammation, and Plunc (palate, lung and nasal epithelium associated), a gene not previously implicated in IPF. Paper-13704290. The highest scoring network was assembled around activation protein 1 ( AP-1), a heterodimer of c-Fos and c-Jun oncoprotein, and five AP-1-related genes ( COX-2, IL-6, AREG, HBEGF and EGR1) with tissue repair function. Paper-13691288. Reporter constructs bearing the EGR-1 binding segment of the TGF-beta 1 promoter was activated 4- to 6-fold relative to a control reporter in either HT-1080 cells that stably expressed or parental cells cotransfected with an EGR-1 expression vector. Paper-732827. Additionally, the transcription factor early growth response-1 ( Egr-1) gene was transcriptionally activated and the levels of non-steroidal anti-inflammatory drug (NSAID)- activated gene-1 ( NAG-1) protein were elevated in platycodon D-treated U937 cells. Paper-13539443. The induction of cyclin D1 transcription by TGFalpha is mediated in part through the induction of the early growth response protein (Egr-1) and its subsequent binding of Egr-1 to a cis-regulatory region spanning nucleotides -144 to -104 of the cyclin D1 promoter. Paper-1277344. E2F1 up-regulated the production of EGR1-induced growth factors, epidermal growth factor, platelet-derived growth factor, and insulin-like growth factor II, which in turn activated the phosphoinositide-3-kinase/Akt pathway to resist drug-induced apoptosis. Paper-13669979. Both TrkC and TrkA mediate qualitatively similar increases in the tyrosine phosphorylation of phospholipase C (PLC)-gamma1, Shc, SNT, and MAPK and the transcription of the c-fos, c-jun, NGFI-A, and NGFI-B immediate early genes. Paper-538481. In vitro, incubation of RAGE-expressing liver dendritic cells (DCs) with recombinant HMGB-1 resulted in increased Egr-1 transcripts, in a manner suppressed by RAGE gene deletion, soluble RAGE and inhibitors of p44/ p42 or JNK MAP kinase. Paper-13729113. Double-target experiments in which both HDAC3 and the early-growth response 1 gene ( EGR1), which is localized in the 5q31.2 region, were used as probes showed that the HDAC3 gene lies in region 5q31.3, immediately distal to EGR1 with respect to the centromere. Paper-1799782. Glucose intake induces an increase in activator protein 1 and early growth response 1 binding activities, in the expression of tissue factor and matrix metalloproteinase in mononuclear cells, and in plasma tissue factor and matrix metalloproteinase concentrations. Paper-10292722. We conclude that the HGF-induced activation of transcription factor Egr-1 by MEK1/2- and PKC-dependent mechanisms differentially contributes to expression of PDGF and VEGF, which are important angiogenesis factors and targets for HNSCC therapy. Paper-10804544. Transfection of Egr1 led to transactivation of TCF4 as well as p300 genes, through specific binding to a promoter region, and thus in turn resulted in nuclear accumulation of beta-catenin mediated by the up-regulating TCF4. Paper-13092792. In addition, overexpression of EGR-1 was sufficient to transactivate the NHE3-reporter gene activity, and knockdown of EGR-1 with gene-specific small interfering RNA resulted in inhibition of the PMA-induced up-regulation of the endogenous NHE3 mRNA expression. Paper-12000009. Overexpression of early growth response-1 ( Egr-1) in VSMC induced Id2 expression while IL-1beta- induced Id2 expression was abrogated in VSMC by the Egr-1 repressor, NGFI-A binding protein 2 ( NAB2), expressed from an adenovirus. Paper-13428818. Induction of NAG-1 and Egr-1 by CDODA-Me was dependent on activation of phosphatidylinositol-3-kinase ( PI3-K) and/or p42 and p38 mitogen- activated protein kinase ( MAPK) pathways but there were differences between Panc28 and Panc1 cells. Paper-13890102. Taken together, the results indicate that GM-CSF activates signaling pathways which regulate EGR-1 gene expression through a pertussis toxin-sensitive G protein and that these events increase EGR-1 mRNA levels by a posttranscriptional mechanism. Paper-7043144. RESULTS: Evolutionary conserved transcription factor binding sites (TFBS) recognized by WT1, EGR1, SP1, SP2, AP2 and GATA1 were identified in the promoters of 24 differentially expressed prostate cancer genes from eight mammalian species. Paper-12904823. The oleate-inducible genes encoding early growth response 1, c-fos, S-phase kinase-associated protein 2, and splicing factor 2 are mapped into a network, which is controlled by signaling pathways of mitogen-activated protein kinase, insulin, or hypoxia. Paper-13506821. This review focuses on the efficacy of various phytochemicals in targeting transcription factors such as AR, Sp1, STATs, E2F, Egr1, c-Myc, HIF-1 alpha, NF-kappaB, AP-1, ETS2, GLI and p53 in the context of prostate cancer intervention. Paper-12592113. We conclude that the signaling pathway involving mitogen-activated protein kinase/extracellular signal- regulated protein kinase has a dual impact on the biology of Egr-1 by controlling the transcription of the Egr-1 gene and the transcriptional activity of the Egr-1 protein. Paper-8890515. By creating zinc finger deletions, we demonstrate that zinc finger 1, but not zinc finger 4, is critical for + P5 binding; whereas zinc finger 4, but not 1, is necessary for the binding of WT1 target sites within EGR1, PDGF A chain and IGF2 promoters. Paper-747124. Differential involvement of calmodulin-dependent protein kinase II-activated AP-1 and c-Jun N-terminal kinase- activated EGR-1 signaling pathways in tumor necrosis factor-alpha and lipopolysaccharide- induced CD44 expression in human monocytic cells. Paper-10740160. Real-time reverse transcriptase-polymerase chain reaction analysis was performed to evaluate the expression of types I, II, and X collagen; aggrecan; cathepsin B; and early growth response protein-1 (Egr-1) and Sry-type high-mobility-group box transcription factor-9 (Sox-9) mRNAs. Paper-10755328. The protein products of these genes are: fos-related antigen 2, apoptotic cysteine protease MCH4, DB1 ( zinc finger protein 91), transcription factor ETR103, integrin alpha, interleukin-4, interleukin-6, 23-kDa highly basic protein, and ribosomal protein S9. Paper-8522489. This involved abrogation of Egr-1 DNA binding in the promoter of CCR5 by curcumin as determined by: (i) electrophoretic mobility shift assay, (ii) transfection studies with truncated CCR5 gene promoter constructs, and (iii) chromatin immunoprecipitation analysis. Paper-10561261. The time-courses of RNA expression observed at 0.5, 1.5, 3, 6 and 15 h after wounding for genes such as c-Fos, c-Jun, Egr1, the plasminogen activator PLAU ( uPA) and the signal transducer and transcription activator STAT3, were consistent with previously published data. Paper-12816804. There were no changes in the expression of the other genes in this brain region. mRNA levels of Arc and Zif268 in striatum and Zif268 in the nucleus accumbens markedly increased both in SA and YC animals; but there was no change in the expression of FGF-2 and BDNF. Paper-13661129. The wt1 gene, a putative tumor suppressor gene located at the Wilms tumor ( WT) locus on chromosome 11p13, encodes a zinc finger-containing protein that binds to the same DNA sequence as EGR-1, a mitogen-inducible immediate-early gene product that activates transcription. Paper-7143882. Overall, EGR-1 mRNA was strongly suppressed (average, 15.2 +/- 13.9%) in 27 of 31 cases (87%), independent of changes in p16/ INK4a/ ARF and Mdm2; whereas 4 of 31 cases with residual EGR-1 expression as well as the highest EGR-1 variance segregated with p53 mutations. Paper-8856147. When formation of phosphatidic acid was inhibited by overexpression of catalytically inactive PLD during etoposide treatment, expression of Egr-1 and PTEN and the apoptotic effect of etoposide were not inhibited. Paper-10829040. The most abundant splicing variants contain a nine-nucleotide insertion encoding lysine, threonine, and serine (KTS) in the H-C link region between the third and fourth WT1 zinc fingers which disrupts binding to a previously defined WT1- EGR1 binding site. Paper-8025472. Secondly, we demonstrated that NT induced the expression of the growth-related gene Krox-24 at the protein level, as assessed by Western-blot analysis, and at the transcriptional level, as demonstrated in CHO cells transfected with hNTR and a reporter gene for Krox-24. Paper-792851. Consistent with this, expression of PDGFA and VEGF but not IL-8 showed corresponding differences with Egr-1 expression in HNSCC tumor specimens and were strongly suppressed by transfection of Egr-1-antisense or small interference RNA (siRNA) oligonucleotides. Paper-10804544. We have recently identified early growth response-1 ( Egr-1), an immediate-early gene transcription factor, as an important contributor to increased LPS- stimulated TNF-alpha secretion by Kupffer cells after chronic ethanol exposure. Paper-11498246. Apoptosis in these cells is triggered by the alteration of the Egr1-PTEN-Akt ( early growth response-1/phosphate and tensin homolog deleted on chromosome 10/Akt) and p53 pathways, which converge on the FOXO3a (Forkhead box transcription factor O class 3a) transcriptional activator. Paper-13480830. Further, some of the genes that show a robust response to estrogen exposure in Ishikawa cells are well known to be estrogen responsive, in various in vivo studies, such as PGR, MMP7, IGFBP3, IGFBP5, SOX4, MYC, EGR1, FOS, CKB, and CCND2, among others. Paper-13495998. To test their roles in cell physiology, we constructed adenoviral recombinants encoding NGFI-A binding protein 2 ( NAB2, a repressor of EGR1, EGR2, and EGR3), EGR1, NAB-insensitive EGR1(I293F) ( EGR1*), EGR2, and the NAB-binding, repressive domain 1 (R1) of EGR1. Paper-8638277. Interaction of early growth response protein 1 (Egr-1), specificity protein 1 (Sp1), and cyclic adenosine 3'5'-monophosphate response element binding protein ( CREB) at a proximal response element is critical for gastrin-dependent activation of the chromogranin A promoter. Paper-9647642. We show also that 1,25D(3) treatment of HL60 cells markedly increases the binding of Egr1 to an element in the p35 gene promoter, whereas transfection of an excess of this Egr1- binding oligonucleotide ("promoter decoy") reduces p35 gene transcription and cell differentiation. Paper-10489512. Here, we show that continuous high frequency (100 Hz) electrical stimulation of the central thalamus generates widespread cortical activation of c-fos across all cortical layers and a selective pattern of regulation of zif268 within the supragranular, granular, and infragranular cortical laminae. Paper-12307208. These data, which were validated by qRT-PCR or Western analysis for ID1, TP53, HPSE, NQO1, EGR1, and VEGFA, showed a two-pronged response where a core set of genes was coordinately regulated by all analogues while each analogue simultaneously uniquely regulated a larger number of genes. Paper-13719206. In addition, hnRNP G overexpression led to up-regulation of the expression of TXNIP, a cell cycle inhibitory gene, and significantly reduced the expression of the genes that promote cellular proliferation, such as EGR1, JUND, JUNB, FOS, FOSL1, ROS, and KIT. Paper-12009775. Deletion of a specific Egr-1- binding site present in the PTEN promoter blocked etoposide- induced PTEN activity and elevated expression of PLD decreased the sensitivity to apoptosis induced by ectopic expression of Egr-1. Paper-10829040. These findings suggest the existence of differentiation-induced pathways in LLC-PK1 cells that alternatively abrogates EGR-1 and promotes WT1 gene expression, thereby modulating a target protooncogene G alpha i-2 that is participatory for growth and differentiation in renal cells. Paper-446747. Our previous studies showed that interaction of Abeta1-40 or fibrilar Abeta1-42 caused activation of nuclear transcription factor, early growth response-1 ( Egr-1), which resulted in increased expression of cytokines ( TNF-alpha and IL-1beta) and chemokines (MIP-1beta, MCP-1 and IL-8) in monocytes. Paper-10561261. However, recent reports have clarified that early growth response 1 gene ( Egr1) positively regulates MDR1 transcription, while Wilms' tumor suppressor gene ( WT1) does negative regulation of MDR1 gene expression in 12-O-tetradecanoylphorbol-13-acetate treated K562 cells. Paper-9344763. Genes encoding the transcription factor early growth response-1 ( EGR-1) and cytokine tumor necrosis factor-alpha ( TNF-alpha) were induced upon irradiation of prostate cancer cells, and inhibition of EGR-1 function resulted in abrogation of both TNF-alpha induction and apoptosis. Paper-1277330. Cells were analyzed throughout the differentiation process (2 h, 1, 2, 3, 4, and 10 days), for neurite outgrowth (light microscopy and computer image analysis), and for mRNA levels of the immediate molecular differentiation markers Egr1, Egr3, PC3 and PC4 (quantitative real-time PCR). Paper-13536507. We show that expression of EGR-1 in human HT-1080 fibrosarcoma cells uses increased secretion of biologically active TGF-beta 1 in direct proportion (rPearson = 0.96) to the amount of EGR-1 expressed and addition of recombinant human TGF-beta 1 is strongly growth-suppressive for these cells. Paper-732827. METHODS: To test the hypothesis that EGR1 is deleted differentially in ER-negative versus ER-positive breast carcinomas, fluorescence in situ hybridization was employed in this study to determine the EGR1 deletion status in 50 breast carcinoma specimens. Paper-10746577. Gene-based candidates for Parkinson's disease (PD) include the ubiquitin-proteosome system, scavengers of reactive oxygen species, brain-derived neurotrophic factor ( BDNF), its receptor, TrkB, and downstream target early growth response 1, Nurr-1, and signaling through protein kinase C and RAS pathways. Paper-13495833. Transactivation studies using an EGR1 expression vector co-transfected with a reporter construct containing the 280-bp region showed EGR1- activated heparanase promoter activity in a dose-dependent manner in prostate or breast adenocarcinoma and colon carcinoma cell lines. Paper-10974272. However, in gel mobility shift assays pure EGR-1 or nuclear extracts of EGR-1- regulated cells specifically bind to two GC-rich elements of the human FN promoter at positions -75/-52 and -4/+18, indicating that the increased secretion of FN is likely due to direct up-regulation by EGR-1. Paper-1748903. In addition, we have shown that the EP(4) receptor, but not the EP(2), can activate the extracellular signal-regulated kinases (ERKs) 1 and 2 by way of PI3K leading to the induction of early growth response factor-1 ( EGR-1), a transcription factor traditionally associated with wound healing. Paper-10165907. Two important transcription factors, i.e., early growth response (EGR) protein EGR-1 and nuclear factors of activated T cells ( NFAT) protein NFATc, regulate transcription of the human IL-2 cytokine and the same combination of EGR and NFAT proteins seems relevant for coordinated cytokine expression. Paper-9741776. The NAB1 and NAB2 ( NGFI-A/ EGR1-binding protein) transcriptional corepressors directly interact with three EGR family members ( Egr1/ NGFI-A/ zif268, Egr2/ Krox20, and Egr3) and repress activation of their target promoters. Paper-12020576. Etoposide-induced activation of Akt was potentiated by overexpression of PLD and PLD- stimulated suppression of Egr-1 was blocked by inhibition of phosphatidylinositol 3-kinase/Akt survival pathway at the both transcriptional and posttranscriptional levels. Paper-10829040. An in silico reconstruction of cellular networks suggested that differences in pathway activity between the two sub-populations of RGCs are controlled by networks interconnected by SP-1, Erk2 ( MAPK1), Egr1, Egr2 and, potentially, regulated via transcription factors C/EBPbeta, HSF1, STAT1- and c-Myc. Paper-12974778. We investigated the effect of glucose intake on 2 other proinflammatory transcription factors, activator protein 1 ( AP-1) and early growth response 1 ( Egr-1), and on the genes regulated by them, ie, the genes for matrix metalloproteinases 2 ( MMP-2) and 9 ( MMP-9) and tissue factor ( TF), respectively. Paper-10292722. Induction of NAG-1 in Panc28 cells was p38- MAPK- and PI3-K-dependent but Egr-1-independent, whereas induction in Panc1 cells was associated with activation of p38- MAPK, PI3-K, and p42-MAPK and was only partially Egr-1-dependent. Paper-13890102. Quantitative polymerase chain reaction ( PCR) and Western blotting were used to assess levels of mRNA and protein for the glucocorticoid receptor, early growth response 1 ( Egr-1), the Sp1 transcription factor (Sp1), and MYC-associated zinc finger protein ( MAZ) in 6 MEN-2 and 13 VHL tumors. Paper-12313302. Wild-type and mutant fusion proteins were assayed for their DNA-binding affinity using four previously identified WT1 DNA targets: an EGR1 consensus site; murine insulin-like growth factor 2 promoter 2 (IGF2P2); a (TCC)n motif from the PDGFA-chain promoter; and +P5, a genomic fragment isolated by its affinity for WT1 + KTS. Paper-275256. The persistent expression of NGFI-A in CA1 neurons destined to die and the persistent expression of NGFI-A, NGFI-C, and egr-3 genes in dentate granule cell neurons that survive may indicate that some transcription factors modulate cell death whereas others support cell survival when expressed for prolonged periods. Paper-760133. Transfection with HCV-core in HepG2 cells stimulated the membrane translocation of protein kinase C (PKC) and the treatment of HCV-core transfected cells with calphostin C, a PKC inhibitor, blocked induction of Sp1 and Egr1 DNA binding activity, and eventually transcriptional transactivations of the IGF-II gene. Paper-8806515. Thus, we examined Fos-like, c-Jun, activating transcription factor 2 ( ATF-2), early growth response 1 ( Egr-1), early growth response 2 (Egr-2), and TH immunoreactivity expression in the LC and mPFC in rats receiving 2, 4, 8, or 15 mg/kg/day olanzapine by s.c. osmotic minipump for 4 h, 1 week, 2 weeks, or 4 weeks. Paper-12319869. CONCLUSIONS: These results indicate that EGR-1 is commonly suppressed in gliomas independent of p16/ INK4a/ ARF and Mdm2 and that suppression is less crucial in tumors bearing p53 mutations, and these results implicate an EGR-1 growth regulatory mechanism as a target of inactivation during tumor progression. Paper-8856147. Four mutants, with deletions of 9-15 bases in the 5' regulatory region of the human interleukin 1 alpha gene, were constructed: three deleted stretches correspond to regions with high sequence similarity to regions in other genes, coding for nerve growth factor-induced proteins, e.g. NGFI-A, NGFI-B, NGFI-C, ERK2 and VGF gene. Paper-978747. Transcript elongation by polymerase II paused at the Egr1 promoter is activated by mitogen-activated protein kinase phosphorylation of the ternary complex factor ( TCF) ELK1 bound at multiple upstream sites and subsequent phospho- ELK1 interaction with mediator through the MED23 subunit. Paper-13755371. Transient transfections with a series of promoter constructs containing overlapping SP and EGR-1 sites and with constructs in which the EGR-1 and SP sites were systematically inactivated by site-directed mutagenesis established the dominance of SP sites in both basal and progestin- enhanced TF transcriptional activity. Paper-9075988. We studied the roles of integrins and ECM proteins ( fibronectin [ FN], type I collagen [COL1], and laminin [LM]) in shear-mediated signaling and the expression of bone formation-related genes ( early growth response-1 [ Egr-1], c-fos, cyclooxygenase-2 [ Cox-2], and osteopontin [ OPN]) in human osteosarcoma MG63 cells. Paper-12844521. While the induction of transcription factors such as IRF1, NF-kappaB, ATF-2, STAT3, Egr1 and C/EBPbeta is thought to promote post-ischemic inflammation, activation of transcription factors such as HIF-1, CREB, c-fos, PPARalpha, PPARgamma and p53 is thought to prevent post-ischemic inflammation and neuronal damage. Paper-13299223. Subsequently, we probe this data set and identify three specific TGF-beta-induced genes with regulation by PNF1 conserved over multiple timepoints-amyloid beta (A4) precursor protein (APP), early growth response 1 ( EGR-1), and matrix metalloproteinase 14 ( MMP14 or MT1-MMP)-that are also implicated in angiogenesis. Paper-13831936. Because the SIRE motif is composed of a c/ EBP binding site and a cAMP response element, both of which are quite divergent from the classical GC-rich Egr1 recognition sequences, we hypothesized that Egr1 may regulate LDLR transcription through interacting with members of the c/ EBP and CREB families. Paper-10043986. These results indicate that HCV-core functions as a positive regulator of IGF-II transcription through the PKC pathway and that Sp1 and Egr1 are direct targets of the transcriptional regulation of the IGF-II gene which plays an important role in hepatitis C virus pathogenesis during the formation of hepatocellular carcinoma ( HCC). Paper-8806515. Induction of Egr-1 mRNA by IL-1 beta and TNF-alpha was completely inhibited by H-7 suggesting the mediation of protein kinase C. The induction by IL-1 beta and TNF-alpha of Egr-1 mRNA was independent of de novo protein synthesis since this induction was also observed in the presence of protein synthesis inhibitor cycloheximide. Paper-619170. In the total series of bladder cancer and normal bladder samples, the combination of promoter CpG methylation and EGR1 expression regulated heparanase expression in a stepwise manner, where heparanase expression was the lowest in methylation-positive and EGR1-negative samples and the highest in methylation-negative and EGR1-positive samples. Paper-11206301. Taken all together, sulindac sulfide activated ERK1/2 MAP kinases which then mediated EGR-1 induction and nuclear translocation, all of which played important roles in the cellular survival from NSAID-mediated cytotoxicity in the human intestinal epithelial cells, implicating the protective roles of EGR-1 in the NSAID-mediated mucosal injuries. Paper-13427028. Our studies clearly demonstrate that Egr1 is the OM- induced transcription factor that binds to the SIRE sequence of the LDLR promoter and also suggest that Egr1 may have a functional role in OM- induced upregulation of LDLR transcription through interaction with other SIRE binding proteins such as c/EBPbeta or CREB. Paper-9626639. In addition, in neuroblastoma cells, the two novel EGR1 target genes EGR3 and NAB2 were identified by using adenoviral transfer of EGR1 and EGR1*. Our results demonstrate that recombinant adenovirus is useful to regulate heterologous and endogenous EGR target gene expression, and suggest that EGR transcription factors can autoregulate themselves. Paper-8638277. When blocking the gene expression of EGR-1 with EGR-1 siRNA or ERK inhibitor, EGCG-induced mPGES-1 was suppressed in both cases. mPGES-1 promoter with deleted or point-mutated EGR-1 binding sites showed significantly less response to the EGCG stimulation, which also implicated the importance of EGR-1 binding in promoting mPGES-1 gene expression. Paper-12373229. These synonyms are used for gene EGR1 (early growth response 1): ZNF225, Zinc finger protein 225, ZIF-268, Transcription factor Zif268, Transcription factor ETR103, TIS8, Protein Krox-24, NGFI-A, Nerve growth factor-induced protein A, KROX-24, G0S30, EGR-1, Early growth response protein 1, AT225. These accession numbers are used for gene EGR1: Q546S1 (UNIPROT__AC), CAA36777 (NCBI_GENBANK__AC), B4DVG0 (UNIPROT__AC), AAA35815 (NCBI_GENBANK__AC). EGR1 is a homologue of EGR1 (early growth response 1) from Bos taurus. EGR1 is a homologue of EGR1 (early growth response 1) from Pan troglodytes. EGR1 is a homologue of EGR1 (early growth response 1) from Gallus gallus. EGR1 is a homologue of EGR1 (early growth response 1) from Canis lupus familiaris. EGR1 is a homologue of Egr1 (early growth response 1) from Mus musculus. EGR1 is a homologue of Egr1 (early growth response 1) from Rattus norvegicus. EGR1 is a homologue of egr1 (early growth response 1) from Danio rerio. Important links ! iHOP - Information Hyperlinked over Proteins . Concept & Implementation by Robert Hoffmann.