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Hepatocyte growth factor receptor (HGF receptor) [5] [6] is a protein that in humans is encoded by the MET gene.The protein possesses tyrosine kinase activity. [7] 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.
MET is an essential process in embryogenesis to gather mesenchymal-like cells into cohesive structures. [1] Although the mechanism of MET during various organs morphogenesis is quite similar, each process has a unique signaling pathway to induce changes in gene expression profiles.
Other non-catalytic tyrosine-phosphorylated receptors carry a conserved inhibitory motif that, when phosphorylated, results in the inhibition of the signaling pathway via recruitment of phosphatases, namely SHP-1, SHP-2 and SHIP1. This serves not only for inhibition and regulation of signalling pathways related to ITAM-based signalling, but ...
c-Met stimulates cell scattering, invasion, protection from apoptosis and angiogenesis. [4] c-Met is a receptor tyrosine kinase, [5] which can cause a wide variety of different cancers, such as renal, gastric and small cell lung carcinomas, central nervous system tumours, as well as several sarcomas [6] when its activity is
[[Category:Signaling pathway templates]] to the <includeonly> section at the bottom of that page. Otherwise, add <noinclude>[[Category:Signaling pathway templates]]</noinclude> to the end of the template code, making sure it starts on the same line as the code's last character.
The epithelial–mesenchymal transition (EMT) is a process by which epithelial cells lose their cell polarity and cell–cell adhesion, and gain migratory and invasive properties to become mesenchymal stem cells; these are multipotent stromal cells that can differentiate into a variety of cell types.
EGFR activates c-Src while EGF also increases the activity of c-Src. In addition, overexpression of c-Src increases the response of EGFR-mediated processes. So both EGFR and c-Src enhance the effects of one another. Elevated expression levels of c-Src were found in human breast cancer tissues compared to normal tissues. [29] [30] [31]
The process of formation begins when the T-cell receptor binds to the peptide:MHC complex on the antigen-presenting cell and initiates signaling activation through formation of microclusters/lipid rafts. Specific signaling pathways lead to polarization of the T-cell by orienting its centrosome toward the site of the immunological synapse. The ...