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Product Feature - cMet Signalling
cMET (Mesenchymal epithelial transition factor) is a member of the MET family of receptor tyrosine kinases that also contains the receptor Ron. The natural ligand for cMET is hepatocyte growth factor/scatter factor, a disulfide-linked heterodimeric molecule produced predominantly by mesenchymal cells. cMET protein is mainly expressed in epithelial and endothelial cells and is also found in neural cells, hepatocytes, haematopoietic cells and melanocytes. Activation of the HGF/cMET pathway leads to a variety of cellular responses including proliferation, survival, angiogenesis, scattering, motility, invasion and branching morphogenesis.
Key cMet signalling compounds now available from Tocris include:
Potent and selective cMET inhibitor
2693 l PHA 665752 Antitumor agent; inhibits tumourigenicity and angiogenesis in mouse lung cancer xenografts.
Receptor tyrosine kinase inhibitor
1683 l K 252a Inhibits the oncogenic properties of Met; prevents autophosphorylation and activation of downstream effectors (MAPK, Akt).
Selective PI 3-Kinase inhibitor
1130 l LY 294002 A highly selective inhibitor of phosphatidylinositol 3-kinase (IC50 = 1.4 μM).
Selective inhibitor of MEK1/2
2605 l PD 198306 Inhibits isolated enzyme at a concentration of 8 nM and inhibits MEK activity in synovial fibroblasts at concentrations of 30-100 nM. Antihyperalgesic; blocks static allodynia in the streptozocin model of neuropathic pain following i.t. administration.
Selective STAT3 inhibitor
2798 l Stattic Inhibits binding of tyrosine-phosphorylated peptide motifs to STAT3 SH2 domain and inhibits STAT3 activation, dimerisation and nuclear translocation. Displays selectivity over STAT1, STAT5, c-Myc/Max, Jun/Jun and Lck. Induces apoptosis in STAT3-dependent cancer cell lines.
View all cMET Signalling Related Products.
cMET and Cancer
cMET is a proto-oncogene frequently mutated or overexpressed in a variety of cancers. Various mutations have been described in multiple sold tumours and some haematological malignancies, including human papillary renal carcinomas, ovarian cancer and gastric cancer. Constitutive activation of cMET results in activation of key oncogenic pathways (Ras, PI3K, STAT, beta-catenin). Many new cancer therapies have been aimed at the HGF/cMET pathway including anti-HGF monoclonal antibodies, truncated variants of cMET and protein kinase inhibitors to block cMET pathways.
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NEW Product Guide
Highlights over 150 new products
More cMET Signalling Compounds
AEG 3482
Inhibitor of JNK signalling
10-DEBC
Selective Akt/PKB inhibitor
Cucurbitacin I
Selective inhibitor of STAT3/JNK signalling
GW 5074
Potent, selective cRaf1 kinase inhibitor
c-JUN peptide
Peptide inhibitor of JNK/c-Jun interaction
SP 600125
Novel and selective JNK inhibitor
U0126
Potent, selective inhibitor of MEK1 and 2
740 Y-P
Cell-permeable PI 3-Kinase activator
ZM 39923
Potent, selective Jak3 inhibitor
ZM 336372
Potent, selective c-Raf inhibitor cMet Structure and Function
Ma et al review the potential therapeutic inhibition of cMet (more)
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