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Human HGF Protein expressed in Insect Cells - ABIN1589618
Rezzola, Dal Monte, Belleri, Bugatti, Chiodelli, Corsini, Cammalleri, Cancarini, Morbidelli, Oreste, Bagnoli, Semeraro, Presta: Therapeutic Potential of Anti-Angiogenic Multitarget N,O-Sulfated E. Coli K5 Polysaccharide in Diabetic Retinopathy. in Diabetes 2015
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Rat (Rattus) HGF Protein expressed in Human Cells - ABIN2009606
Comoglio: Structure, biosynthesis and biochemical properties of the HGF receptor in normal and malignant cells. in EXS 1993
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Human HGF Protein expressed in HEK-293 Cells - ABIN2722630
Ueda, Ito, Shiraishi, Taniguchi, Kayukawa, Nakanishi, Nakamura, Naya, Hongo, Kamoi, Okihara, Kawauchi, Miki: PAX2 promoted prostate cancer cell invasion through transcriptional regulation of HGF in an in vitro model. in Biochimica et biophysica acta 2015
Met has a role in promoting formation of double minute chromosomes induced by Sei-1 (show SERTAD1 Proteins) in NIH-3T3 murine fibroblasts
Genetic activation of the antioxidant transcription factor Nrf2 improves liver damage and repair in hepatocyte-specific c-met-deficient mice mainly through restoring a balance in the cellular redox homeostasis.
MET promoted the development of squamous tumors by stimulating the synthesis and release of ligands that activate the epidermal growth factor receptor (EGFR (show EGFR Proteins)).
through the activation of EGFR, MET activation parallels a RAS pathway to contribute to human and mouse cutaneous cancers.
Results show that c-MET expression is significantly low in pancreatic neuroendocrine tumors (PNETs) and is under the regulation of Meg3-mediated transcriptional and epigenetic mechanisms which contributes to the pathogenesis of PNETs.
Findings indicate a role for the hepatocyte growth factor receptor HGFR/c-MET pathway in neutrophil recruitment and function and suggest that c-MET inhibitor co-treatment may improve responses to cancer immunotherapy in settings beyond c-MET-dependent tumors.
Results demonstrate a new mechanism for the modulation of synapse formation, whereby MET activation induces an alignment of presynaptic and postsynaptic elements that are necessary for assembly and formation of functional synapses by subsets of neocortical neurons that express MET/beta-catenin (show CTNNB1 Proteins) complex.
MET signaling regulates intestinal homeostasis and regeneration, as well as adenoma formation. These activities of MET are promoted by the stem cell CD44 (show CD44 Proteins) isoform CD44v4-10.
Study used biochemical and morphological analyses to demonstrate that two discrete intracellular signaling pathways underlie distinct HGF-induced biological outcomes in developing neocortical neurons. Further, it identified a key developmental epoch, corresponding to the period of dendritic outgrowth and synaptogenesis, during which HGF stimulation elicits maximal activation of MET in the neocortex.
a c-Met/ETS-1 (show ETS1 Proteins)/matrix metalloproteinase-14 (MMP-14 (show MMP14 Proteins)) axis that controls VE-cadherin (show CDH5 Proteins) degradation, endothelial mesenchymal transition, and vascular abnormality.
cabozantinib suppressed MMP1 (show MMP1 Proteins) expression by blocking HGF-MET signaling and that HGF-MET-MMP1 (show MMP1 Proteins) signaling is involved in the invasiveness and proliferation of BCa (show BLNK Proteins) cells. These results suggest that cabozantinib might prove useful for future treatment of muscle-invasive BCa (show BLNK Proteins).
The results suggested that HGF may inhibit TEMT (show INMT Proteins) by inhibiting AngII through the JAK2 (show JAK2 Proteins)/STAT3 (show STAT3 Proteins) signaling pathway in HK2 (show HK2 Proteins) cells and HGF may prevent apoptosis induced by AngII. The present study provides a basis for understanding the mechanisms involved in the inhibition of TEMT (show INMT Proteins) by HGF, which requires further investigation
The identification of novel small-molecule inhibitors of microtubule polymerization highlights the role of the microtubule cytoskeleton in HGF-induced epithelial scattering.
miRNA-200a expression was inverse correlation with HGF expression in stromal fibroblasts. High miRNA-200a and low HGF expression in stromal fibroblasts may predict a good prognosis in patients with non-small cell lung cancer.
Activation of proHGF by St14 (show ST14 Proteins) induces mouse embryonic stem cell differentiation.
Study shows that Met and HGF have a multi-factorial relationship to the biology and outcome of breast cancer, influenced by gene copy number and protein expression, activation status, stromal environment, and cellular localisation.
These results reveal the effect of HGF on the distinct pathways of eosinophil secretory functions and also provide novel insights into the role of HGF in the pathogenesis of allergic inflammation.
The hepatocyte growth factor (HGF)-MET receptor tyrosine kinase (show RET Proteins) signaling pathway
MiRNA199a-3p suppresses tumor growth, migration, invasion and angiogenesis in hepatocellular carcinoma by targeting VEGFA (show VEGFA Proteins), VEGFR1 (show FLT1 Proteins), VEGFR2 (show KDR Proteins), HGF and MMP2 (show MMP2 Proteins)
High HGF expression is associated with castration-resistant progression in androgen dependent metastatic prostate cancer.
acute pulmonary embolism associated with an enhanced HGF expression in the lungs, the right ventricle, and the liver
SNPs within bovine HGF gene were significantly associated with growth traits. This will provide a background for application of bovine HGF gene in the selection program in Chinese cattle.
Treatment of the bovine satellite cells (BSC (show SLC12A2 Proteins)) with ephrin-A5 (show EFNA5 Proteins) causes a reduction in velocity with a concomitant increase in directed migration. Treatment of BSC (show SLC12A2 Proteins) with hepatocyte growth factor had no immediate effect on cell motility or migration.
HGF transiently increases gene transcription of angiotensin-converting enzyme (show ACE Proteins)
Combined administration of mesenchymal stem cells overexpressing IGF-1 (show IGF1 Proteins) and HGF enhances neovascularization but moderately improves cardiac regeneration in a porcine model.
In an animal model of acute myocardial infarction relevant to human disease, intracoronary administration of IGF-1 (show IGF1 Proteins)/hepatocyte growth factor (HGF) is a practical and effective strategy to reduce pathological cardiac remodeling.
Hepatocyte growth factor regulates cell growth, cell motility, and morphogenesis by activating a tyrosine kinase signaling cascade after binding to the proto-oncogenic c-Met receptor. Hepatocyte growth factor is secreted by mesenchymal cells and acts as a multi-functional cytokine on cells of mainly epithelial origin. Its ability to stimulate mitogenesis, cell motility, and matrix invasion gives it a central role in angiogenesis, tumorogenesis, and tissue regeneration. It is secreted as a single inactive polypeptide and is cleaved by serine proteases into a 69-kDa alpha-chain and 34-kDa beta-chain. A disulfide bond between the alpha and beta chains produces the active, heterodimeric molecule. The protein belongs to the plasminogen subfamily of S1 peptidases but has no detectable protease activity. Alternative splicing of this gene produces multiple transcript variants encoding different isoforms.
hepatocyte growth factor
, scatter factor
, fibroblast-derived tumor cytotoxic factor
, lung fibroblast-derived mitogen
, hepapoietin A
, HGF alpha-chain
, hepatocyte growth factor /scatter factor
, HGF receptor
, HGF/SF receptor
, SF receptor
, hepatocyte growth factor receptor
, met proto-oncogene tyrosine kinase
, proto-oncogene c-Met
, scatter factor receptor
, tyrosine-protein kinase Met