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S- MK may be a useful tumor marker for esophageal SCC. Paper-9903689.
GPC3, MDK, and SERPINI1 encode known serum proteins. Paper-13123813.
MK and PTN expression also increases upon ischemic injury. Paper-9614858.
The dissociation constant of binding between LRP and MK was 3.5 nM. Paper-10586018.
The expressions of MK and PTN were not correlated with vascular density. Paper-9841919.
ARAP is a single-chain, extremely hydrophilic, heparin-binding protein. Paper-6896307.
Carcinoma-associated antigens MK-1 and CEA in urological cancers. Paper-2206167.
Angiogenic activity of MK and PTN was confirmed in the rabbit corneal assay. Paper-991835.
OBJECTIVE: This study was to clarify the roles of midkine ( MK) in the brain. Paper-12691443.
The HBNF gene shows high sequence homology to another gene, MK (midkine). Paper-7076801.
These findings suggest that LRP is a component of the receptor complex for MK. Paper-10586018.
The biological properties of the MK protein are remarkably similar to those of HBNF. Paper-7076801.
ACTH (1 nm) increased MK mRNA by 3.5-fold (48 h, P < 0.01) in isolated FZ cells. Paper-12261053.
MK was expressed in choroid plexus of normal brain and released there. Paper-12691443.
A total of 14 HCC but none of the noncancerous specimens were positive for the MK mRNA. Paper-9975387.
Recently, the urine and serum MK concentration was analyzed in gastric cancer patient. Paper-13225310.
Therefore, MK and PTN are candidate molecular targets for therapy for human carcinomas. Paper-10402110.
Moreover, the protein expression of MK, but not of PTN, correlated with tumor stage and size. Paper-9841919.
Increased preoperative S- MK in patients with esophageal SCC is associated with poor survival. Paper-9903689.
Furthermore, antisense oligonucleotides for MK and ribozymes for PTN show anti-tumor activity. Paper-10402110.
The newly identified genes were: IFI27, EPST11, APAF1, LAP3, STK6, and MDK. Paper-12176543.
MK and PTN mRNA and protein expressions were examined with respect to tumor stage and size. Paper-9841919.
Underweight, midkine and VEGF-A were found independent indicators of weight loss. Paper-12626726.
Midkine ( MK) has been shown to be present in amyloid deposits in Alzheimer's disease (AD). Paper-891193.
Knockdown of MDK expression significantly attenuated ACSL5-mediated survival under acidic state. Paper-13567773.
Most myotubes labeling for desmin showed MK immunoreactivity 5-7days after the injury. Paper-12281218.
However, the biologic mechanism of MK in hepatocellular carcinoma has not been clarified to date. Paper-10303362.
Pleiotrophin ( PTN) and midkine ( MK) form a distinct family of heparin binding growth factors. Paper-1764460.
Both MK and VEGF promoters also resulted in a high activity in primary cervical cancer cells. Paper-10931830.
ARP sequence has been found to be identical to protein encoded by human MK gene. Paper-6896307.
Chromosomal assignment of the heparin-binding cytokine genes MDK and PTN in mouse and man. Paper-156399.
MK bound to heparan sulfate chains of glypican-2 in a manner similar to syndecan-3. Paper-10707915.
Thus, the HS chains of ryudocan appear to be responsible for its binding to bFGF, MK, and TFPI. Paper-538502.
Western blot and polymerase chain reaction analyses showed that leukocytes were MK positive. Paper-12691443.
CONCLUSIONS: Our study demonstrates that the promoters for MK and VEGF are active in cervical cancer. Paper-10931830.
Midkine ( MK) and pleiotrophin ( PTN) are low molecular weight proteins with closely related structures. Paper-9614858.
Prognostic value of p53 protein and MK-1 (a tumor-associated antigen) expression in gastric carcinoma. Paper-13307369.
Conversely, all of the resected lung cancers (n = 20) expressed MK but only one expressed PTN. Paper-7610284.
Midkine ( MK) and pleiotrophin ( PTN) are two related peptides associated with carcinogenesis and angiogenesis. Paper-9411037.
A chondroitin sulfate proteoglycan, protein-tyrosine phosphatase zeta (PTPzeta), is a receptor for MK and PTN. Paper-9614858.
Human MK, p53, Bax, Bcl-2, and caspase-3 protein content were detected by Western blotting. Paper-13113311.
The expressions of MK and PTN protein in cancerous tissue were higher than those in the normal cervix (P < 0.05). Paper-9841919.
This analysis revealed that all normal lung tissues examined (n = 17) expressed PTN but only two expressed MK. Paper-7610284.
Midkine ( MK) is a heparin- binding growth factor that occurs as a product of the retinoic acid-inducible gene. Paper-9515426.
Retinoic acid induced the expression of HBNF and MK 6- and 11-fold, respectively, in this cell line. Paper-6860636.
In the first set, only the native E1A promoter was replaced by the COX-2, MK, or E2F1 promoter, respectively. Paper-11342422.
After binding to cells, MK enters cells by an active process in which nucleolin and lipid rafts appear to be implicated. Paper-11391872.
These cells do not express ALK and IRS family members, and do not respond to exogenously added PTN or MK. Paper-13102117.
These results suggested that MK induced growth of ameloblastoma is through the MAPK and Akt pathways. Paper-10207352.
In this study, we investigated the roles of ESCRTs in EGFR recycling after stimulation with amphiregulin ( AR). Paper-14030913.
Microbeads coated with MK or poly-L-lysine induced clustering of glypican-2 as well as syndecan-3. Paper-10707915.
OBJECTIVE: The aim of this study was to determine midkine ( MK) and pleiotrophin ( PTN) expression in cervical cancer. Paper-9841919.
These results demonstrated a striking reciprocal expression pattern of MK and PTN in normal versus malignant lung tissue. Paper-7610284.
We describe a child with Wilms' tumor ( WT) which occurred in an unequivocal multicystic dysplastic kidney ( MDK). Paper-7950833.
In this study, we investigated TXS expression as a model of a gene regulated by NF-E2 during MK differentiation. Paper-8414789.
Total RNA was extracted and reverse transcribed into cDNA, and QC-PCR was performed to evaluate PTN and MK mRNA expression. Paper-9411037.
MDK may be especially susceptible to calcineurin-inhibitor ( CI) mediated vasoconstriction and nephrotoxicity. Paper-9947578.
However, urokinase-type plasminogen activator ( uPA) expression and tumor invasiveness did not correlate with MK expression. Paper-1176118.
In the third set, we substituted the viral E1A and E4 promoters with the COX-2, MK, or E2F1 promoter, respectively. Paper-11342422.
The HBNF gene is expressed in the brain of adult mice and rats, but only minimal expression of MK was observed in this tissue. Paper-6860636.
HBNF is structurally and most likely functionally related to the product of a developmentally regulated gene, MK (midkine). Paper-118824.
Pleiotrophin ( PTN) and midkine ( MK) are members of a family of developmentally regulated, secreted heparin-binding proteins. Paper-701555.
Pleiotrophin ( PTN) and midkine ( MK) mRNA expression in eutopic and ectopic endometrium in advanced stage endometriosis. Paper-9411037.
ES and NB are sensitive to Ad infection, and advanced NBs express a high level of the growth/differentiation factor midkine ( MK). Paper-9088186.
Objective: The objective of this study was to investigate expression, proliferative effects, and ACTH regulation of MK in the HFA. Paper-12261053.
The aim of this study is to evaluate the clinical significance of S- MK in patients with esophageal squamous cell cancer ( SCC). Paper-9903689.
METHODS: The expression of p53 protein and MK-1 antigen was investigated in specimens from 42 patients with gastric carcinoma. Paper-13307369.
The apparent dissociation constants for purified ryudocan were as follows: bFGF, 0.50 nM; MK, 0.30 nM; and TFPI, 0.74 nM. Paper-538502.
Construction of a fusion protein expression vector MK- EGFP and its subcellular localization in different carcinoma cell lines. Paper-12357067.
The expressions of MK and PTN mRNA and protein were examined by quantitative competitive PCR and by immunohistochemistry. Paper-9841919.
Polymerase chain reaction revealed the presence of a short MK mRNA in 7 among 12 human tumor cells which expressed MK mRNA. Paper-533718.
STS cells also expressed the MK receptors protein tyrosine phosphatase zeta and lipoprotein receptor-related protein. Paper-12907068.
An affinity purified antibody specific for midkine ( MK) stained senile plaques in the brain of Alzheimer disease (AD) patients. Paper-7861978.
The midkine ( MK) family consists of only two members, namely heparin-binding growth factors MK and pleiotrophin ( PTN). Paper-10402110.
Like HBNF, the MK gene is developmentally regulated, however, high expression occurs in most fetal tissues during mid-gestation. Paper-7076801.
To examine a role for MK and the related pleiotrophin ( PTN) in tumorigenesis, they were overexpressed in MCF-7 breast carcinoma cells. Paper-991835.
The specific binding of MK to the surface nucleolin is independent of heparan sulfate and chondroitin sulfate proteoglycans. Paper-11391872.
We have investigated by RNase protection analysis the expression of MK in 47 primary bladder tumors and 7 normal bladder samples. Paper-569467.
The expression of MK and PTN is increased in various human tumors, making them promising as tumor markers and as targets for tumor therapy. Paper-9614858.
METHODS: Quantitative changes in protein levels of MDK and EAAT1 were investigated in alcoholic and control cases using Western blots. Paper-13021330.
In contrast, the appican CS from SH-SY5Y neuroblastoma cells contained no E disaccharide and showed no binding to either MK or PTN. Paper-10373887.
Our results suggest increased MK and PTN expression may be related to the initiation of ectopic endometrial implants and peritoneal invasion. Paper-9411037.
We conclude that MK can act as a growth, survival, and angiogenic factor during tumorigenesis and signals through the ALK receptor. Paper-9171245.
Enhanced tumor growth correlated with increased vascular density and endothelial proliferation, implicating an angiogenic role for MK and PTN. Paper-991835.
MK may have a role for differentiation during skeletal muscle regeneration and may be taken up in an autocrine fashion with LRP. Paper-12281218.
During embryogenesis, MK is highly expressed in the mid-gestational period, whereas PTN expression reaches the maximum level around birth. Paper-10402110.
HBNF and MK, members of a novel gene family of heparin-binding proteins with potential roles in embryogenesis and brain function. Paper-7076801.
Correspondingly, the combination of exogenous MK and high glucose enhanced MCP-1 expression in Mdk(-/-) cells. Paper-13391917.
Impact of weight loss on circulating IL-1, IL-6, IL-8, TNF-alpha, VEGF-A, VEGF-C and midkine in gastroesophageal cancer patients. Paper-12626726.
We developed a CI-free protocol of antibody induction, sirolimus, mycophenolate mofetil, and prednisone in recipients with MDK or DGF. Paper-9947578.
Full-length HB-GAM is not a mitogen for Balb/3T3 clone A31, Balb MK, NRK, or human umbilical vein endothelial cells. Paper-55997.
The purpose of this study was to examine regulation of MK by GC and RA during postnatal alveolar formation in rats. Paper-13979252.
Most patients with p53- and MK-1-positive gastric carcinomas and those more than five metastatic lymph nodes had a poor prognosis. Paper-13307369.
We have examined the expression of midkine ( MK), a neurotrophic factor with heparin-binding activity, in human esophageal cancer cells. Paper-1890405.
Midkine ( MK) and heparin-binding growth-associated molecule/pleiotrophin form a new family of heparin-binding growth/differentiation factors. Paper-7641216.
Autopsy brain samples from patients with meningitis expressed MK weakly in mononuclear cells on immunohistochemical examination. Paper-12691443.
MK significantly enhanced STS cell growth potentially via the Src and extracellular signal-regulated kinase pathways. Paper-12907068.
Interestingly, KAF stimulated the growth of BALB/ MK cells at high cell density but failed to stimulate these cells at clonal density. Paper-30347.
BACKGROUND/AIMS: Aberrant expression of Midkine ( MK) has been found in various human carcinomas including hepatocellular carcinoma ( HCC). Paper-2070690.
In MK-producing lymphocytes, MK is detectable at the cell surface where it colocalizes with the surface- expressed nucleolin. Paper-8713803.
Our results suggest that the cell surface-expressed nucleolin serves as a low affinity receptor for MK and could be implicated in its entry process. Paper-9171541.
Consistently, a significant increase in serum midkine, encoded by MDK, was associated with HCC patients, including those with normal serum AFP. Paper-13123813.
From the microarray study, we selected five candidate genes (i.e., GPC3, PEG10, MDK, SERPINI1, and QP-C), which were overexpressed in HCCs. Paper-13123813.
Immunohistochemical expression of MK and CD34 was evaluated in pancreatic head carcinoma specimens from 75 patients who underwent surgical resection. Paper-13364955.
RESULTS:: All cytokines were elevated in cancer patients with further up-regulation of IL-6, IL-8, midkine and VEGF-A in cachexia. Paper-12626726.
This sequence was compared to those of HBGAM and MK protein, two other heparin binding proteins exhibiting growth and/or neurotrophic activities. Paper-6970760.
Purified KAF stimulated the growth of normal human keratinocytes, mouse AKR-2B cells, and a mouse keratinocyte cell line (BALB/ MK). Paper-30347.
In addition, deposits of MK and/or PTN are found in neurodegenerative diseases, such as Alzheimer's disease and multiple system atrophy. Paper-10402110.
An epidermal growth factor-like growth factor, amphiregulin ( AR), which was not expressed by untreated cells, was strongly induced by PGE(2). Paper-10829074.
As amphiregulin ( AREG) is another heparin-binding factor of the EGF family, we investigated its role in multiple myeloma ( MM). Paper-10971552.
4) This peptide abolished the biological activity of MK to enhance the plasminogen activator activity in bovine aortic endothelial cells. Paper-974744.
S- MK values in patients with esophageal SCC were significantly higher than those in healthy controls (417 +/- 342 pg/ml vs. 154 +/- 76 pg/ml, P < 0.001). Paper-9903689.
A drug coupled to an NGR peptide has more potent antitumor effects than the free drug [W. Arap et al., Science ( Washington DC), 279: 377-380, 1998]. Paper-2107871.
RESULTS: TGFalpha, Amphiregulin ( ARG) and CM from Rasmt cells (Rasmt-CM) resulted in an increased clonogenic survival of irradiated Raswt cells. Paper-11536694.
Thus, AR and IGF1 cooperate to prevent apoptosis by activating a specific PKC-p90(rsk)-dependent pathway, which leads to Bad and Bax inactivation. Paper-10758315.
We investigated the expression of the truncated MK mRNA in specimens of 47 surgically removed human gastrointestinal organs using polymerase chain reaction. Paper-1532708.
Amphiregulin ( AR) and insulin-like growth factor-1 ( IGF1) are growth factors known to promote non-small cell lung cancer (NSCLC) survival. Paper-10758315.
CI-free protocols may allow expansion of the kidney donor pool by encouraging utilization of MDK at high risk for DGF or CI-mediated nephrotoxicity. Paper-9947578.
CONCLUSIONS: These results suggest that MK is expressed in the majority of HCC tissues and rarely in surrounding tissues in chronic liver diseases. Paper-2070690.
These results suggest that dimer formation through transglutaminase- mediated cross- linking is an important step as to the biological activity of MK. Paper-974744.
Within the NF1 group, MK levels increased dramatically at puberty from an average of 0.79 ng/mL in patients <18 years to 1.18 ng/mL in patients >18 years old. Paper-10858362.
The results demonstrate that expression of MK and Abeta is not an exclusive feature of amyloid deposits in Alzheimer brain, but is also found in LB brain. Paper-891193.
Midkine ( MK) is a 13 kDa heparin-binding polypeptide which enhances neurite outgrowth, neuronal cell survival and plasminogen activator activity. Paper-1282614.
CONCLUSIONS: The conclusion is that VUR contralateral to the MDK is associated with small kidneys and reduced renal growth both at birth and at 2 years of life. Paper-8999184.
After formic acid treatment, plaque staining was dramatically enhanced, and almost all beta-amyloid protein ( BAP) deposits were also immunoreactive for MK. Paper-7861978.
The regression equations were Y=0.005X+0.498 (Y, CSF MK level; X, cell number) and Y=0.007X+0.326 (Y, MK level; X, protein level) for all CSF samples. Paper-12691443.
Confocal immunofluorescence laser microscopy revealed the colocalization of MK and the cell-surface- expressed nucleolin at distinct spots. Paper-9171541.
Confocal immunofluorescence laser microscopy revealed the colocalization of MK and the cell-surface- expressed nucleolin at distinct spots. Paper-11391872.
Complementary DNA constructs coding for the mature HBNF and MK proteins were expressed in bacteria and purified by heparin affinity chromatography. Paper-6860636.
These data suggest that the MK promoter can activate a therapeutic gene preferentially in HCC and is as useful as the AFP promoter in clinical settings. Paper-9975387.
Using real-time reverse transcriptase-polymerase chain reaction, we found that MM cells expressed ErbB receptors and that AREG promoted their growth. Paper-10971552.
We found that MK mediated an integrin-dependent tyrosine phosphorylation of FAK and activation of paxillin and Stat1alpha pathways. Paper-13093370.
Recruitment of insulin receptor substrate-1 and activation of NF-kappaB essential for midkine growth signaling through anaplastic lymphoma kinase. Paper-13102117.
Stem cell factor and MK concentrations above a defined threshold in serum of NF1 patients are of diagnostic benefit for 96% of patients in the cohort tested. Paper-10858362.
Conclusion: Antisense oligonucleotides targeting MK shows therapeutic effects on HCC; ASODN5 has the possibility to be developed as an effective antitumor agent. Paper-12320973.
The combination of AR and IGF1 increases p90(rsk) and Bad phosphorylation as well as inhibiting the conformational change of Bax by a PKC-dependent mechanism. Paper-10758315.
The second human gene identified in this study, called MK, codes for a 143-residue protein (including a 22-amino acid signal sequence) which is 46% homologous with HBNF. Paper-6860636.
Pharmacological interventions indicated that MK-induced DZ cell proliferation may be mediated by phosphatidylinositol 3-kinase, MAPK kinase, and Src family kinases. Paper-12261053.
The available evidence suggests that HBNF and MK are members of a new family of genes with potential roles in fetal development and in brain function or maintenance. Paper-7076801.
RESULTS: A combination of the RNAs CDC2, MDK, IGFBP5, and HOXA13 detected 48%, 90%, and 100% of stage Ta, T1, and >T1 TCCs, respectively, at a specificity of 85%. Paper-12720500.
MK and PTN share receptors, and show similar biological activities that include fibrinolytic, anti-apoptotic, mitogenic, transforming, angiogenic, and chemotactic ones. Paper-10402110.
In addition, MK protein expression in cultured human alveolar type 2-like cells treated with DEX and RA was also determined. Paper-13979252.
MK and PTN promote the growth, survival, and migration of various cells, and play roles in neurogenesis and epithelial mesenchymal interactions during organogenesis. Paper-9614858.
In studies reported here, the expression of the angiogenic growth factor pleiotrophin ( PTN) and homolog midkine ( MK) was assessed in resected normal and malignant lung tissues. Paper-7610284.
This study showed that MK mRNA expression increased in association with differentiation by E5166, but not by dbcAMP in SK-N-SH and KP-N-RTBM1 human NB cell lines. Paper-877170.
Preparation of human IgG and IgM monoclonal antibodies for MK-1/ Ep-CAM by using human immunoglobulin gene-transferred mouse and gene cloning of their variable regions. Paper-11768942.
This aim of this study is to screen for suitable antisense oligonucleotides (ASODN) targeting MK in hepatocellular carcinoma ( HCC) cells and evaluate its antitumor activity. Paper-12320973.
Furthermore, FAS promoter can drive the therapeutic gene in a wider range of human breast cancers than cerbB2 promoter and exhibit a stronger activity than midkine ( MK) promoter. Paper-13352466.
MK and PTN mRNA expression in ectopic endometrium was significantly lower than that in eutopic endometrium from women with and without endometriosis (P < 0.05). Paper-9411037.
Midkine ( MK), a retinoic acid-inducible growth/differentiation factor, serves as a substrate for tissue transglutaminase (Kojima, S. , Muramatsu, H., Amanuma, H., and Muramatsu, T. Paper-974744.
Midkine ( MK) is a heparin- binding growth factor with its gene first identified in embryonal carcinoma cells at early stages of retinoic acid-induced differentiation. Paper-13580179.
Milder hydrolysis conditions removed from O-3 other side-chains containing Fucp and Araf nonreducing end-units and internal Arap, and 2-O- and 3-O-substituted Araf units. Paper-9949318.
Strong expression of PTN is also detected in several carcinomas, although, in general, MK is expressed more intensely and in a wide range of carcinomas than PTN. Paper-10402110.
Using 300 pg/ml as the cut-off value (representing the mean + 2 standard deviations of the S- MK of healthy controls), 61% of patients with esophageal SCC were classified as positive. Paper-9903689.
Expression of human recombinant HBNF and MK in Escherichia coli lead to the formation of insoluble aggregated protein that accounted for about 25% of the total cellular protein. Paper-118824.
In conclusion, this study shows that TXS is coordinately expressed with the other platelet proteins during MK differentiation but is not directly involved in platelet formation. Paper-8414789.
We found that inhibition of mitochondrial respiration and mitochondrial DNA ( mtDNA) depletion resulted in induction of amphiregulin ( AR) expression in HepG2 cells. Paper-13887583.
Our data indicate that MK plays a critical role in the tubulointerstitial inflammation associated with diabetic nephropathy through activation of the MCP-1 pathway. Paper-13391917.
CPK and MDK isozyme patterns of the heart muscle in cases of sudden death were studied to investigate the relationship between their changes and the causes of death. Paper-3610285.
We show that expression of ALK plus IRS-1 renders these cells independent of IL-3 owing to the activation of ALK by endogenous MK. Paper-13102117.
CONCLUSION: A CI-free protocol with antibody induction and sirolimus results in low rates of AR and PNF and excellent early patient and graft survival in patients with MDK and DGF. Paper-9947578.
The growth factor midkine ( MK) has been reported to bind heparan sulfate and nucleolin, two components of the cell surface implicated in the attachment of HIV-1 particles. Paper-8713803.
The analysis revealed that ACSL5 was critical to the expression of tumor-related factors including midkine ( MDK), a heparin-binding growth factor frequently overexpressed in cancer. Paper-13567773.
Midkine ( MK) is a novel heparin- binding growth factor whose gene has been identified in embryonal carcinoma cells in early stages of retinoic acid-induced differentiation. Paper-8509962.
Real-time polymerase chain reaction confirmed expression level changes seen by microarray analysis of candidate genes such as PLA2G2A, CDK8, CASP7, MDK, and NKX3. Paper-11610667.
Midkine ( MK), a neurotrophic polypeptide of which expression is developmentally regulated in embryogenesis, is expressed in malignant tumor tissues including neuroblastoma ( NB). Paper-877170.
We conclude that the recruitment of IRS-1 to activated ALK and the activation of NF-kappaB are essential for the autocrine growth and survival signaling of MK. Paper-13102117.
The aim of this study was to evaluate the clinicopathological significance of serum midkine concentration (S- MK) in patients with superficial esophageal squamous cell carcinoma ( SCC). Paper-9751011.
Our studies indicate that HBNF and MK are members of a new family of highly conserved, developmentally regulated genes that may play a role in nervous tissue development and/or maintenance. Paper-6860636.
Here, we identified the growth factor midkine ( MK) as a novel key molecule involved in inflammation associated with Streptozotocin- induced diabetic nephropathy. Paper-13391917.
In vitro experiments using human umbilical vein endothelial cells confirmed the potent angiogenic action of MK via the PI3K/ Akt pathway. Paper-13524060.
Here, we investigated the tumor specificity of both MK and COX-2 promoters in human pancreatic cancer, with the aim to improve the selectivity of therapeutic gene expression. Paper-8904212.
RESULTS: Concentrations of midkine ( MK) and stem cell factor, but not epidermal growth factor, were substantially increased in serum of NF1 patients when compared with healthy controls. Paper-10858362.
Eutopic endometrium from endometriosis patients showed increased expression of MK and PTN mRNA compared with endometrium from normal women in the luteal phase (P < 0.05). Paper-9411037.
Additionally, the study aimed to expand our understanding of MDK and EAAT1 action by localizing their expression within morphologically and functionally distinct layers of this brain region. Paper-13021330.
A conditionally replicative Ad in which the expression of E1 is controlled by the MK promoter achieved good levels of viral replication in NB or ES and induced remarkable tumor cell killing. Paper-9088186.
In this study, the appican CS chain from rat C6 glioma cells was shown to specifically bind several growth/differentiation factors including midkine ( MK) and pleiotrophin ( PTN). Paper-10373887.
Consistent with the findings in the mouse model, MK expression was detected in the glomeruli, tubular epithelium and interstitium of kidneys from patients with diabetic nephropathy. Paper-13391917.
In the inflammatory synovitis of rheumatoid arthritis and osteoarthritis, MK was detected in synovial fluid, synoviocytes, and endothelial cells of new blood vessels. Paper-1200172.
We conclude that MK-1 containing HS is highly beneficial for overcoming the in vitro developmental block of IVF-derived feline embryos and increasing the success rate of IVF/ET. Paper-1475714.
S- MK was measured by enzyme-linked immunosorbent assay in 135 healthy controls, 16 patients with benign esophageal disease, and 93 patients with primary esophageal SCC before surgery. Paper-9903689.
This report describes the cloning, expression and characterization of two members of a novel human gene family of proteins, HBNF and MK, which exhibit neurite outgrowth-promoting activity. Paper-6860636.
High glucose upregulated MK expression in primary-cultured tubular epithelial cells, and induced MCP-1 to a larger extent in Mdk(+/+) cells than in Mdk(-/-) cells. Paper-13391917.
The growth factor midkine ( MK) is a cytokine that inhibits the attachment of human immunodeficiency virus particles by a mechanism similar to the nucleolin binding HB-19 pseudopeptide. Paper-9171541.
Using human alveolar type 2 (AT2)-like cells differentiated in culture, we confirmed that DEX and cAMP decreased, and RA increased MK expression. Paper-13979252.
MK immunoreactivity was observed in the myoblast-like cells and myotubes, which were desmin-positive cells, whereas it was not detectable in the surviving normal muscle fibers. Paper-12281218.
We concluded that MK could be an important factor in differentiation of NB cells, and further, that there could be at least two pathways in differentiation of NB cells at molecular mechanism. Paper-877170.
Increased cellular response to MB was limited to the MS and OND groups, whereas high and low values of stimulation index to MK and ML were similarly observed in all groups of individuals examined. Paper-3612366.
The use of various deletion constructs of nucleolin then indicated that the extreme C-terminal end of nucleolin, containing repeats of the amino acid motif RGG, is the domain that binds MK. Paper-9171541.
The use of various deletion constructs of nucleolin then indicates that the extreme C-terminal end of nucleolin, containing repeats of the amino acid motif RGG, as the domain that binds MK. Paper-11391872.
OBJECTIVE:: Proinflammatory cytokines are involved in cancer-related weight loss, but the involvement of VEGF-A, VEGF-C, IL-8 and midkine in gastroesophageal cancer patients remains unknown. Paper-12626726.
Elucidating the molecular mechanisms of PTN and MK action could lead not only to a deeper understanding of developmental processes, but also to the ultimate identification of targets for tumor therapy. Paper-701555.
Cell cultures derived from four independent fetal skin donations were consistent for cell growth, protein concentration, and gene expression of MDK, PTN, TGF-beta1, and OPG. Paper-12608691.
AIMS/BACKGROUND: Midkine ( MK) is a novel heparin- binding growth factor whose gene was identified in embryonal carcinoma cells in the early stages of retinoic acid-induced differentiation. Paper-8659573.
The effects of PSK on proliferation and apoptosis induced by TXT in gastric cancer cells were evaluated in vitro using a human gastric cancer cell line, MK-1. Paper-13751728.
In the present study, human mAbs were prepared against a pancarcinoma antigen, MK-1 ( Ep-CAM), using a genetically-engineered mouse (KM mouse) that contains the human immunoglobulin genes. Paper-11768942.
BACKGROUND/AIMS: Midkine ( MK) is a novel heparin- binding growth factor whose gene has been identified in embryonal carcinoma cells in early stages of retinoic acid-induced differentiation. Paper-8643189.
In addition, staining by anti- TXS antibody of proplatelet bearing MKs was not increased in comparison to that observed in mature MK, suggesting that TXS is not upregulated during platelet formation. Paper-8414789.
The present results showed for the first time that intestinal inflammation upregulates the MK- RPTP-beta system, which may stimulate mucosal regeneration during the process of healing of colitis. Paper-12214492.
In Experiment II, the effect of dish type ( tissue culture dish, TCD, versus suspension culture dish, SCD) on embryo development was evaluated in MK-1 supplemented with either HS or BSA. Paper-1475714.
In addition, we observed different localization of epitope-tagged glypican-2 and syndecan-3 on the surface of N2a cells; the result suggested that they may play different roles in MK-mediated neural function. Paper-10707915.
The widespread downregulation of PTN and MK in the adult human is reverted in a number of cancers, in which polypeptides are able to act as both transforming growth factors and promoters of angiogenesis. Paper-701555.
Small interfering RNA-mediated knockdown of the endogenous MK or p65/NF-kappaB revealed that both these are rate limiting for the transformed phenotype induced by ALK plus IRS-1. Paper-13102117.
Heparin affin regulatory peptide (HARP), also called Pleiotrophin ( PTN), is a polypeptide that displays a high affinity for heparin and that shares approximately 50% sequence homology with Midkine ( MK). Paper-689362.
In the ex vivo experimental system, PSK enhanced the growth inhibition and apoptosis induced by TXT in the MK-1 cells and reduced the increased invasive ability induced by TXT. Paper-13751728.
However, the relevance of PTN expression itself is unknown especially since, besides PTN, at least one more growth factor, midkine ( MK), signals through ALK and is expressed in glioblastoma. Paper-11240319.
AIM: To synthesize antisense oligonucleotides (ASODNs) of midkine ( MK), package the ASODNs with nanoparticles, and to inhibit hepatocellular carcinoma ( HCC) growth using these nanoparticles. Paper-13740601.
However, in contrast to HAT, PAR-2 AP could not cause AR release into extracellular space; it appears that activation of PAR-2 is not sufficient for HAT- induced AR release. Paper-11514033.
Finally, PKCdelta, PKCzeta, or p90(rsk) small interfering RNAs block the antiapoptotic activity of AR/ IGF1 combination but have no effect on partial apoptosis inhibition observed with each factor used alone. Paper-10758315.
PTN and MK are expressed during embryogenesis, showing an expression pattern that suggests functions in neurogenesis, cell migration, secondary organogenetic induction, and mesoderm-epithelial interaction. Paper-701555.
We showed for the first time that MK interacted with TSPAN1 and facilitated the association between TSPAN1 and integrin alpha6beta1 proteins in head and neck squamous cell carcinoma (HNSCC) cells. Paper-13093370.
RESULTS: When analyzed by flow cytometry, MK-1 was positive in 2 out of 3 bladder, 3 out of 3 prostate and one out of 4 renal tumor cell lines, whereas CEA was negative in all the 10 tumor cell lines. Paper-2206167.
Thus, PGE(2)-activated myofibroblasts promoted the proliferation and migration of intestinal epithelial cells, which were attenuated by neutralizing antibodies to AR and HGF, respectively. Paper-10829074.
METHODS: We determined cerebrospinal fluid MK levels in patients with neurological disorders by enzyme- linked immunoassay and immunostained autopsied brain samples in patients with meningitis. Paper-12691443.
CONCLUSION: Using the minimal promoter region of MK to drive the HSV-TK gene and in vivo electroporation to transduce IL-21 DNA into the tumors produced an efficient gene therapy with improved safety. Paper-13386768.
Altogether, our data provide strong evidence that AREG plays an important role in the biology of MM and emphasize the advantages of using ErbB inhibitors, which might target myeloma cells as well as the tumor environment. Paper-10971552.
We indicate a current nonsurgical approach to MDK, but stress the probable malignant degeneration of blastemal cells, the need to search carefully for the WT in the MDK, and the necessity on 3-monthly follow-up US studies. Paper-7950833.
Among these, midkine ( MDK), a heparin-binding growth factor, was overexpressed in all drug-resistant cell lines, strongly suggesting that MDK might contribute to multidrug resistance in gastric cancer cells. Paper-10347976.
Midkine, pleiotrophin ( PTN), and their receptors syndecan-3 and receptor protein tyrosine phosphatase beta/zeta, were highly expressed in the striatum during development. Paper-13188435.
These observations show that HAT induces AR production through the PAR-2 mediated ERK pathway, and then causes AR release by a TACE-dependent mechanism. Paper-11514033.
EGF, FGF-2, IGF-1, IGF-2, TGF-beta1, and TGF-beta2 were chemotactic for one or two of the cell lines (2- to 4-fold effects), whereas PDGF-AA, PDGF-BB, VEGF, PTN, and MK had no effect. Paper-9734356.
In addition, phosphorylation of PKCdelta and PKCzeta/lambda, but not of PKCalpha/beta(II), increases in serum-starved H358 cells and in H322 cells treated with an AR/ IGF1 combination and is blocked by calphostin C. Paper-10758315.
The binding of labeled MK to cells is prevented by excess unlabeled MK or by the anti-HIV pseudopeptide HB-19 that blocks HIV entry by forming a stable complex with the cell-surface- expressed nucleolin. Paper-8713803.
CONCLUSION: Our findings suggested that MK may maintain normal adult brain as a neurotrophic factor, and that MK may be released from leucocytes in brain of patients with meningitis as an immunological mediator. Paper-12691443.
METHODS: Adult renal transplant recipients who received MDK or had DGF were treated with a CI-free protocol consisting of antibody induction (basiliximab or thymoglobulin), sirolimus, mycophenolate mofetil, and prednisone. Paper-9947578.
BACKGROUND: MK-1, the target molecule of FU- MK-1, is encoded by the GA733-2 gene, which is currently being used as a target in clinical trials for gastric, intestinal and biliary cancer treatment with monoclonal antibodies. Paper-13307369.
The results thus suggest that MK expression is involved in the development and progression of pancreatic ductal adenocarcinomas induced by BOP in hamsters, with loss of upregulation by retinoic acid. Paper-8580016.
These in vivo changes induced by exogenous MK were associated with activation of PI3K/ Akt and MAPKs ( ERK, p38) and expression of syndecans in the left ventricular tissue. Paper-13524060.
METHODS: Different dosages of Cd (0.5-1-5-10 mug/mL) were applied to Hep3B cells and their effects to apoptosis, lactate dehydrogenase ( LDH) leakage and midkine secretion were evaluated as time dependent manner. Paper-12680608.
Previous results have shown that HAT enhances the release of amphiregulin ( AR); further, it causes MUC5AC gene expression through the AR-epidermal growth factor receptor pathway in the airway epithelial cell line NCI-H292. Paper-11514033.
MK-1 expression was more frequent in cardia tumors (71%), in large (>3 cm) tumors (60%-64%), and in specimens from patients with more than five metastatic lymph nodes (69%). p53 expression was present in 20 (48%) of the 42 cases. Paper-13307369.
Midkine ( MK), a heparin binding growth factor, and cyclooxygenase-2 ( COX-2), a key enzyme in the conversion of arachidonic acid to prostaglandin, are both up-regulated at the mRNA or protein level in many human malignant tumors. Paper-8904212.
CONCLUSION: The study found that the expression of both p53 and MK-1 was frequent in aggressive gastric carcinomas; however, extensive lymph node involvement (more than five nodes) was the only significant factor related to overall survival. Paper-13307369.
Initially, metanephric kidney ( MK) explants harvested from embryonic day 15 Sprague-Dawley rats were infected with adenoviral vectors (rAd) encoding human bFGF or LacZ genes and transplanted under the renal capsule of adult female rats. Paper-12059746.
Immunoreactivity of low-density lipoprotein receptor-related protein ( LRP), a cell membrane receptor of MK, was detected in the regenerating muscle cells, whereas it was not detected in the normal adult skeletal muscle and surviving muscle. Paper-12281218.
DEX treatment of rat pups decreased, and RA treatment increased lung MK expression, whereas concurrent DEX+RA treatment prevented the DEX- induced decrease in MK expression. Paper-13979252.
We recently demonstrated that the growth factors pleiotrophin (PTN) and midkine ( MK) are ligands for ALK and that upon ALK activation, insulin receptor substrate-1 ( IRS-1) and other substrates are phosphorylated. Paper-13102117.
CONCLUSIONS:: IL-6 and IL-8, and probably midkine and VEGF-A, appear to participate in the development of cancer-related cachexia in gastroesophageal malignancies, although a detailed mechanism underlying cytokine involvement needs to be elucidated. Paper-12626726.
Transcript differentials were validated using real-time PCR and subsequent immunohistochemical analysis confirmed protein expression for several of the most interesting changes ( MDK, c-MET, VEGF, POSTN, CYP17A1, ITGB1BP3/ MIBP and TRIM63). Paper-13601305.
AIM: To construct an expression plasmid encoding human wild-type midkine ( MK) and enhanced green fluorescence protein ( EGFP) fusion protein ( MK- EGFP), and to analyze the subcellular localization of MK in different carcinoma cell lines. Paper-12357067.
Luciferase assays showed that the SUR regulatory region exhibited the greatest activity and that the MK regulatory region activated the reporter gene better than the enhancer- linked AFP promoter even in high- AFP-producing cells. Paper-9835731.
We have previously published that 1) AR and IGF1, secreted by H358 NSCLC cells, cooperate to protect those cells and H322 NSCLC cells from serum-starved apoptosis; 2) H358 cells resist Bax-induced apoptosis through an inhibition of Bax conformational change. Paper-10758315.
Finally, HAT-induced AR release was eliminated by blockade of tumour necrosis factor alpha-converting enzyme ( TACE) by the TAPI-1 and RNA interference, suggesting that TACE activity is necessary for HAT- induced AR release. Paper-11514033.
MK binds to anaplastic lymphoma kinase ( ALK), the receptor for PTN, with an apparent K(d) of 170 pm in intact cells, and this receptor binding of MK is competed by PTN with an apparent K(d) of approximately 20 pm. Paper-9171245.
Methylation analysis and oligosaccharide analysis showed that A-I and A-II also contained highly branched Ara chains possessing Araf side-chains attached at positions 3 of some 4- or 5- linked Ara and that a small proportion of Arap was present in each acidic unit. Paper-5645698.
HAT-induced AR gene expression was mediated by extracellular signal-regulated kinase ( ERK) pathway, as pretreatment of cells with ERK pathway inhibitor eliminated the effect of HAT on AR mRNA. Paper-11514033.
DESIGN AND METHODS:: Serum IL-1, IL-6, IL-8, TNF-alpha, VEGF-A, VEGF-C, and midkine were evaluated in 96 cancer patients and 42 controls using ELISAs and were related to the occurrence of weight loss, patient's age, gender and BMI, cancer TNM status and blood cell counts. Paper-12626726.
Pleiotrophin ( PTN) is a heparin- binding growth/differentiation inducing cytokine that shares 50% amino acid sequence identity and striking domain homology with Midkine ( MK), the only other member of the Ptn/Mk developmental gene family. Paper-11254346.
Methylation analysis, partial acid hydrolysis, and (13)C NMR spectroscopy indicated that it was an arabinogalactan containing a (1-->4)-linked beta-Galp main chain, substituted at O-6 with Ara units, which were in turn substituted at O-5 ( Araf) and/or O-4 ( Arap), O-3, O-3,5, and O-2,5. Paper-10246573.
The prevalence of the antinucleolar antibodies (ANoA) demonstrated by indirect immunofluorescence technique in 1,662 sera of patients with a known or suspected rheumatic disease increased from 1.97% when mouse kidney ( MK) was used as substrate to 4.9% when HEp-2 cells were used as substrate. Paper-7952338.
The expression of midkine ( MK) was investigated in pancreatic ductal hyperplasias, atypical hyperplasias and adenocarcinomas induced by N-nitrosobis(2-oxopropyl)amine ( BOP) in hamsters, and in hamster ductal adenocarcinoma cell lines (HPD-1NR, -2NR and -3NR). Paper-8580016.
In our current study, we developed oncolytic adenoviruses which preferentially lyse pancreatic and colon cancer cells by replacing viral E1 and/or E4 promoter with the tumor/tissue-specific promoters, cyclooxygenase-2 ( COX-2), midkine ( MK), or the cell cycle-dependent promoter, E2F1. Paper-11342422.
Comparison of the HBNF protein sequence with sequences stored in the Protein Identification Resource/ Genbank databases reveals high homology to the translation product of the MK-1 gene, which is retinoic acid-inducible in embryonic carcinoma cells and developmentally expressed during gestation in mice. Paper-7121346.
A recent study investigated the mRNA expression of selected genes in the prefrontal cortex and found that the levels of mRNA encoding the neurotrophic factor, midkine ( MDK), and the excitatory amino acid transporter 1 ( EAAT1) were significantly higher in alcoholics compared with nonalcoholic controls. Paper-13021330.
In each cell line, we examined MK mRNA expression by TaqMan real-time quantitative polymerase chain reaction, MK promoter activity, after plasmid transfection, using a luciferase assay, and the transduction efficiency by co-transfection with the cytomegalovirus-beta-gal plasmid. Paper-12638086.
From these results, and because it has been reported that AdMKTk and AdCOX-2L Tk in combination with GCV did not reveal significant liver toxicity, we conclude that the MK as well as the COX-2 promoters are promising tumor-specific promoters for Ad vector-based gene therapy of pancreatic cancer. Paper-8904212.
Accordingly, the nucleolin- binding HB-19 pseudopeptide has no effect on the MK binding to the high affinity binding site, whereas it prevents the binding of MK to the low affinity binding site, thus suggesting the low affinity receptor of MK is the cell-surface- expressed nucleolin. Paper-11391872.
MATERIALS AND METHODS: We examined the expression of MK-1 in 10 urological tumor cell lines using flow cytometry and reverse transcription-polymerase chain reaction ( RT-PCR) and in 15 cancer tissue specimens by immunohistochemical staining, and then compared it with that of carcinoembryonic antigen ( CEA). Paper-2206167.
Moreover, PAR-2 AP induced AR gene expression subsequent to protein production in the cellular fraction through the ERK pathway indicating that PAR-2- mediated activation of ERK is essential for HAT- induced AR production. Paper-11514033.
MK could induce phosphorylation of p44/42 MAPK (Thr202/Tyr204) and Akt (Ser473 and Thr308), and by pretreatment of PD98059, MEK1 inhibitor, or LY294002, PI3K inhibitor, MK- stimulated-phosphorylation of MAPK and Akt and MK-stimulated growth of AM-1 cells were inhibited. Paper-10207352.
Human midkine ( hMK), a novel heparin-binding neurotrophic factor consisting of 121 amino acid residues with five intramolecular disulphide bonds, was synthesized by solution procedure in order to demonstrate the usefulness of our newly developed solvent system, a mixture of dichloromethane or chloroform and trifluoroethanol. Paper-1169343.
Furthermore, MK stimulates ALK phosphorylation in WI-38 human fibroblasts and activates PI3-kinase and MAP kinase signal transduction in WI-38, HUVEC, neuroblastoma (SH SY-5Y) and glioblastoma (U87MG) cells that express the ALK protein. Paper-9171245.
Our study also shows that MDK activates both the Akt and ERK1/2 pathways and upregulates the expression of several cell-cycle-related proteins, including cyclin A, cyclin D1, Cdk2, Cdk4, and Cdk6, which in part explains the contribution of MDK to gastric cancer cell survival and growth. Paper-13760501.
RESULTS: The expressions of midkine and pleiotrophin mRNA in cervical cancer were higher than those in the normal cervix ( MK, 175.59 +/- 63.3 vs 1.00 +/- 0.18 fmol, respectively; PTN, 3.18 +/- 1.25 vs. 0.86 +/- 0.12 fmol, respectively, P < 0.05), and their expressions were not correlated with cervical cancer stage or size of the tumor. Paper-9841919.
We constructed recombinant adenoviral (Ad) vectors containing either the luciferase (Luc) reporter gene under the control of the COX-2 or MK promoter or the herpes simplex virus thymidine kinase (HSV Tk) gene under the control of the COX-2 promoter and compared the expression with the cytomegalovirus (CMV) promoter. Paper-8904212.
A 2.3-kb genomic fragment in the regulatory region of the MK gene could activate a fused reporter gene in both AFP- producing and -nonproducing HCC lines, and the MK fragment- mediated transcriptional activity was comparable to the AFP enhancer-linked AFP promoter in AFP-producing cell lines. Paper-9975387.
Interestingly, the cross-linking of surface-bound MK with a specific antibody results in the clustering of surface nucleolin along with glycosylphosphatidylinositol- linked proteins CD90 and CD59, thus, pointing out that MK binding induces lateral assemblies of nucleolin with specific membrane components of lipid rafts. Paper-9171541.
Forty-seven patients with multiple sclerosis ( MS), 21 subjects with neurological diseases other than MS (OND), 7 with miscellaneous disease (MD) and 21 healthy individuals (HI) were examined by the standard procedure of blast transformation for the in vitro response to mouse brain (MB), mouse kidney ( MK) and mouse lung (ML) tissue extracts. Paper-3612366.
Main Outcome Measures: The main outcome measures were MK mRNA levels (measured by quantitative real-time RT-PCR); MK localization (measured by immunostaining); MK proliferative effects and mechanism (measured by proliferation assays, flow cytometry, pharmacological interventions); and ACTH regulation (measured by quantitative real-time RT-PCR). Paper-12261053.
RESULTS: Analysis of patient array data versus universal RNA identified elevated expression of transcripts related to angiogenesis ( ANGPTL2, HIF-1 alpha, MDK, c-MET, VEGF, TIMP-2), cell proliferation ( PRL, IGFBP1, NTSR2, PCSK1), metastasis ( ADAM9, ECM1, POSTN) and steroid biosynthesis ( CYP17A1 and STS). Paper-13601305.
The NOP activity of the higher molecular weight fraction and that of the embryonic pig brain-derived CS/ DS fraction were also sup pressed to a large extent by antibodies against HGF, PTN, and their individual receptors cMet and anaplastic lymphoma kinase, revealing the involvement of the HGF and PTN signaling pathways in the activity. Paper-12441693.
Specifically, differentially expressed genes included those encoding extracellular matrix components ( COL16A1, DPT), proteases (CATD, PRSS11), cytokines ( MDK, IL8), transport proteins ( SLC1A3, ATP10B), cytoskeleton constituents ( ACTA2, ACTSG, NEFL), DNA repair enzymes ( WRN, ADPRTL2), and G-protein signaling components ( GNA12, RGS3, RGS4). Paper-10211790.
METHODS: Plasmid DNA-based luciferase reporter gene assays and adenovirus type 5 ( Ad5) infection were combined to examine the effect of the Ad5 (nt 1-353) element and/or adenoviral gene products on tissue-specific ( Midkine ( MK) and COX-2), cell cycle associated (Ki-67 and E2F1) and viral promoters ( Ad5 E1, Ad5 E4 and SV40). Paper-11113323.
Exogenous 500-5000 pg/mL midkine application during 5 mug/mL Cd toxicity prevented caspase-3 activation (control, Cd toxicity, 250, 500, 1000, 2500, 5000 pg/mL midkine+ Cd toxicity, respectively: 374 +/- 64, 1786 +/- 156, 1545 +/- 179, 1203 +/- 113, 974 +/- 116, 646 +/- 56, 556 +/- 63 cfu) LDH leakage and cell death in Hep3B cells (P < 0.001). Paper-12680608.
These synonyms are used for gene MDK (midkine (neurite growth-promoting factor 2)): Neurite outgrowth-promoting protein, Neurite outgrowth-promoting factor 2, NEGF2, MK1, MK, Midkine, Midgestation and kidney protein, FLJ27379, ARAP, Amphiregulin-associated protein.
These accession numbers are used for gene MDK: Q9UCC7 (UNIPROT__AC), Q2LEK2 (UNIPROT__AC), CAA38908 (NCBI_GENBANK__AC), AAH11704 (NCBI_GENBANK__AC).
MDK is a homologue of mdkb (midkine-related growth factor b) from Danio rerio.
MDK is a homologue of mdka (midkine-related growth factor) from Danio rerio.
MDK is a homologue of MDK (midkine (neurite growth-promoting factor 2)) from Bos taurus.
MDK is a homologue of MDK (midkine (neurite growth-promoting factor 2)) from Bos taurus.
MDK is a homologue of MDK (midkine (neurite growth-promoting factor 2)) from Gallus gallus.
MDK is a homologue of Mdk (midkine) from Mus musculus.
MDK is a homologue of Mdk (midkine) from Rattus norvegicus.
Important links !
iHOP - Information Hyperlinked over Proteins .
Concept & Implementation by Robert Hoffmann.