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Subject cui: C0062534 Name: Hepatocyte Growth Factor Sem. type: aapp Novel: true

Predicate: STIMULATES

Object cui: 4233|8731|79811 Name: MET|RNMT|SLTM Sem. type: gngm|gngm|gngm Novel: true

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Hepatocyte Growth Factor STIMULATES MET|RNMT|SLTM Correct? #Y/N
The kinase activity of the c-MET receptor was also stimulated by HGF in an in vitro assay, after detergent solubilization and partial purification of p190c-met. (PMID: 1827664) 0/0
Treatment with hepatocyte growth factor increased phospho-Met levels, and this was inhibited in a concentration-dependent manner by EGCG and SU11274 (IC(50) 3.0 vs. (PMID: 20361925) 0/0
Reverse transcription-polymerase chain reaction revealed that FGFs and HGF enhanced c-met expression. (PMID: 12543460) 0/0
However, only two-chain HGF stimulates Met signaling. (PMID: 20937841) 0/0
HGF activated the c-Met receptor in HCE cells up to 30 minutes and was downregulated by 2 hours. (PMID: 18579758) 0/0
HGF stimulated c-Met and Akt phosphorylation, but did not affect the phosphorylation of extracellular signal-regulated kinase-1/2 or stress-activated protein/c-jun N-terminal kinase. (PMID: 21892609) 0/0
HGF activated Met signaling in all lines but elicited different responses: HGF induced cell dispersion (scattering) and collagen gel invasion in IOSE-Ov29 and IOSE-Ov29/T4 but did not alter the growth pattern of IOSE-29. (PMID: 15302591) 0/0
HGF activates the tyrosine kinase receptor c-met , initiating a series of complex events that regulate cell morphology, cell-cell interactions, and cell-matrix interactions and eventually result in the formation of branching tubular structures. (PMID: 11095644) 0/0
Hepatocyte growth factor (HGF)-stimulated Met signaling influences tumor survival, growth and progression, all processes involving the transcription factor NF-kappaB. (PMID: 15240510) 0/0
Conversely, stimulation with hepatocyte growth factor increased both phospho-MET and phospho-EGFR. (PMID: 21774103) 0/0
Here we demonstrate that fibroblast secretion of HGF activates Met and leads to EGFR/Met crosstalk and resistance to EGFR TKIs in triple-negative breast cancer (TNBC). (PMID: 22788954) 0/0
On the other hand, although TGF-beta1 treatment did not affect tyrosine phosphorylation of c-Met and EGFR, MAPK activity, and cyclin D1 expression, which were stimulated by HGF and EGF, DNA synthesis was completely inhibited through a marked decrease in cyclin E expression. (PMID: 11162525) 0/0
HGF induced c-met expression by L2 cells and neutralizing antibodies to HGF inhibited the mitogenic activity in the BALF. (PMID: 12042032) 0/0
However, when fetal hepatocytes were incubated in the presence of HGF , a 10-fold increase in c-met mRNA levels was observed 30 min after addition of the factor. (PMID: 7526865) 0/0
In normal peripheral blood B cells, which are c-MET-, c-MET expression was induced by PMA, ConA, HGF/ SF, and Epstein-Barr virus (EBV) infection. (PMID: 9028331) 0/0
(2) HGF -activated Met and src cooperate in inducing invasion; (PMID: 9010033) 0/0
These results identify syndecan-1 as a functional coreceptor for HGF that promotes HGF/Met signaling in MM cells, thus suggesting a novel function for syndecan-1 in MM tumorigenesis. (PMID: 11830493) 0/0
Under hypoxia, HGFA might be overexpressed and secreted from pancreatic cancer cells, which contributes to accelerate processing of HGF from fibroblast, resulting in the activation of the c-Met pathway. (PMID: 18422749) 0/0
Primary hepatocytes respond to the proliferating signals of Hepatocyte Growth Factor (HGF) through activation of the tyrosine kinase activity of the met (p145) receptor. (PMID: 8573137) 0/0
Most notably, in vitro cell stimulation with peptide V8 in the presence of pro-HGF leads to Akt phosphorylation, enhances cell survival, and facilitates cell migration between 75 and 100% of that found with two-chain HGF , thus revealing a novel approach for activation of Met signaling that bypasses proteolytic processing of pro-HGF. (PMID: 20937841) 0/0
Using several chimeric constructs consisting of various lengths of the met promoter region fused to the reporter gene of chloramphenicol acetyl transferase (CAT), and by performing transient transfection of these constructs into HepG2 cells, we show that induction of met gene expression by HGF and other cytokines is, at least in part, through up-regulation of met gene promoter activity. (PMID: 9214452) 0/0
Treatment with HGF slightly enhanced the expression of c-met mRNA only in COLO-357 cells. (PMID: 10452684) 0/0
Hepatocyte growth factor (HGF) binds the extracellular domain and activates the Met receptor to induce mitogenesis, morphogenesis, and motility. (PMID: 15261143) 0/0
On the other hand stimulation of c-met receptor with HGF leads to enhanced integrin-mediated adhesion of activated B cells to vascular cell adhesion molecule (VCAM-1) and fibronectin. (PMID: 11328385) 0/0
Hepatocyte growth factor (HGF) and Ephrin-A3 (EFNA3) were upregulated in all treatment groups suggesting a possible activation of c-Met and Ephrin-Eph signaling pathways. (PMID: 18549507) 0/0
Analysis by real-time PCR and western blot showed that after an EGF but not HGF or insulin-like growth factor-I treatment, HC11 mammary cells exhibited an increase in MET expression at both the mRNA and protein levels, which was dependent on the AKT pathway. (PMID: 19850646) 0/0
As it involves the activation of c-met, the receptor of HGF, we could show that MMP-19-dependent processing of plasminogen decreases the phosphorylation of c-met. (PMID: 21787393) 0/0
They are fibroblast growth factor (FGF), hepatocyte growth factor (HGF), and mast cell growth factor (MGF), which activate the FGF receptor, c-Met , and c-Kit, respectively, known to be receptor tyrosine kinases. (PMID: 1445804) 0/0
Activation of the c-Met receptor for HGF and of focal adhesion kinase (FAK) was investigated by immunoprecipitation with anti-phosphotyrosine antibody, gel electrophoresis, and immunostaining on Western blot. (PMID: 12556370) 0/0
Since HGF plays a critical role in neurotrophic activity, activation of the HGF/c-Met signaling system might be involved in the process of post-traumatic regeneration. (PMID: 17425951) 0/0
To investigate the role of HGF/c-met signaling on metastasis in cancer cells stimulated with HGF, we examined the effects of a specific MEK1 inhibitor (PD98059) and a p38 MAP kinase inhibitor (SB203580) on HGF-induced uPA expression in pancreatic cancer cell lines, L3.6PL and IMIM-PC2. (PMID: 14598883) 0/0
The N-terminal and first Kringle domains (NK1) of HGF comprise a naturally occurring splice variant that retains the ability to activate the Met receptor. (PMID: 21788476) 0/0
The FSH and HGF each down-modulated c-Met mRNA accumulation, whereas Bu(2)-cAMP increased c-Met mRNA content. (PMID: 10819792) 0/0
Activation of the hepatocyte growth factor (HGF)-Met system in papillary thyroid cancer: biological effects of HGF in thyroid cancer cells depend on Met expression levels. (PMID: 15192042) 0/0
In addition to the well-acknowledged role of HGF -Met in cancer invasion and metastasis, recent studies indicate that activation of the HGF-Met pathway makes tumor-initiating cells invasive and resistant to chemical and radiation therapy. (PMID: 20015005) 0/0
However, exogenous HGF failed to significantly reduce albuminuria in podo-met(-/-) mice, suggesting that podocyte-specific c-met activation by HGF confers renal protection. (PMID: 20375988) 0/0
We show that MCJs are naturally more endocytic than other sites of the apical membrane, that endocytosis and Lm invasion of MCJs depends on functional dynamin, and that c-Met activation by soluble InlB or hepatocyte growth factor (HGF) increases MCJ endocytosis. (PMID: 20485518) 0/0
Several mechanisms, including bypass signaling by hepatocyte growth factor (HGF)-triggered Met activation , are implicated as mediators of resistance. (PMID: 23690929) 0/0
Hepatocyte growth factor (HGF) activation of MET receptors rescued cells from lapatinib-induced growth inhibition by restimulating the downstream pathways and restoring normal cell-cycle progression. (PMID: 22238368) 0/0
By comparing the differences between the protein phosphorylation profiles obtained using the protein microarrays, we were able to recover many of the proteins that are known to be specifically activated (i.e., phosphorylated) upon c-Met activation by the hepatocyte growth factor (HGF). (PMID: 24023761) 0/0
The present study investigated whether or not hypoxia increases HGFA expression in PK8 cells and promotes the processing of HGF , and leads to c-Met activation . (PMID: 18422749) 0/0
Consistent with these findings, c-Met activation by DeltaEGFR also elevated HGF expression, and the inhibition of DeltaEGFR with AG1478 reduced HGF levels. (PMID: 23359207) 0/0
This study examines podocytopenia and the role of decreased paracrine Met activation on podocytes by decreased glomerular hepatocyte growth factor (HGF) levels in the development of podocytopenia in TxG. (PMID: 21514418) 0/0
However, sustained MET activation by hepatocyte growth factor did not modulate the cellular effects of gefitinib or erlotinib. (PMID: 19808904) 0/0
Inhibition of phosphoinositide 3-kinase (PI3-kinase) substantially reduced c-met induction by SF/HGF in T98G cells but had no effect in U-373 MG cells. (PMID: 11238734) 0/0
Transfection of either cell line with TAM-67, a dominant negative for the jun transactivation domain, completely inhibited AP-1 and c-met induction by SF/HGF. (PMID: 11238734) 0/0
These results support a model of c-met induction by SF/HGF in human glioma cells that uniformly involves Ras, MAPK, and AP-1 and additionally involves PI3-kinase and PKC in some cell lines. (PMID: 11238734) 0/0
In this study we evaluated MET activation by HGF and HGF action in prostate cancer cell lines. (PMID: 10875259) 0/0
In this study we evaluated MET activation by HGF and HGF action in prostate cancer cell lines. (PMID: 10875259) 0/0
Furthermore, both HGF and HGF activator were also expressed in several of these cell lines, providing evidence of a possible autocrine loop of Met activation . (PMID: 19379214) 0/0
Interestingly, although a CD44 splice variant contributes to MPNST cell invasion and interacts with c-Met and HGF in ST8814 cells, it is not required for c-Met activation . (PMID: 14730703) 0/0
Using several chimeric constructs consisting of various lengths of the met promoter region fused to the reporter gene of chloramphenicol acetyl transferase (CAT), and by performing transient transfection of these constructs into HepG2 cells, we show that induction of met gene expression by HGF and other cytokines is, at least in part, through up-regulation of met gene promoter activity. (PMID: 9214452) 0/0
We show here that Met activation by HGF impairs Fas-triggered apoptosis of primary embryonic hepatocytes and cell survival correlates with inhibition of caspase-8 and caspase-3 activities. (PMID: 17464994) 0/0
Met activation by hepatocyte growth factor (HGF) is associated with decreased E-cadherin-dependent cell-cell contacts. (PMID: 17336101) 0/0
Inversely, enhancement of the c-Met activation by exogenous HGF blocked endothelial/tubular apoptotic injuries and acute renal failure. (PMID: 15920173) 0/0
Thus, c-Met activation is reciprocally regulated by phosphorylation between c-Met serine and tyrosine residues through PP2A induction in the presence or absence of mutant SOD1 expression, and HGF functions more efficiently in ALS and ALS-related diseases. (PMID: 19595710) 0/0
In addition, hepatocyte growth factor was found to block the ability of EGFR-TKIs to inhibit MET activation . (PMID: 19808904) 0/0
Using several HCC cell lines as a model system, we show that HGF, as well as other cytokines, such as epidermal growth factor (EGF), interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor alpha (TNF-alpha), induce met and ron expression. (PMID: 9214452) 0/0