The most recent information on IGF1 is here. Click here for the function of IGF1. Edit this page in Wiki Genes - IGF1 or see Wiki Gene. The effects of IGF-1 were inhibited by hEAG inhibitors. Paper-13321989. PDGF-alpha positively regulated transcription of IGF1. Paper-15171987. The effect of IGF-I was mediated through the IGF-I receptor. Paper-1729740. Hepatic IGF-I isoforms were regulated in parallel by GH. Paper-10922021. IGF-I induced SNCG expression in various cancer cells. Paper-15402611. IGF-I induced both Src/ SHP-2 and Src/ SHPS-1 association. Paper-12197181. IGF-1 activates p21 to inhibit UV-induced cell death. Paper-9857486. IGF-1 activated the MAPK/ ERK and PI-3K pathways. Paper-14308212. Reduced IGF1 activity might also be associated with longevity in humans. Paper-13497984. IGF-I and IGFBP-1 had no effect on IGFBP-3 binding to FN. Paper-8797411. However, how IGF-I- induces VEGF expression is not yet fully understood. Paper-10846384. Estrogen receptor alpha rapidly activates the IGF-1 receptor pathway. Paper-8387162. Coincubation with anti- IGFBP-3 further enhanced IGF-I-induced DNA synthesis. Paper-10549484. Two haplotype variants in the IGF2R were associated with the level of IGF1. Paper-15237012. IL-21 stimulates human myeloma cell growth through an autocrine IGF-1 loop. Paper-14463503. We found that IGF-I up-regulated VEGF mRNA expression and protein secretion. Paper-10040654. IGF-I regulated phosphorylation and translocation of PDK-1 in neurons. Paper-13715515. SNCG blockade may suppress IGF-I-induced cell proliferation and migration. Paper-15402611. IGF-1 controls GLUT3 expression in muscle via the transcriptional factor Sp1. Paper-12611706. Finally, SNCG knockdown suppressed IGF-I-induced cell proliferation and migration. Paper-15402611. Likewise, variants of IGF1 and IRS2 interacted with the LEP rs2167270 polymorphism. Paper-12721451. Finally, IGF1 receptor inhibitor blocks amphiregulin and IGF1 release by H358 cells. Paper-9306038. The WISP3-deficient cells are extremely sensitive to the growth stimulatory effects of IGF-1. Paper-13166351. Further analysis showed that Shc and SHP-2 can be coimmunoprecipitated after IGF-I stimulation. Paper-11096449. In addition, IGF-1 prevents the UV irradiation- mediated suppression of p21 and MDM2 expression. Paper-9857486. IGF-I- stimulated growth of AML blasts was blocked by an inhibitor of the PI3K/Akt pathway. Paper-13400449. Exposure to this peptide also inhibited IGF-I- stimulated Shc and MAPK phosphorylation. Paper-11096449. In conclusion, E2 and IGF-1 differentially regulate ER transcription at ERE and AP-1 sites. Paper-12451830. In this study, we show that IGF-1 activates p21 protein expression in a p53-dependent manner. Paper-9857486. Knockdown of survivin-2B rescued the ability of IGF-1 to promote survival when WTAP was overexpressed. Paper-13976442. IGF-I induced rapid recruitment of integrin beta1 to lipid rafts is Caveolin-1 dependent. Paper-14529669. Accordingly, caveolin-1 expression dramatically enhances IGF-I-dependent MCF-7 cell migration. Paper-12923340. All four IGFBP-3 SNPs (including rs2854744) were associated with IGF-I and IGFBP-3 levels. Paper-14398728. IGF-1 induces Pin1 expression in promoting cell cycle S-phase entry. Paper-9354285. Growth hormone- stimulated IGF-1 generation in cirrhosis reflects hepatocellular dysfunction. Paper-12825738. As expected, E2F-1 small interfering RNA blocks the ability of IGF-I to increase synthesis of E2F-1. Paper-10399603. Filamin A is a novel caveolin-1-dependent target in IGF-I-stimulated cancer cell migration. Paper-12923340. IGF-1 treatment also enhanced PDK1 interaction with IGF-1 receptor (IGF-1R) in intact MCF-7 cells. Paper-14172534. Treatment of beta-CTF-expressing cells with IGF-1 increased the levels of beta-CTF and secreted Abeta. Paper-13615926. These results suggest that IGF-I induces 14-3-3sigma expression in a manner that is independent of p53. Paper-10522890. BMP-2 was both proliferative and pro-chondrogenic while the effect of IGF-1 in our system was variable. Paper-13049153. TGFbeta- induced chondrocyte proliferation was inhibited by suppression of IGF-1 signaling. Paper-14378655. There was no significant effect of IGF-I on net arginine- induced GH release over control conditions. Paper-9221513. Likewise, the ability of IGFBP-5 to inhibit IGF-I-stimulated receptor phosphorylation was attenuated. Paper-8387130. The addition of anti- TNF-alpha did not neutralize the effects of IGF-I on CB DC maturation and apoptosis. Paper-10197121. We show that H(2)O(2) up-regulates and IGF-1 down-regulates PML expression in a Pin1-dependent manner. Paper-14675880. AMPK activation inhibits the expression of HIF-1alpha induced by insulin and IGF-1. Paper-11368237. The activation of raf-1/ MEK1 reversed the effect of IGF-1 treatment by the depletion of intracellular CgA. Paper-10886406. IGF-1 increased DNA synthesis 88 +/- 21% at 2 nM and the effect of insulin at 2 nM was 34 +/- 12%. Paper-96649. In summary, residues 68, 69, 70, 73, and 74 in IGFBP-5 appear to be critical for high affinity binding to IGF-I. Paper-8387130. IGF-1 phosphorylates AMPK-alpha subunit in ATM-dependent and LKB1-independent manner. Paper-10657189. CONCLUSIONS: IGF-I protects neuroblastoma cells from apoptosis and increases Bcl-2 expression. Paper-9394367. In addition, leptomycin B prevented IGF-I stimulated nuclear export of GFP- FKHR. Paper-11541990. Women have the trend of progressive hypoactivity of GH to stimulate IGF-I and IGFBP-3 secretions with age. Paper-13866021. Insulin-like growth factor I triggers nuclear accumulation of cyclin D1 in MCF-7S breast cancer cells. Paper-9292871. BRCA1 silencing by siRNA was used to investigate the effect of BRCA mutations on IGF-I protein expression. Paper-13435311. This population-based study examined whether CRP is inversely associated with IGF-I and IGFBP-3 concentrations. Paper-14017165. Here, we studied how 17-beta-estradiol (E2) and IGF-1 affect ER transcriptional machinery in MCF-7 cells. Paper-12451830. Lack of stroma IGF-1 reduction after castration was associated with low stroma AR expression before therapy. Paper-12372407. IGF-1 and IGFBP-3 gene variants influence on serum levels and prostate cancer risk in African-Americans. Paper-12518232. Intratumoral IGF-I protein expression is selectively upregulated in breast cancer patients with BRCA1/2 mutations. Paper-13435311. Growth factors like insulin-like growth factor-I induce mTOR to prevent cell death during cellular stress. Paper-13031160. TGF-beta1 but not BMP-2 or IGF-1 siRNA inhibited OBCM- induced IL-8 release in human cancer cells. Paper-12836593. Using Western analysis, IGFBP-3 expression was enhanced in IGF-I-stimulated SN12K1 cells exposed to exogenous IGF-I. Paper-10549484. IGF-I- induced VEGF expression in HUVEC involves phosphorylation and inhibition of poly(ADP-ribose)polymerase. Paper-10846384. The IGF-I- mediated phosphorylation and inhibition of PARP represent a novel mechanism of VEGF protein expression. Paper-10846384. PD98059 suppressed both IGF-1- induced cell proliferation as well as IGF-1- stimulated VEGF production. Paper-14563557. The GHRL single-nucleotide polymorphism rs375577 was associated with a 5% increase in IGF-I levels ( P = 0.01). Paper-12901531. Furthermore, also IGF-I and IGF-II induced DNA synthesis was significantly suppressed by anti- IGF-IR mAb. Paper-9173896. IGF-1- induced invasion was reproduced when ARK5 was overexpressed in Burkitt's lymphoma and plasmacytoma lines. Paper-11440040. Insulin-like growth factor I ( IGF-I) inhibits GH secretion via effects at the pituitary and/or hypothalamus. Paper-9221513. CONCLUSIONS: Our results suggest that PC cells that have metastasized to bone have an upregulated IGF-I regulatory system. Paper-10374312. Taken together, these data indicate that IGF-1 may activate p21 in executing its survival function upon genotoxic insults. Paper-9857486. Conclusions The induction of the raf-1/ MEK1 pathway blocks IGF-1-mediated intracellular neuroendocrine hormone regulation. Paper-10886406. Here, we report that activation of P2Y(2) receptors by extracellular UTP inhibits the IGF-I- induced p110alpha- PI3K activation. Paper-14274569. The p38 MAPK inhibitor decreased production of TNF- stimulated VEGF, HGF, and IGF-I in hMSCs and hAPCs. Paper-12220121. We investigated whether IGF-I affects VEGF gene expression and protein secretion in human mesangial cells. Paper-10024097. Cleavage of IGFBP-3 by PSA resulted in a marked reduction in the binding affinity of the fragments to IGF-I, but not IGF-II. Paper-72038. Modification of androgen receptor function by IGF-1 signaling implications in the mechanism of refractory prostate carcinoma. Paper-13643294. Insulin-like growth factor-i regulates Kruppel-like factor-6 gene expression in a p53-dependent manner. Paper-14298254. Interestingly, we found that H(2)O(2)- and IGF-1- mediated alteration in PML accumulation regulate MDA-MB-231 cell migration. Paper-14675880. These results show that AICAR and insulin/ IGF-1 regulate VEGF expression through different mechanisms. Paper-11368237. Our data reveal a novel mechanism whereby IGF-I and c-Abl control RACK1 association with FAK to facilitate adhesion signaling. Paper-13780937. Here we show that IGF-1 and its receptor regulate post-translational changes in RUNX2 to activate DNA binding in proliferating EC. Paper-10564271. None of the ALS or IGFBP3 SNPs were statistically significantly associated with IGF-I levels or mammographic density. Paper-15164649. Treatment of BON cells with IGF-1 stimulated the release of CgA, while high intracellular CgA levels were maintained. Paper-10886406. Several RIZ1- regulated genes involved in insulin-like growth factor-1 ( IGF-1) signaling were identified using cDNA microarrays. Paper-13143489. Circulating insulin-like growth factor-I (IGF-I) and IGF- binding protein-3 ( IGFBP-3) levels have been associated with common diseases. Paper-13655801. Furthermore, the dominant-negative mutant of Akt abolished the ability of IGF-I to suppress activity of the SR-BI/ CLA-1 promoter. Paper-10634507. IGF-1 treatment prevented the glucose- induced neurite degeneration and UCP3 down-regulation. Paper-10457684. Moreover, AICAR and metformin inhibited the ability of insulin and IGF-1 to induce HIF-1alpha expression. Paper-11368237. Moreover, using a pulse-chase experiment, we showed that IGF-I enhances the stability of beta-catenin in prostate cancer cells. Paper-10782813. IGF1 and IGFBP3 tagging polymorphisms are associated with circulating levels of IGF1, IGFBP3 and risk of breast cancer. Paper-11339927. MAIN OUTCOME MEASURE(S): The PCOS and control patients' serum IGF-I and IGFBP-3 levels were compared and correlated with IVF outcome. Paper-13327805. AICAR stimulated VEGF mRNA expression, but did not modify the insulin- and IGF-1- induced VEGF expression. Paper-11368237. These results indicate that IGF-I- stimulated migration of WM1341D cells requires PI3K activation but is independent of MAPK/ERK signaling. Paper-9756906. Stress and IGF-I differentially control cell fate through mammalian target of rapamycin ( mTOR) and retinoblastoma protein (pRB). Paper-13031160. IGF1 promotes resistance to apoptosis in melanoma cells through an increased expression of BCL2, BCL-X(L), and survivin. Paper-14320457. IGF-1 released by corneal epithelial cells induces up-regulation of N-cadherin in corneal fibroblasts. Paper-13902412. AMP-activated protein kinase ( AMPK) inhibits IGF-I actions, but the mechanism by which AMPK functions is undefined. Paper-15129510. The authors hypothesize that IGF-I may protect neuroblastoma cells from apoptosis by upregulating their Bcl-2 expression. Paper-9394367. Little is known regarding sex steroid regulation of ghrelin and the effects of IGF-I on ghrelin in severe undernutrition. Paper-10514098. IGF-I also activated both the extracellular signal- regulated protein kinase (ERK) and phosphatidylinositol 3-kinase ( PI3K) pathways. Paper-10754501. In this study, the role of ERK1 and 2 in mediating the chemotactic and mitogenic actions of IGF-I in cultured porcine VSMCs was investigated. Paper-9957760. In this study, we performed several experiments to test whether beta-catenin is involved in IGF-I- induced AR-mediated transcription. Paper-10782813. Given the role of the IGF system in prostate cancer, ALS may influence carcinogenesis by modulating IGF-I levels or bioavailability. Paper-14241759. Cav-1 down regulated Hacat cells were then stimulated with IGF-I and analyzed by immunofluorescence and flow cytometry. Paper-14529669. Here, we demonstrated in prostate cancer DU145 cells that IGF-1 induced EGFR transactivation, leading to ERK activation. Paper-12245536. Insulin-like growth factor I induces MDM2-dependent degradation of p53 via the p38 MAPK pathway in response to DNA damage. Paper-9161511. These results suggest that IGF-1 promotes Abeta production through a secretase-independent mechanism involving APP phosphorylation. Paper-13615926. Thus, in RPE cells IGF-1 stimulates the second messenger Ca(2+) and increases VEGF secretion which, in turn, induces neovascularization. Paper-10616284. The nuclear receptor coactivator AIB1 mediates insulin-like growth factor I-induced phenotypic changes in human breast cancer cells. Paper-10865552. In addition, IGF-I rescue from serum withdrawal- induced apoptosis is associated with a rapid export of GFP- FKHR into the cytoplasm. Paper-11541990. IGF-1 induces SREBP-1 expression and lipogenesis in SEB-1 sebocytes via activation of the phosphoinositide 3-kinase/Akt pathway. Paper-14308212. CONCLUSION: IGF-I induces VEGF gene expression and protein secretion in human mesangial cells via a Src-dependent mechanism. Paper-10024097. There was also an IGF-1- induced increase in VEGF synthesis as measured quantitatively by [(14)C]methionine- VEGF immunoprecipitation. Paper-14563557. Specifically, an early mean GH </= 4.8 mU L-1 is as predictive for a satisfactory effect of treatment as a normalized IGF-1 3 months after surgery. Paper-8394339. Treatment with U0126, which inhibits ERK1/2 activation, reduced IGF-1- stimulated RUNX2 DNA binding without affecting RUNX2 protein levels. Paper-10564271. In contrast, the C and D domains of IGF-I allow higher affinity binding to the IGF-1R than the analogous domains of IGF-II. Paper-10646911. Increased circulating IL-8 is associated with reduced IGF-1 and related to poor metabolic control in adolescents with type 1 diabetes mellitus. Paper-14066810. IGF-I can bind to the extracellular matrix protein vitronectin ( VN) through the involvement of IGF-binding proteins-2, -3, -4, and -5. Paper-12753017. Regulation of multisite phosphorylation and 14-3-3 binding of AS160 in response to IGF-1, EGF, PMA and AICAR. Paper-12558619. These data also demonstrate that increases in circulating IGF-I are not responsible for changes in hypothalamic function observed after GH treatment. Paper-1509224. Hyperglycemia also reduces the basal IRS-1 concentration and IGF-I- stimulated IRS-1-linked signaling. Paper-15111902. Taken together, our results suggest that IGF-I regulates the expression of FLIP in FRTL cells by activating the PI3K/ NF-kappaB cascade. Paper-13280279. We hypothesized that the induction of parallel raf-1/ MEK1 pathways will block IGF-1- mediated chromogranin A ( CgA) maintenance. Paper-10886406. Growth hormone may promote SHBG synthesis in the liver while somatomedin-C may stimulate its extravasation and uptake in target tissues. Paper-6263147. Having an IGF-1 genotype other than homozygous for the 19-repeat allele was associated with higher IGFBP-3 levels (1,945 versus 2,052 ng/mL). Paper-10983085. Antioxidants and catalase inhibited IGF-1- stimulated EGFR phosphorylation, indicating that H(2)O(2) is required for EGFR activation. Paper-12245536. SDF-1alpha or the M351E-M358L mutant of API were attached at the C-terminal end of IGF I and synthesized by a stable insect cell expression technique. Paper-9740659. Depletion of IGF-1 in epithelial cells by RNA interference abolished the effect of these cells on N-cadherin expression in fibroblasts. Paper-13902412. Insulin-like growth factor-I ( IGF-I) has been shown to promote angiogenesis by enhancing vascular endothelial growth factor ( VEGF) expression. Paper-10846384. Thus, Foxo-1 is a novel corepressor for AR and IGF-1/ insulin signaling may confer stimulatory effects on AR by attenuating Foxo-1 inhibition. Paper-13643294. Immunoprecipitates of ATM collected from IGF-1- stimulated cells also caused the phosphorylation of the AMPK-alpha subunit in vitro. Paper-10657189. IGF-1 activates hEAG K(+) channels through an Akt-dependent signaling pathway in breast cancer cells: role in cell proliferation. Paper-13321989. The latter observation suggests that the rise in SmC levels associated with low dose estrogen may not be mediated through a change in GH secretion. Paper-5780541. In contrast, similar concentrations of either wortmannin or LY294002 were required to inhibit both IGF-I- induced PI3K activation and migration. Paper-9756906. Furthermore, inhibition of the PI3-K pathway also blocked the IGF-1- induced transcription of SREBP target genes and sebocyte lipogenesis. Paper-14308212. Here, we show that IGF-I (but not E(2)) is able to induce nuclear accumulation of cyclin D1 by a phosphatidylinositol 3-kinase-dependent mechanism. Paper-9292871. Together, these data indicate the importance of IGFBPs in modulating IGF-I binding to VN and that this binding has functional consequences in cells. Paper-9741104. The results of our studies showed that endogenous expression of SR-BI/ CLA-1 was suppressed by exposure to GH or IGF-I in cultured HepG2 cells. Paper-10634507. PI3-K inhibitor, LY294002, reduced IGF-I- stimulated phosphorylation of FKHR, FKHRL1, and Akt, but did not affect Erk phosphorylation. Paper-11541990. In contrast, in rGH-treated hypophysectomized rats, induced GH (but not PRL) binding sites showed significant positive correlation with SM-C levels. Paper-4532289. Recombinant IGF-1 exhibited similar basophil-selective effects as IGF-2, and both growth factors were detected in nasal polyp extracts by ELISA. Paper-10653208. However, IGF-I- induced tyrosine-phosphorylation of IGF-I receptor and IRS-I and AKT phosphorylation were unaffected by ErbB2 overexpression. Paper-10206195. Thus, blockade of KCC4 trafficking and surface expression may provide a potential target for the prevention of IGF-I- or EGF-dependent cancer spread. Paper-14571005. These results suggest that IGF-1 induces AMPK-alpha subunit phosphorylation via an ATM-dependent and LKB1-independent pathway. Paper-10657189. IGF-1- induced Akt phosphorylation was abolished by PIK-75 suggesting the contribution of PI3-K p110alpha for activation of Akt by IGF-1. Paper-12629242. Thus, we demonstrated by quantitative PCR that IL-21 induced clonogenicity through an autocrine IGF-1 secretion in HMCL and primary myeloma cells. Paper-14463503. Single nucleotide polymorphisms (SNP) in IGF1 and IGFBP3 have been reported to be associated with the expression of the IGF-I/ IGFBP3 axis. Paper-14249613. Finally, we show that IGF-1 mediated this delay in the onset of UVB- induced apoptosis through activation of the AKT signaling pathway. Paper-9169468. Serum insulin-like growth factor I (IGF-I) and IGF- binding protein 3 ( IGFBP-3) in IVF patients with polycystic ovary syndrome: correlations with outcome. Paper-13327805. Hybrids behaved very similarly to type I receptors with respect to the inhibition of 125I- IGF-I binding by unlabelled IGF-I and insulin. Paper-7757102. Milk samples were analyzed for VEGF, b-FGF and PDGF by enzyme-linked immunosorbent assay and IGF-I was measured by radioimmunoassay method. Paper-14695074. In the metastatic cancer tissues, KCC4 colocalizes with IGF-I or EGF, indicating a likely in vivo stimulation of KCC4 function by growth factors. Paper-14571005. The EPO- induced DNA synthesis and the cooperative effect of EPO/ IGF-I were significantly inhibited by the inducible expression of dn-STAT5 or dn-Ras. Paper-1577577. Most important, this E2F-1 small interfering RNA also blocks the ability of IGF-I to increase cyclin A accumulation and to hyperphosphorylate RB. Paper-10399603. In addition, IGF-I increased the IGFBP-3 levels five- to eightfold with TGF-beta acting in synergy to enhance the IGFBP-3 levels 12- to 17-fold. Paper-12279199. IGF-I- induced association of Src and SHPS-1 was also impaired in SHP-2Delata10-expressing cells, although SHP-2/ SHPS-1 association was unaffected. Paper-12197181. The purpose of this investigation was to examine the mechanisms that IGF-I uses to induce skeletal alpha-actin gene expression in C2C12 myoblasts. Paper-10384925. These results suggest that IGF-1 released from corneal epithelial cells up-regulates the expression of N-cadherin in corneal fibroblasts. Paper-13902412. Additionally, it's been demonstrated that IGF-II binds directly to the extracellular matrix protein vitronectin ( VN), whereas IGF-I does not. Paper-10267907. Moreover, IGF-I interacted directly with TGF-beta activation of the TbetaR complex by enhancing phosphorylation and nuclear translocation of Smad2. Paper-12279199. An antisense construct of beta-catenin that decreases the cellular level of beta-catenin can reduce IGF-1 receptor- mediated enhancement of AR activity. Paper-10782813. Synthesis and characterization of insulin-like growth factor-binding protein (IGFBP)-7. Recombinant human mac25 protein specifically binds IGF-I and -II. Paper-794767. IGF-I may act to limit atrophy and apoptosis during reverse remodeling and to promote repair and regeneration in concert with stromal cell derived factor. Paper-10781358. Parallel application of IGFBP-3 had borderline inhibitory effects while the addition of 40ng/mL of IGFBP-5 enhanced the chemotactic effect of IGF-I on MPC. Paper-12022949. Total alanine-scanning mutagenesis of insulin-like growth factor I ( IGF-I) identifies differential binding epitopes for IGFBP-1 and IGFBP-3. Paper-1855946. IGF-I- induced VEGF production rose by 6 hours with a peak at 12 hours, and declined by 24 hours (52%, 72%, and 34%, respectively; P < 0.01 at 12 hours). Paper-10024097. Polymorphisms in IRS1 and IGF1 were also associated with an approximately two-fold increased risk of specific TP53 mutations relative to controls without cancer. Paper-11838461. The CC genotype for rs1908751 ( IGFBP1) was associated with lower levels of IGF-I (110.9 ng/ml) compared to the CT/TT genotypes (115.7 ng/ml) ( P = 0.04). Paper-15164649. SK-N-MC cells were chosen for further investigation since they express IGF-I, IGF-I receptor and IGFBP-2 mRNA and secrete IGF-I and IGFBP-2 protein. Paper-11103179. In conclusion, decreased serum IGF-1 levels were associated with HCC and the decrease was remarkably noted in those patients concomitant with chronic hepatitis C. Paper-15118313. Most biological effects of GH are mediated by IGF-I; however, the relationship between height, weight and rate of growth has not been systematically studied in CF. Paper-13782732. Immunoneutralization of IGF-I also prevented or reversed the effects of leptin on P, E, IGF-I, IGFBP-3, PGF, but not on OT. Paper-11217899. To determine the mechanism by which AMPK inhibited IGF-I signaling, the role of insulin receptor substrate-1 ( IRS-1) was examined. Paper-15129510. Furthermore, for Shc to be phosphorylated in response to IGF-I requires that Shc must associate with SHPS-1 and this association is mediated in part by SHP-2. Paper-11096449. We speculate that the reduction in bioactive IGF-I may be related to the higher levels of free IGFBP-1 and the faster disappearance of IGFBP-1- bound IGF-I. Paper-12155061. In conclusion, the mutant WISP3 lose is the function of inhibiting IGF-1 and disturbs the maintenance of a stable phenotype in articular chondrocytes. Paper-13166351. At the same time, chronic undernutrition is characterized by low IGF-I that might also influence ghrelin, either directly or through changes in the GH axis. Paper-10514098. Data from literature indicate that iNOS is expressed in vascular smooth muscle cells (VSMC) and that IGF-1-induced release of NO is both rapid and delayed. Paper-13263623. MAPK phosphorylation was examined using the Western blot method. siRNA was used to inhibit the expression of TGF-beta1, BMP-2, and IGF-1. Paper-12836593. IGF-I increased the secretion of VEGF(165) into PrEC growth medium and stimulated transcription of a reporter gene driven by a 1.5-kb region of the VEGF promoter. Paper-9897301. IGF-1 increases expression of sterol response element- binding protein-1 ( SREBP-1), a transcription factor that regulates numerous genes involved in lipid biosynthesis. Paper-14308212. Insulin-like growth factor (IGF)-binding protein-3 ( IGFBP-3) binds to fibronectin ( FN): demonstration of IGF-I/ IGFBP-3/fn ternary complexes in human plasma. Paper-8797411. Finally, estrogen receptor alpha but not beta is required to induce the activation of the estrogen receptor-responsive reporter ERE-LUC in IGF-1-stimulated cells. Paper-8387162. We demonstrate that huntingtin is a substrate of Akt and that phosphorylation of huntingtin by Akt is crucial to mediate the neuroprotective effects of IGF-1. Paper-9485238. RIZ1 was shown to associate with promoter regions of IGF-1 and to increase histone H3 lysine 9 methylation using chromatin immunoprecipitation assays. Paper-13143489. These results suggest that IGF-I promotes proliferation and inhibits osteoblastic differentiation and mineralization of vascular cells via both ERK and PI3K pathways. Paper-10754501. Role of SHPS-1 in the regulation of insulin-like growth factor I- stimulated Shc and mitogen-activated protein kinase activation in vascular smooth muscle cells. Paper-11096449. OBJECTIVE: Animal and human studies suggest that C-reactive protein ( CRP) may be inversely associated with serum insulin-like growth factor-I ( IGF-I) concentrations. Paper-14017165. Insulin-like growth factor-I protects neuroblastoma against starvation- induced apoptosis and is associated with increased Bcl-2 expression. Paper-9394367. A combination of EGF and IGF-I resulted in hepatic injury and function parameters in both liver types similar to those obtained by EGF and IGF-I separately. Paper-15339596. Therefore, raf-1/ MEK1 activation may be a viable method to block IGF-1-mediated cellular effects and serve as a therapeutic target in gastrointestinal carcinoid tumors. Paper-10886406. We next established that TNFalpha dose-dependently inhibits IGF-I- induced phosphorylation of both RB and histone H1 by cyclin A-dependent cyclin-dependent kinases. Paper-10399603. These results indicate that the angiogenic growth factor, IGF-1, can regulate RUNX2 DNA binding through sequential activation of the PI3K/Pak1 and ERK1/2 signaling cascade. Paper-10564271. However, in these cell lines PTEN regulates hypoxia- and IGF-1- induced angiogenic gene expression by regulating Akt activation of HIF-1 activity. Paper-2146355. IGF-I levels were significantly associated with PCa risk (P(trend) = 0.02) with a 21% increase of PCa risk when compared with the highest quartile to the lowest quartile. Paper-15212503. OP-1 was found to enhance mRNA levels of IGF-1 and the IGF-1 receptor, the latter of which appeared to be responsible for the combined effect of IGF-1 and OP-1. Paper-9777518. Recombinant human IGFBP-2 significantly attenuated IGF-1- stimulated MCF-7 cell proliferation with coaddition of 20 or 100 nM IGFBP-2 (50 or 80% inhibition, respectively). Paper-11316716. The effect of IGF-I is inhibited by the PI3K inhibitor wortmannin, indicating that IGF-I- stimulated phosphorylation of filamin A occurs via the PI3K/Akt pathway. Paper-12923340. The enhanced SULT1E1 activity may have a role in inhibiting GH- stimulated STAT5b phosphorylation and IGF-1 synthesis via the sulfation and inactivation of E2. Paper-13494803. Overexpression of PAPP-A led to degradation of the IGFBP-2 produced by C2C12 myoblasts and increased free IGF-I concentrations without affecting total IGF-I concentrations. Paper-11542791. Secretion of VEGF, HGF, and IGF-I in hMSCs and hAPCs was significantly increased by stimulation with TNF and was associated with increased activation of p38 MAPK. Paper-12220121. Insulin-like growth factor-binding protein-3 and -5 ( IGFBP-3 and -5) have been shown to bind insulin-like growth factor-I and -II ( IGF-I and -II) with high affinity. Paper-8387130. In human RCC cells, we recently showed that insulin-like growth factor I ( IGF-I) has growth- promoting effects regulated by IGF-binding protein 3 ( IGFBP-3). Paper-12279199. Our data indicate that common variants in the IGF1 and IGFBP3 genes are associated with differences in circulating levels of IGF1 and IGFBP3 and with breast cancer risk. Paper-11339927. We aimed to correlate GH- stimulated IGF-1 responses with both MELD and Child-Pugh scores and determine the impact of portal hypertension and nutrition on IGF-1 responses. Paper-12825738. The biological effects of estrogens are mainly mediated by the activation of estrogen receptor (ERalpha) whose activity is deeply influenced by the insulin/ IGF-I signaling pathway. Paper-14469982. This notion was confirmed by overexpression of constitutively active GSK3beta, which blocks IGF-I- induced nuclear accumulation of cyclin D1 as well as S phase transition. Paper-9292871. The presence of IGF-I/ IGFBP-3/ FN ternary complexes in human plasma was demonstrated by coimmunoprecipitation of IGFBP-3 and [(125)I]IGF-I with anti- FN monoclonal antibody. Paper-8797411. The elevated IGFBP-5 protein levels were associated with a similar increase in IGF-I mRNA abundance (4-fold, P<0.01) and a significant increase in IGFBP-5 mRNA abundance (1.5-fold). Paper-11251872. IGF-1 mediates PTEN suppression and enhances cell invasion and proliferation via activation of the IGF-1/PI3K/Akt signaling pathway in pancreatic cancer cells. Paper-14525660. IGF-1 upregulates electroneutral K-Cl cotransporter KCC3 and KCC4 which are differentially required for breast cancer cell proliferation and invasiveness. Paper-12389656. GH replacement increased free and total IGF-I to levels similar to those observed during plain fasting and decreased IGFBP-1, however, without affecting IGFBP-1- bound IGF-I. Paper-9768104. In this study, we tested the hypothesis that IGF-I stimulates IL-8 expression at the transcriptional level through induction of Fos/Jun activator protein (AP)-1 complex formation. Paper-12072466. UTP was also found to efficiently attenuate, within few minutes, the IGF-I- induced PI3K-controlled translocation of the actin-nucleating protein cortactin to the plasma membrane. Paper-14274569. PURPOSE: Disruption of the balance of insulin-like growth factor I (IGF-I) and IGF- binding protein 3 ( IGFBP3) has been implicated in the etiology and progression of lung and other cancers. Paper-14249613. This finding is in agreement with our previous observation that IGF-I is able to enhance basal IL-8 production in peripheral blood mononuclear cells (PBMC) in the absence of other stimuli. Paper-12072466. Insulin-like growth factor-I stimulates Shc-dependent phosphatidylinositol 3-kinase activation via Grb2- associated p85 in vascular smooth muscle cells. Paper-12821263. We further demonstrate that GH and IGF-I can synergize in acute aspects of signaling and that IGF-I enhances GH-induced assembly of conformationally active GHRs. Paper-10422464. RESULTS: IGF-I induced a dose-dependent increase in VEGF protein levels (10(-11) mol/L, 5%; 10(-10) mol/L, 14%; 10(-9) mol/L, 46%; 10(-8) mol/L, 66%; 10(-7) mol/L, 68%; P < 0.001). Paper-10024097. RESULTS: AGS cells possessed a single class of high-affinity binding sites for IGF-1 (dissociation constant [Kd], 0.51), with a binding capacity approximately 4 x 10(4) sites per cell. Paper-91213. These results demonstrate that DICE1 has a growth- suppressing activity and interferes with anchorage-independent growth of IGF-IR transformed tumor cells dependent upon IGF-I signaling. Paper-10502104. The expression of an activator protein (AP)-1 dominant negative in an immortalized prostate epithelial cell line PZ-HPV-7 suppressed the IGF-I- induced increase in VEGF promoter activity. Paper-9897301. These results demonstrate that IGF-1 activates the IGF receptor/IRS/ PI3K/ PKB pathway, and that PI3Kalpha is essential for the potentiatory effect of IGF-1 on platelet responses. Paper-12629250. Angiotensin II and IGF-1 regulate connexin43 expression via ERK and p38 signaling pathways in vascular smooth muscle cells of coronary artery bypass conduits. Paper-13402750. Leptin levels were significantly different in the prepubertal CDGP group compared with controls but in the pubertal CDGP group only IGF-I levels were significantly different from controls. Paper-10681085. Compared to the strong and sustained MAPK activation induced by platelet-derived growth factor-BB, the IGF-I- induced MAPK activation was weaker and more transient. Paper-9957760. This study identified signaling events that were induced by AMPK that mediated inhibition of IGF-I- stimulated phosphoinosotide-3-kinase ( PI3K) pathway activation. Paper-15129510. Gab1 underwent tyrosine phosphorylation and subsequent complex formation with protein-tyrosine phosphatase SHP2 upon IGF-I stimulation in C2C12 myoblasts. Paper-12917253. When medium containing either hGH or Sm-C was changed frequently so as to remove factors secreted by fibroblasts only those cells exposed to exogeneous somatomedin-C entered DNA synthesis. Paper-3800269. Thus, the determinants of IGF-II binding to IGFBPs partially overlap those for the IGF-II/ mannose 6-phosphate receptor and overlap those for the IGF-I receptor to a lesser extent. Paper-7858548. In the present study in neuroblastoma, NDGA inhibits IGF-I- mediated activation of the IGF-IR and disrupts activation of ERK and Akt signaling pathways induced by IGF-I. Paper-12620104. The MCF-7 cell proliferation induced by IGF-1 is inhibited pharmacologically by Astemizole or Quinidine or more specifically using siRNA against hEAG channel. Paper-13321989. Studies using IGF-I analogs determined this stimulation to be dependent on both heterotrimeric IGF-I-IGFBP- VN complex formation and the involvement of the IGF-I receptor ( IGF-IR). Paper-12753017. These results indicate that IGF-I interacts with E2 to promote the proliferation of breast carcinoma cells via ROS-dependent MAPK activation and c-Jun protein expression. Paper-13321986. Overexpression of RACK1 in either R+ fibroblasts or MCF-7 cells inhibited IGF-1-induced phosphorylation of Akt, whereas it enhanced phosphorylation of Erks and Jnks. Paper-9164730. Knockdown of Pin1 leads to decreased cell migration, lower levels of ITGB1 expression and resistance to IGF-1- and H(2)O(2)- induced changes in cell migration and ITGB1 expression. Paper-14675880. The degradation may result in a decrease of IGF-I binding, contributing to increase in free IGF-I that may stimulate the cells to produce extracellular matrix ( ECM) components. Paper-9626751. Estrogen receptor alpha and the activating protein-1 complex cooperate during insulin-like growth factor-I- induced transcriptional activation of the pS2/ TFF1 gene. Paper-13184342. Our findings suggest that IGF-I may regulate neuronal PDK-1 differently than in non-neuronal cells, which may indicate a novel role for PDK-1 in IGF-I-mediated neuroprotective signaling. Paper-13715515. IGFBP-4, IGFBP-5, and nonglycosylated IGFBP-3 were shown to significantly enhance binding of IGF-I to VN, whereas IGFBP-2 and glycosylated IGFBP-3 had a smaller effect. Paper-9741104. Adenovirus-mediated expression of dominant-negative AMPK totally abolished the effects of metformin on cell proliferation and phosphorylation of P70S6K in response to IGF1. Paper-14219958. CONCLUSIONS/SIGNIFICANCE: Our findings demonstrate for the first time that extracellular cell survival signal IGF1 regulates MST2 and that Akt is a key upstream regulator of MST2. Paper-14278295. By binding to its receptor, GH1 stimulates the production of IGF-I and its binding protein IGFBP3, resulting in the regulation of cell proliferation, differentiation and apoptosis. Paper-11009148. The current studies were undertaken to define the upstream signaling components that are required for IGF-I- stimulated MAPK activation and the role of SHPS-1 in regulating this process. Paper-11096449. CONCLUSIONS: In our study, CRP levels are inversely associated with IGF-I concentrations in black male smokers; however, the causal nature of the association is unclear and should be studied further. Paper-14017165. Suppression of PTEN phosphorylation strongly enhanced cell proliferation and invasion stimulated with IGF-1 via activation of PI3K/Akt/NF-small ka, CyrillicB signaling pathway. Paper-14525660. Further investigations are required to determine if other IGF-1 effects and more particularly neuroprotective mechanisms are altered in prion-associated neurodegenerative diseases. Paper-13667849. Overexpression of IRS-1 S794A was associated with increased IGF-I- stimulated IRS-1 tyrosine phosphorylation, p85 association, and protein synthesis. Paper-15129510. H358-conditioned medium and amphiregulin induce IGF1 receptor phosphorylation in H322 cells, which is prevented by anti- amphiregulin neutralizing antibody but not by AG556 or ZD1839. Paper-9306038. Tumor necrosis factor alpha inhibits cyclin A expression and retinoblastoma hyperphosphorylation triggered by insulin-like growth factor-I induction of new E2F-1 synthesis. Paper-10399603. Results obtained showed that IGF-I stimulated KLF-6 transcription in cells with normal, but not disrupted, p53, suggesting that KLF6 is a downstream target for IGF-I action. Paper-14298254. In a human interleukin-3 or erythropoietin (EPO)-dependent cell line, F-36P, IGF-I alone failed to stimulate DNA synthesis but did augment the EPO-dependent DNA synthesis of F-36P cells. Paper-1577577. Both PDGF and EGF provoked a rapid and transient rise in [Ca++]i, while Sm-C did not alter [Ca++]i. Nifedipine (3 X 10(-6) M) suppressed the rise in [Ca++]i provoked by PDGF and EGF. Paper-6372023. Indeed, because the effects of conformational averaging and aggregation are eliminated in IGF-I and -II bound to IGFBP-2, the spectra of the complexes are actually superior to those of the free ligands. Paper-11190786. In particular, the transformed cells showed a down-regulation of both PDGF receptors and expressed the 105-kDa isoform of the IGF-1 beta receptor, which was not present in the normal control cells. Paper-9033599. This finding is consistent with experimental data that indicate that IGFBP-3 can inhibit cellular proliferation and induce apoptosis independent of IGF-I and the IGF-I receptor. Paper-9460639. In addition, the PI3 kinase inhibitor, LY294002, upregulates IGFBP-3 expression but downregulates IGF-I and IGF-II, indicating that PTEN controls IGFBP-3 and IGFs by an Akt-dependent pathway. Paper-10807123. Here, we investigate the relationship between these factors and show that prolactin up-regulated transcript levels of both IGF-I and IGF-II, but only after increases in cyclin D1 protein were observed. Paper-14307445. Surprisingly, these IGF-1- mediated effects on RUNX2 were not regulated by Akt phosphorylation, a common downstream target of PI3K, as determined by pharmacological or genetic inhibition. Paper-10564271. The results show that IGF-I- induced Shc phosphorylation and its subsequent binding to Grb2 is required for sustained phosphorylation of MAPK and increased cell proliferation in SMCs. Paper-11096449. WTAP down-regulation by IGF-1 was mediated by an IGF-1 receptor-phosphatidylinositol 3-kinase-Akt signaling axis that directed WTAP degradation via a nuclear 26 S proteasome. Paper-13976442. The IGF-1/Akt pathway has a dual effect on huntingtin-induced toxicity, since activation of this pathway also results in a decrease in the formation of intranuclear inclusions of mutant huntingtin. Paper-9485238. Interaction of scaffolding adaptor protein Gab1 with tyrosine phosphatase SHP2 negatively regulates IGF-I-dependent myogenic differentiation via the ERK1/2 signaling pathway. Paper-12917253. Although substitution of residues 54 and 55 with the analogous residues from IGF-I (Arg-Arg) abolished binding to the IGF-II/ mannose 6-phosphate receptor, binding to IGFBPs was not substantially affected. Paper-7858548. Using a specific phosphatidylinositol 3-kinase ( PI3K) inhibitor, LY294002, we also found that PI3K was involved in the pathway by which IGF-I activated NF-kappaB and increased FLIP expression. Paper-13280279. The scaffolding protein RACK1 (receptor for activated C kinases) integrates insulin-like growth factor I ( IGF-I) and integrin signaling, but whether RACK1 is required for FAK function is unknown. Paper-13780937. Treatment of PI3K inhibitor LY294002 and the MAP kinase inhibitor PD098059, but not p38 inhibitor SB203580, effectively blocks IGF-1- induced upregulation of Pin1, cyclin D1 and RB phosphorylation. Paper-9354285. OBJECTIVE: Insulin receptor substrate-1 ( IRS-1) acts as a docking protein between the insulin-like growth factor-1 ( IGF-1) receptor and intracellular signaling molecules in the IGF-1 signaling pathway. Paper-12912172. IGF-I and insulin promoted the growth of human AML blasts in vitro and activated the phosphoinositide 3-kinase (PI3K)/Akt and the extracellular signal-regulated kinase ( Erk) pathways. Paper-13400449. Taken together, our work identifies PML as a common target for H(2)O(2) and IGF-1 and supports a novel tumor suppressive role for PML in controlling cell migration through the expression of ITGB1. Paper-14675880. We conclude that IGF-I and insulin enhance TRPV1 protein expression and activity, and impaired pain sensation might result from distorted TRPV1 regulation in the peripheral nervous system. Paper-13211622. By contrast, maximum effective concentrations of IGFBP-3 (52 nM) potentiated the effect of IGF-1 50-200% when preincubated with bovine fibroblasts for 48 h prior to the addition of IGF-1. Paper-609477. Mutant WISP3 triggers the phenotype shift of articular chondrocytes by promoting sensitivity to IGF-1 hypothesis of spondyloepiphyseal dysplasia tarda with progressive arthropathy (SEDT-PA). Paper-13166351. CONCLUSION: Common genetic variation in the IGF1 and SSTR5 genes seems to influence circulating IGF-I levels, and variation in IGFBP3 and IGFALS seems to influence circulating IGFBP-3. Paper-15501534. The C and D domains of IGF-II promote higher affinity binding to the IR-A than the equivalent domains of IGF-I, resulting in an affinity close to that of insulin for the IR-A. Paper-10646911. Taken together, these data indicate that the IGFBP-binding domain on IGF-1 contacts the distal third of IGFBP-2, providing evidence that the IGF-1- binding domain is located within the C terminus of IGFBP-2. Paper-8952879. Our results confirm that the C-domain of IGFBP-2 plays a key role in binding regions of IGF-I and -II that are also involved in binding to the type-1 IGF receptor and thereby blocking ligand binding to this receptor. Paper-11190786. Competition studies revealed that EGF and IGF-I share a common binding site on the cathepsin B enzyme, with native IGF-I displaying the lowest affinity for the protease ( IC50 approximately 1.5 microM). Paper-11242275. ARK5 is transcriptionally regulated by the Large-MAF family and mediates IGF-1-induced cell invasion in multiple myeloma: ARK5 as a new molecular determinant of malignant multiple myeloma. Paper-11440040. The availability of these mutants will make it possible to determine if there are direct, non- IGF-I-dependent effects of IGFBP-3 and -5 on cellular physiologic processes in cell types that secrete IGF-I. Paper-8387130. The antibody inhibits rat IGF-1 binding to IGF-1 receptors, and prevents IGF-1- stimulated receptor and IRS-1 phosphorylation in LISN C4 cells, an IGF-1 receptor-transfected cell line. Paper-1321066. Here, we study the long-term effects on TRPV1 expression mediated by insulin-like growth factor type-I ( IGF-I) and insulin in a stably TRPV1-expressing SH-SY5Y neuroblastoma cell line. Paper-13211622. In conclusion, AMPK functions to inhibit IGF-I- stimulated PI3K pathway activation through stimulation of IRS-1 serine 794 phosphorylation. Paper-15129510. Immunocytochemistry using an alphaIR3 antibody confirmed the presence of IGF-I receptor in human blastocysts and the same antibody completely inhibited the stimulation of blastocyst formation by IGF-I. Paper-1729740. In the human pancreatic cancer cell line PANC-1, AMPK-alpha subunit phosphorylation promoted by IGF-1 was suppressed by antisense ataxia telangiectasia mutated ( ATM) expression. Paper-10657189. In summary, these results suggest that IGF-1/PI-3 kinase inhibited C2-ceramide-induced apoptosis due to relieving oxidative damage, which resulted from the inhibition of catalase by activated caspase-3. Paper-9229300. We showed that after 4-nitroquinoline 1-oxide-induced DNA damage, IGF-I induced exclusion of the p53 protein from the nucleus and led to its degradation in the cytoplasm, whereas p53 mRNA was unaffected. Paper-9161511. IGF-1- stimulated tyrosine phosphorylation of IRS-1 and IRS-2 and subsequent p85 binding is transient and precedes phosphorylation of protein kinase B ( PKB) on Ser473. Paper-12629250. IGF-I- stimulated activation of AKT was reduced by AIB1 small interfering RNA treatment, whereas mitogen-activated protein kinase (extracellular signal-regulated kinase 1/2) activation by IGF-I was unaffected. Paper-10865552. Deletion of an E2F recognition site from this reporter eliminates the regulatory effects of both IGF-I and TNFalpha on cyclin A transcription, indicating the essential role of E2F-1 in mediating their cross-talk. Paper-10399603. This hypothesis was sustained both by the fact that IL-21 treatment induced an IGF-1 mRNA synthesis and that an antagonistic anti- IGF-1 receptor mAb (AVE1642) strongly inhibits the IL-21-induced clonogenicity. Paper-14463503. Pregnancy-associated plasma protein A ( PAPP-A) is an IGF-binding protein-4 ( IGFBP-4) metalloproteinase that cleaves inhibitory IGFBP-4 to amplify local IGF-I bioavailability in vitro. Paper-9986815. CONCLUSION: A high IGFBP-3 level might affect LUTS by decreasing the bioavailability of IGF-1 or independent of IGF-1 by up-regulating apoptosis, and, thus, limiting its growth promoting effects on the prostate. Paper-12507849. This decrease in IGF-1 receptor may confer a survival advantage to prostate cancer cells that have entered the circulation by making them resistant to the differentiative effects of IGF-1 at metastatic sites such as bone. Paper-10654763. Furthermore, IGF-1 stimulates tyrosine phosphorylation of insulin receptor substrate-1 ( IRS-1) and IRS-2 and their association with the p85 subunit of phosphoinositide-3 kinase ( PI3K). Paper-12629250. RESULTS: Clear cell RCC were characterized by significant increases in the mRNA expression of IGF-I, IGFBP-3 and IGFBP-6 while papillary RCC exhibited down-regulated expression of IGF-I, IGFBP-4 and IGFBP-5. Paper-10986279. Competitive hormone-binding analysis revealed that the cell line expressed approximately 4 x 10(3) high affinity insulin binding sites and 1.1 x 10(4) high affinity IGF-1 binding sites per cell. Paper-96649. There was a suggestion of an interaction between ALS and total IGF-I, whereby high circulating IGF-I was associated with an increased risk of advanced prostate cancer among men with low but not higher ALS levels. Paper-14241759. We found that IGF-1 also induced AMPK-alpha subunit phosphorylation in the human normal fibroblast TIG103 cell line, but failed to do so in a human fibroblast AT2-KY cell line lacking ATM. Paper-10657189. In the present study, by using MSC from the BM of IRS-1(- / - ) mice we show that IRS-1 mediates almost 50% of the IGF-I mitogenic response and the MAPK-MEK/ERK signalling accounts for the other 50%. Paper-13984810. We hypothesized that if the dominant action of IGF-I is to suppress GH release at the level of the pituitary, then the arginine-induced net increase in GH concentration would be unaffected by an IGF-I infusion. Paper-9221513. The protein in conditioned medium and the molecular weight of IGF-1 receptors on AGS cells were determined by affinity cross- linking with 125I- IGF-1 followed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Paper-91213. In summary, the results of this study revealed that both stratifin and KCM stimulate the expression of MMP-1-in fibroblasts and this effect can be abrogated by either IGF-1, TGF-beta1, or a combination of both. Paper-13151484. Very low plasma GH levels (less than 1 mU/l or 0.5 ng/ml) were associated with normal SMC values and clinical cure, high GH levels (greater than 10 mU/l or 5 ng/ml) with elevated SMC levels and persisting acromegaly. Paper-5681577. Therefore, it is suggested that GH levels of 80-100 micrograms 1(-1) maximally activate Somatomedin-C production in man and that further increases in GH in general will not result in a further increase in SM-C generation. Paper-5467588. Blockade of gene transcription by actinomycin D abolished IGF-1- mediated increase in KCC3 and KCC4 mRNA, indicating that IGF-1 increases KCC abundance through the regulation of KCC genes. Paper-12389656. Thus, these data suggest that the mitogenic function of IGF-1 is at least partially linked to the induction of Pin1, which in turn stimulates cyclin D1 expression and RB phosphorylation, therefore contributing to G0/G1-S transition. Paper-9354285. A significant inverse association between IGF-I and all markers of inflammation persisted in individuals with hsCRP below 3.0 mg/L whereas only YKL-40 was significantly associated with IGF-I in individuals with hsCRP above 3.0 mg/L. Paper-15153077. Insulin-like growth factor-I ( IGF-I) stimulates phosphorylation of filamin A on Ser-2152 in MCF-7 cells and further enhances Ser-2152 phosphorylation over its already high basal level in MCF-7/ Cav1 cells. Paper-12923340. In analyses stratified by IL-6 tertiles, IGF-I was an independent predictor of muscle function only in subjects in the lowest IL-6 tertile, suggesting that the effect of IGF-I on muscle function depends on IL-6 levels. Paper-9800928. Insulin-like growth factor-I- stimulated insulin receptor substrate-1 negatively regulates Src homology 2 domain-containing protein-tyrosine phosphatase substrate-1 function in vascular smooth muscle cells. Paper-15111902. BACKGROUND: The acid-labile subunit ( ALS) acts in the insulin-like growth (IGF) system by binding circulating IGF-I in a ternary complex with binding protein (IGFBP)-3 to prevent IGF-I from crossing the endothelial barrier. Paper-14241759. Polymorphic variants in the CYP3A4, IGF1, and AIB1 genes are associated with increases in the plasma levels of IGF-I among oral contraceptive users and the variant alleles are much more common in black women than in white women. Paper-8710662. RESULTS: Only black men had positive findings: log CRP was significantly associated with IGF-I (beta=-13.1 ng/ml, p=0.02) and the difference in mean IGF-I concentrations between the highest and lowest quartiles of CRP was 26 ng/ml. Paper-14017165. RESULTS: IGF-I concentrations were negatively associated with ghrelin concentrations in the analysis of all subjects before (beta=-0.32, p<0.001) and after adjustments for BMI, insulin levels, sex and age (beta=-0.40, p<0.001). Paper-11077566. Using specific inhibitors of each pathway, we found that the increase in expression of SREBP-1 induced by IGF-1 was blocked in the presence of the PI3-K inhibitor but not in the presence of the MAPK/ ERK inhibitor. Paper-14308212. Furthermore, the ability of the IGF-binding protein-3 mutants to inhibit IGF-I-stimulated phosphorylation of its receptor was a reflection of their affinity for IGF, with the lowest affinity mutants having the least inhibitory effect. Paper-9077442. CONCLUSIONS: Blocking Hsp90 disrupts IGF-I and IL-6- induced proangiogenic signaling cascades by targeting IGF-IR and STAT3 in pancreatic cancer, leading to significant growth-inhibitory effects. Paper-12591181. However, in contrast to KCM, whose efficacy on MMP-1 expression was modestly reduced by either IGF-1 and TGF-beta1, or a combination of both, these factors abrogated the MMP-1 stimulatory effect of stratifin in fibroblasts. Paper-13151484. The observations that IGF-I enhances the TGF-beta signaling and that TGF-beta promotes IGFBP-3 production and thus influence the biological activity of IGF may be of importance for future therapeutic options. Paper-12279199. Genotypic analyses revealed that persons with the IGF-I [cytosine-adenine (CA)](19) or the IGFBP-3 A-202C C allele were associated with lower circulating concentrations of IGF-I (P(trend)=0.01) and IGFBP-3 (P(trend)=0.002), respectively. Paper-12610288. We conclude that SHPS-1 functions as an anchor protein that recruits both Shc and SHP-2 and that their recruitment is necessary for IGF-I-dependent Shc phosphorylation, which is required for an optimal mitogenic response in SMCs. Paper-11096449. These studies were undertaken to determine whether Src kinase activity is required to phosphorylate Shc in response to IGF-I in SMC and because SHP-2 binds to Src whether their interaction was also required for IGF-I-stimulated mitogenesis. Paper-12197181. IGFBP-1 and IGFBP-6 are most sensitive to changes in IGF-II structure, although IGFBP-1 binds IGF-I and IGF-II with equal affinity, whereas IGFBP-6 has a marked preferential binding affinity for IGF-II. Paper-7858548. GH treatment up regulates the level of IGF-I gene expression in older people and when combined with resistance exercise more is spliced towards MGF and hence should improve the ability of muscle to respond to physical activity. Paper-10613098. CONCLUSIONS: In adolescents with T1DM and chronic, poor glucose control, increased serum IL-8 is associated with reduced IGF-1 suggesting a pro-inflammatory milieu that may contribute to alterations in the GH/ IGF-1 axis. Paper-14066810. These data indicate that caveolin-1 specifies filamin A as a novel target for Akt- mediated filamin A Ser-2152 phosphorylation thus mediating the effects of caveolin-1 on IGF-I-induced cancer cell migration. Paper-12923340. Interference with KCC activity by either an inhibitor or a dominant-negative loss-of-function mutant profoundly suppressed the IGF-I- induced membrane trafficking of KCC4 and the structural interaction between KCC4 and ezrin near the cell surface. Paper-14571005. An early mean GH > 4.8 mU L-1 had a 77.8% predictive value for persistent or recurrent disease, compared with 85.7% for persistently increased SmC/ IGF-1 and 68.8% for an abnormal GH release after TRH 3 months after surgery. Paper-8394339. Insulin-like growth factor I ( IGF-I) stimulates smooth muscle cell (SMC) proliferation, and the mitogen-activated protein kinase ( MAPK) pathway plays an important role in mediating IGF-I-induced mitogenic signaling. Paper-11096449. We investigated the mechanism by which IGF-1 affects cell proliferation and invasion by suppression of PTEN phosphorylation and interaction with PI3K/ PTEN/Akt/NF-small ka, CyrillicB signaling pathway in pancreatic cancer. Paper-14525660. IGF-1 and OP-1 each significantly reduced the basal level as well as fibronectin fragment- or IL-1beta- stimulated transcription of the MMP-13 gene in a dose-dependent fashion with the corresponding decreases in the protein level of MMP-13. Paper-9777518. OBJECTIVE: The aim of the study was to determine whether the serum concentration of insulin-like growth factor-I (IGF-I) and its binding protein-3 ( IGFBP-3) correlates with the mineral metabolism markers in children with idiopathic decrease in bone mass. Paper-11408862. Conversely, IGF-I- induced extracellular signal-regulated kinase 1/2 ( ERK1/2) activation was significantly repressed in myoblasts overexpressing Gab1(DeltaSHP2) but enhanced in those overexpressing either Gab1(WT) or Gab1(Deltap85). Paper-12917253. However, an inhibitor of the p21-activated protein kinase-1, glutathione S-transferase-Pak1-(83-149), inhibited both basal and IGF-1- stimulated RUNX2 DNA binding, suggesting that Pak1 mediates IGF-1 signaling to increase RUNX2 activity. Paper-10564271. The IGF-1- induced phosphorylation of the novel phosphorylated Ser666-Pro site was suppressed by AICAR, and by combined mutation of a TOS (mTOR signalling)-like sequence (FEMDI) and rapamycin. Paper-12558619. In the present study, the changes in circulating IGF-1 and its binding protein IGFBP-3 were determined in adult patients with active inflammatory bowel disease (IBD) in order to assess the effect of this inflammatory condition on the IGF system. Paper-9134255. We conclude that IRS-1 is an important factor for maintaining VSMCs in the non-proliferative state and that its down-regulation is a component of the VSMC response to hyperglycemic stress that results in an enhanced response to IGF-I. Paper-15111902. Understanding how iNOS and sodium pump activity are regulated by IGF-1 activation of the PI3K/cPLA(2)/Akt cascade should provide novel and fundamental knowledge regarding the regulatory actions of IGF-1 in promoting vasodilation. Paper-13263623. METHODOLOGY/PRINCIPAL FINDINGS: Using immunoblotting, in vitro kinase and in vivo labeling assays, we show that IGF1 inhibits MST2 cleavage and activation induced by DNA damage through the phosphatidylinosotol 3-kinase (PI3K)/Akt pathway. Paper-14278295. Expression of constitutively active forms of AMPK suppressed IGF-I- stimulated activation of Akt/ TSC2/mTOR/p70S6K and protein synthesis, whereas AMPK knockdown resulted in enhanced responses to IGF-I. Paper-15129510. Insulin-like growth factor I ( IGF-I) stimulates proliferation but also increases caspase-3 activity, Annexin-V binding, and DNA-fragmentation in human MG63 osteosarcoma cells: co-activation of pro- and anti-apoptotic pathways by IGF-I. Paper-10173623. In vitro studies demonstrated that IL-6 inhibits the secretion of insulin-like growth factor I ( IGF-I) and its biological activity, suggesting that the negative effect of IL-6 on muscle function might be mediated through IGF-I. Paper-9800928. When treated with IGF-I and LY294002, decreased NF-kappaB DNA binding activity and increased expression of IkappaBalpha protein were detected in cultured thyroid cells, which further confirmed that NF-kappaB was under the control of the PI3K pathway. Paper-13280279. In addition, when the cells were pre-incubated with LY294002 before IGF-I stimulation, the phosphorylation of Akt-Ser473 and FoxO1-Ser256 was inhibited, implying that phosphorylation of Akt and FoxO1 was downstream of IGF-I- induced PI3K signaling. Paper-9807336. Ceramide-activated caspase-3 was inhibited by IGF-1/PI-3 kinase and enhanced by wortmannin, while the addition of a specific caspase-3 inhibitor DMQD-CHO significantly enhanced the restoration by IGF-1 of ceramide-depleted catalase function. Paper-9229300. Collectively, these results establish that TNFalpha targets IGF-I- induced E2F-1 synthesis, leading to inhibition of the subsequent accumulation in cyclin A, formation of cyclin A- Cdk2 complexes, hyperphosphorylation of RB, and cell cycle arrest. Paper-10399603. Somatomedin-A ( SM-A), insulin-like growth factor II ( IGF-II) and two forms of multiplication stimulating activity (MSA) were less than 5% as potent as SM-C/ IGF-I in the RIA and less than 50% that of SM-C/IGFi in the SM-C receptor assay. Paper-3531654. Either mitogen-activated protein kinase ( MAPK) or phosphatidylinositol 3-kinase ( PI3K) are known to mediate IGF-1 cell proliferative signals through the activation of extracellular signal-regulated kinase 1/2 (Erk 1/2) and Akt, respectively. Paper-13321989. At multivariate analysis, a high transfemoral gradient of CRP was independently associated with a low transfemoral gradient of IGF-1 (beta coefficient = -0.48, P < 0.01), and a high transfemoral gradient of IGFBP-3 (beta coefficient = 0.22, P < 0.05). Paper-13071364. IGF-I, long-R(3)-IGF-I (only binds IGF-I receptor), AL(31)Leu(60)-IGF-I (only binds IGFBPs), antihuman IGF-I receptor antibodies, and IGFBP-1 were then added to LNCaP cultures to determine the independent effects of IGF-I and IGFBP-1 on cell growth. Paper-9708394. Our data indicate that in the physiologically relevant model of primary cultured MSC, IGF-I induces a temporally regulated nuclear or cytoplasmic localization of IRS-1 that correlate with the transition from proliferation to chondrogenic differentiation. Paper-13984810. IGF-1 treatment triggered phosphatidylinositol 3-kinase and mitogen-activated protein kinase ( MAPK) cascades which were differentially required for IGF-1- stimulated biosynthesis of KCC3 and KCC4. Paper-12389656. Inhibition of either phosphatidylinositol 3-kinase ( PI3-K) or Mek1/2 signaling pathways completely abrogated the IGF-I- induced increase in VEGF secretion and promoter activity, indicating a dependence on coordinate signaling from both pathways to produce this effect. Paper-9897301. Insulin induces hepatic IGF-1 secretion, and both hormones amplify the stimulatory effect of GH on sebocytes and augment mitogenic downstream signalling pathways of insulin receptors, IGF-1 receptor and fibroblast growth factor receptor-2b. Paper-13996581. Cyclin-dependent kinase 2 ( Cdk2) mediates this suppression because co-immunoprecipitation experiments revealed that TNFalpha reduces the amount of IGF-I- induced cyclin A that binds Cdk2, leading to a reduction in Cdk2 enzymatic activity. Paper-10399603. Augmentation of basal IGF-I receptor phosphorylation was associated with coordinate increases in basal tyrosine phosphorylation of insulin receptor substrate (IRS)-2 and activation of Erk, which were also minimally responsive to IGF-I stimulation. Paper-12753010. We conclude that in VSMCs exposed to hyperglycemia, IGF-I stimulation of Shc facilitates the transfer of Grb2 to p85 resulting in enhanced PI3K activation and AKT phosphorylation leading to enhanced cell proliferation and migration. Paper-12821263. We have previously shown that the synergistic action of E(2) and IGF-I emanates from the ability of both hormones to induce cyclin D1 expression and that IGF-I action is required to induce activity of the cyclin D1-CDK4 complex, which triggers cell cycle progression. Paper-9292871. Therefore, we investigated the dynamic changes in circulating total, free, and bioactive IGF-I, IGF-binding protein (IGFBP)-1, IGFBP-2, and IGFBP-1- bound IGF-I (binary complex) during an oral glucose tolerance test ( OGTT) in patients with liver cirrhosis. Paper-12155061. Preincubation of cells with a peptide that contains a phospho-tyrosine binding motif sequence derived from SHPS-1 inhibited IGF-I- stimulated SHP-2 transfer to SHPS-1, the association of Shc with SHPS-1, and IGF-I-dependent Shc phosphorylation. Paper-11096449. Because activation of p70s6 kinase is downstream of both PI-3 kinase and p42/44 MAPK activation in osteoblasts treated with IGF-I, this ribosomal kinase represents a convergence point for IGF-I- induced PI-3 kinase and p42/44 MAPK signaling in osteoblastic cells. Paper-10040359. Liganded AR stimulates IGF-1 receptor expression, suggesting the presence of local positive feedback between IGF-1 and AR signaling in PC cells, presumably resulting in higher IGF-1 signaling tension and further enhancing the functions of the receptor itself. Paper-13643294. The link for this point of view comes from the original function of IGF1 during ontogeny/ phylogeny, the promotion of cell survival and control of neural cell numbers, whereas one of the IGF1 functions in the adult brain is the control of hippocampal neurogenesis. Paper-13680742. These data suggest that IGF-I- induced activation of the skeletal alpha-actin promoter is regulated by the L-type VGCC and calcineurin but independent of nuclear factor of activated T-cell transcriptional activity as C2C12 myoblasts differentiate into myotubes. Paper-10384925. Genes with early and sustained regulation by IGF-I were highly enriched for transcriptional targets of the estrogen receptor ( ER), Ras/extracellular signal-related kinase 1/2, and phosphatidylinositol 3-kinase/Akt/mammalian target of rapamycin pathways. Paper-12923051. Insulin receptor substrate 1 ( IRS1) was identified as a target of the GLI1 transcription factor and inhibition of GLI1 was sufficient to obstruct IRS1 protein expression and IGF-I induced mitogen-activated protein kinase ( MAPK) activation. Paper-15643185. IL-6 infusion had no effect on GH binding protein, IGFBP-3, and acid-labile subunit levels. rhIL-6 levels similar to the levels found after strenuous exercise induced a typical exercise-associated GH-->IGF-I axis response (increase GH, decreased IGF-I, and elevated IGFBP-1). Paper-12300784. Overexpression of catalytic-inactive SHP2 modulated IGF-I- induced myogenic differentiation and ERK1/2 activation similarly to that of Gab1(DeltaSHP2), suggesting that Gab1- SHP2 complex inhibits IGF-I-dependent myogenesis through ERK1/2. Paper-12917253. Using a GFP-tagged S1P1 receptor as a biological sensor for the generation of physiologically relevant S1P levels, we found that IGF-1 and IGF-2 induced GFP- S1P receptor internalization and that the effect was blocked by pretreatment with the SK inhibitor, dimethylsphingosine. Paper-12272163. Additionally, 3-OH flavone, baicalein, and quercetin showed effective inhibitory activities against E2/ IGF-I- induced proliferation through suppressing proliferative events such as phosphorylation of IRS-1, ERKs, and JNKs proteins, and induction of c-Jun protein and colony formation. Paper-13321986. Ni(+) [ T-type voltage-gated Ca(2+) channel (VGCC) inhibitor] reduced basal-induced activation of the skeletal alpha-actin promoter by approximately 84%, and nifedipine (L-type VGCC inhibitor) inhibited IGF-I- induced activation of the skeletal alpha-actin promoter by 29-48%. Paper-10384925. The AMPK activator metformin stimulated AMPK Thr172 phosphorylation and inhibited IGF-I- stimulated phosphorylation of Akt/ tuberous sclerosis 2 (TSC2)/mammalian target of rapamycin (mTOR)/p70S6 kinase (p70S6K). Paper-15129510. Here, we report that Pin1(-/-) MEF cells display a delayed cell cycle S-phase entry in response to IGF stimulation and that IGF-1 induces Pin1 protein expression which correlates with the induction of cyclin D1 and RB phosphorylation in human breast cancer cells. Paper-9354285. IGF-1- stimulated ATM phosphorylation at both threonine and tyrosine residues, and our results demonstrated that the phosphorylation of tyrosine in the ATM molecule is important for AMPK-alpha subunit phosphorylation during IGF-1 signaling. Paper-10657189. Mutation of the hypoxia response element (HRE), which mediates hypoxic stimulation of VEGF transcription, did not inhibit the effect of IGF-I on the VEGF promoter, despite the fact that this mutation inhibited PI3-K- stimulated VEGF promoter activity in prostate cancer cells. Paper-9897301. There was a significant combined IGF1 cytosine adenine (CA) repeat gene effect, which included both the IGF1 CA repeat main effect and IGF1 CA repeat x PPP3R1 insertion-deletion (I/ D) gene x gene interaction effect, on the changes in strength ( P < 0.01) and MQ ( P < 0.05) with ST. Paper-12586132. Chemical shift perturbations in 15N- and 2H/15N-labelled IGF-I or -II upon binding to unlabelled thioredoxin-tagged bovine IGFBP-2 (Trx(1-279)IGFBP-2) have been monitored to identify residues involved directly in the binding interaction as well as any affected by conformational changes associated with the interaction. Paper-11190786. In this report, we have identified a new mechanism of apoptosis inhibition by amphiregulin through an IGF1-dependent survival pathway in non-small cell lung cancer (NSCLC) cells: amphiregulin activates the IGF1 receptor that in turn induces the secretion of amphiregulin and IGF1. Paper-9306038. Our previous studies have shown that IGF-I-induced Shc phosphorylation is necessary for sustained activation of MAPK and increased cell proliferation of SMCs, and both Shc and the tyrosine phosphatase SHP-2 must be recruited to the membrane protein SHPS-1 in order for Shc to be phosphorylated. Paper-12197181. This result was confirmed by expressing an IRS-1 mutant that had both impaired binding to IGF-IR and to SHP-2 IGF-I increased SHPS-1 phosphorylation, SHP-2 association with SHPS-1, Shc MAPK phosphorylation, and proliferation in cells expressing the mutant. Paper-15111902. Insulin-like growth factor I ( IGF-I) and epidermal growth factor ( EGF) stimulate KCC4 recruitment from a presumably inactive cytoplasmic pool of endoplasmic reticulum and Golgi to plasma membrane along actin cytoskeleton that is significantly inhibited by LY294002 and wortmannin. Paper-14571005. Further study demonstrated that IGF-I induced the DNA- binding activity of NF-kappaB in association with decreased expression of the NF-kappaB inhibitory protein IkappaBalpha . These findings implied that IGF-I increased FLIP expression by enhancing the activation of NF-kappaB in FRTL thyroid cells. Paper-13280279. We hypothesized that tumor necrosis factor-alpha ( TNF-alpha) stimulated progenitor cell secretion of vascular endothelial growth factor ( VEGF), hepatocyte growth factor ( HGF), and insulin-like growth factor I ( IGF-I) by a p38 mitogen-activated protein kinase (MAPK)-dependent mechanism. Paper-12220121. Cellular exposure to 25 mm glucose, which is required for Shc phosphorylation in response to IGF-I, resulted in enhanced Grb2 binding to p85, activation of PI3K activity, and increased AKT phosphorylation as compared with cells exposed to 5 mm glucose. Paper-12821263. The phosphatidylinositol 3-kinase ( PI3K) inhibitor, LY294002, reduced both basal and IGF-1- stimulated RUNX2 DNA binding activity in the absence of changes in RUNX2 protein as did the overexpression of the phosphatidylinositol 3-phosphate phosphatase, confirming that PI3K signaling mediates RUNX2 activation. Paper-10564271. The responses of growth hormone ( GH) to administration of growth hormone- releasing hormone (GHRH-1 micrograms/kg b.w.) and of clonidine (clon-2.5 micrograms/kg b.w.) and basal levels of somatomedin C ( SmC) were measured in nine peripubertal patients with Major Depressive Disorder ( MDD) and in 9 age- and gender-matched controls. Paper-7959084. By blocking phosphatidylinositol-3-kinase [PI(3)K] or mitogen-activated protein kinase ( MAPK) signaling, we concluded that the increase in total TRPV1 protein content induced by IGF-I was controlled by PI(3)K signaling, whereas insulin seemed to regulate TRPV1 protein expression via both PI(3)K and MAPK pathways. Paper-13211622. These data indicate that IGF-I stimulates VEGF synthesis in thyroid carcinomas in an Akt-dependent pathway via AP-1 and HIF-1 alpha and provide the framework for clinical use of small-molecule inhibitors, including geldanamycin analogs, to abrogate proangiogenic cascades in thyroid cancer. Paper-10040654. Thus, our results demonstrated that: (1) MGF mRNA in skeletal muscle is expressed in parallel with GH action; (2) MGF mRNA in muscle is produced preferentially in the situation of GH deficiency in contrast to the pattern in the GH-sufficient state; and (3) the induction of IGF-I isoforms by GH is tissue-specific. Paper-10922021. Sequence analysis of the IGF1 and IGF1 receptor ( IGF1R) genes of female centenarians showed overrepresentation of heterozygous mutations in the IGF1R gene among centenarians relative to controls that are associated with high serum IGFI levels and reduced activity of the IGFIR as measured in transformed lymphocytes. Paper-14290744. To delineate the role of Gab1 in IGF-I-dependent signaling, we examined the effect of adenovirus-mediated forced expression of wild-type Gab1 (Gab1(WT)), mutated Gab1 that is unable to bind SHP2 (Gab1(DeltaSHP2)), or mutated Gab1 that is unable to bind p85 (Gab1(Deltap85)), on the differentiation of C2C12 myoblasts. Paper-12917253. Having isolated AS160 by 14-3-3-affinity chromatography, we found that binding of AS160 to 14-3-3 isoforms in HEK (human embryonic kidney)-293 cells was induced by IGF-1 ( insulin-like growth factor-1), EGF ( epidermal growth factor), PMA and, to a lesser extent, AICAR (5-aminoimidazole-4-carboxamide-1-b-D-ribofuranoside). Paper-12558619. OBJECTIVE: To investigate whether common genetic variation in IGF1, IGF binding protein 1 ( IGFBP1), and IGFBP3 influences circulating levels of IGF-I, IGFBP-1, and IGFBP-3, we conducted a cross-sectional study of African-American, Native Hawaiian, Japanese-American, Latino, and white men and women in the Multiethnic Cohort. Paper-13425253. IGF-I- induced VEGF protein secretion was not affected by the addition of wortmannin ( IGF-I, 76% vs. IGF-I + wortmannin, 79% increase over control; P = NS), but was abolished by alpha IR3 ( IGF-I, 69% vs. IGF-I +alpha IR3, 0%; P < 0.001) and significantly reduced by PP2 ( IGF-I, 50% vs. IGF-I + PP2, 14%; P < 0.01). Paper-10024097. OBJECTIVE: Our objective was to assess the induction of phosphatase and tensin homolog deleted on chromosome 10 ( PTEN) expression with insulin treatment and effects of PTEN on IGF-I- induced granulosa cell proliferation as well as the correlation of PTEN levels with the concentration of insulin in follicular fluid in PCOS and non- PCOS patients. Paper-13821044. The c-Met ribozyme inhibited IGF-I- and HGF-mediated migration and invasion, indicating that c-Met is essential for these processes. uPA and uPAR inhibition blocked IGF-I- and HGF-mediated migration and invasion, suggesting that uPAR is downstream of IGF/ IGF-IR and HGF/ c-Met in the signaling pathways that mediate cell migration and invasion. Paper-10777532. These synonyms are used for gene IGF1 (insulin-like growth factor 1 (somatomedin C)): Somatomedin-C, MGF, Mechano growth factor, Insulin-like growth factor I, IGF-I, IGFI, IGF1A, IBP1. These accession numbers are used for gene IGF1: P01343 (UNIPROT__AC), BC152321 (NCBI_GENBANK__AC), BC148266 (NCBI_GENBANK__AC), B2RWM7 (UNIPROT__AC). IGF1 is a homologue of IGF1 (insulin-like growth factor 1 (somatomedin C)) from Pan troglodytes. IGF1 is a homologue of IGF1 (insulin-like growth factor 1 (somatomedin C)) from Canis lupus familiaris. IGF1 is a homologue of IGF1 (insulin-like growth factor 1 (somatomedin C)) from Bos taurus. IGF1 is a homologue of IGF1 (insulin-like growth factor 1 (somatomedin C)) from Gallus gallus. IGF1 is a homologue of Igf1 (insulin-like growth factor 1) from Mus musculus. IGF1 is a homologue of Igf1 (insulin-like growth factor 1) from Rattus norvegicus. IGF1 is a homologue of igf1 (insulin-like growth factor 1) from Danio rerio. Important links ! iHOP - Information Hyperlinked over Proteins . Concept & Implementation by Robert Hoffmann.