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Rat (Rattus) MET Primary Antibody for - ABIN2009011
Bottaro, Rubin, Faletto, Chan, Kmiecik, Vande Woude, Aaronson: Identification of the hepatocyte growth factor receptor as the c-met proto-oncogene product. in Science (New York, N.Y.) 1991
Show all 6 references for ABIN2009011
Dog (Canine) MET Primary Antibody for - ABIN2008841
Weidner, Di Cesare, Sachs, Brinkmann, Behrens, Birchmeier: Interaction between Gab1 and the c-Met receptor tyrosine kinase is responsible for epithelial morphogenesis. in Nature 1996
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Mouse (Murine) MET Primary Antibody for - ABIN2008064
Stephenson, Tronick, Aaronson: Isolation from BALB/c mouse cells of a structural polypeptide of a third endogenous type C virus. in Cell 1975
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Human MET Primary Antibody for - ABIN2003243
Birchmeier, Birchmeier, Gherardi, Vande Woude: Met, metastasis, motility and more. in Nature reviews. Molecular cell biology 2003
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Human MET Primary Antibody for - ABIN2003239
Pennacchietti, Michieli, Galluzzo, Mazzone, Giordano, Comoglio: Hypoxia promotes invasive growth by transcriptional activation of the met protooncogene. in Cancer cell 2003
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Cynomolgus MET Primary Antibody for - ABIN2010132
Boccaccio, Comoglio: Invasive growth: a MET-driven genetic programme for cancer and stem cells. in Nature reviews. Cancer 2006
Show all 6 references for ABIN2010132
Human MET Primary Antibody for - ABIN2180662
Rubin, Chan, Bottaro, Burgess, Taylor, Cech, Hirschfield, Wong, Miki, Finch: A broad-spectrum human lung fibroblast-derived mitogen is a variant of hepatocyte growth factor. in Proceedings of the National Academy of Sciences of the United States of America 1991
Study provides evidence that AXL (show AXL Proteins) and MET are associated with cell proliferation and metastasis in lung cancer, and the crosstalk between these receptors affects tumor progression.
overexpression of HGF resulted in resistance to c-MET tyrosine kinase inhibitors through an autocrine manner in gastric cancer cells
CMET overexpression and CMET amplification are commonly found in non-small cell lung cancer (NSCLC) brain metastases and may represent a promising therapeutic target.
Study shows that MET was directly regulated by miR (show MLXIP Proteins)-23b and miR (show MLXIP Proteins)-27b. Moreover, downregulating the MET gene by use of siRNA significantly inhibited cell migration and invasion by oral squamous cell carcinoma cells.
Activation of the HGF (show HGF Proteins)-mediated MET pathway is involved in escape to selective VEGFR (show KDR Proteins) inhibition in neuroblastoma (show ARHGEF16 Proteins) suggesting combined inhibition of MET and VEGFR (show KDR Proteins) signaling to reduce secondary resistance and enhanced invasiveness.
miR (show MLXIP Proteins)-27b was frequently downregulated in NSCLC tissues and cell lines and could inhibit the malignant phenotypes of NSCLC cells by directly targeting the MET oncogene (show RAB1A Proteins). The identification of miR (show MLXIP Proteins)-27b-mediated novel signaling pathways may help reveal the molecular mechanism underlying the development and malignant progression of this disease.
Therefore, our findings suggested miR (show MLXIP Proteins)-34a could modulate human gastric cancer(GC) cell Cisplatin sensitivity by regulation of cell proliferation and apoptosis via targeting MET, potentially benefiting human GC treatment in the future.
miR1 (show FSD1 Proteins) expression inversely correlated with MET, cyclin D1 (show CCND1 Proteins) and CDK4 (show CDK4 Proteins) expression in esophageal squamous cell carcinoma cells.
c-Met is expressed in malignant pleural mesothelioma, with significant differences in expression among histologic subtypes
High c-MET expression is associated with esophageal squamous cell carcinoma.
study demonstrates that co-activation of AKT (show AKT1 Proteins) and c-Met induces hepatocellular carcinoma development that depends on the mTORC1/FASN (show FASN Proteins) pathway.
Molecular and functional studies revealed that ectopic Met expression in limb mesenchyme does not alter HGF (show HGF Proteins) expression patterns and levels, but impairs HGF (show HGF Proteins) bioavailability
miR-206 suppressed c-Met expression in gastric cancer and could function as a potent tumor suppressor in c-Met overexpressing tumors.
Meg3 overexpression in insulinoma cells down-regulated the expression of the protooncogene c-met.
our results support the concept of the acrosome as a lysosome-related organelle and provide evidence for the identification of MET as a tyrosine kinase receptor (show KDR Proteins) that may play a role in fertilization.
We show that a subset of adult calcitonin gene-related peptide (CGRP (show CALCA Proteins))-expressing myenteric neurons produce MET, the receptor for hepatocyte growth factor (show HGF Proteins).
HGF and c-met inhibition by means of a novel monoclonal neutralizing antibody inhibits tumor growth in prostate cancer cells and in mouse xenografts.
facilitates T cell recruitment to the heart via CCR5 receptor by inducing autocrine CCR5 ligand release
C-Met pathway is suggested to contribute to the lymphomagenesis in the MALT lymphoma after H. heilmannii infection.
c-Met targeting enhances the effect of irradiation and chemical agents against malignant colon cells harboring a KRAS mutation.
possible cooperative role of the EGF (show EGF Proteins) and HGF (show HGF Proteins) pathways and indicate that cross-talk between their respective receptors may modulate mammary gland development in the cow
The proto-oncogene MET product is the hepatocyte growth factor receptor and encodes tyrosine-kinase activity. The primary single chain precursor protein is post-translationally cleaved to produce the alpha and beta subunits, which are disulfide linked to form the mature receptor. Various mutations in the MET gene are associated with papillary renal carcinoma. Two transcript variants encoding different isoforms have been found for this gene.
, 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
, HGF receptor c-Met