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The structure of tivantinib in complex with the c-Met kinase domain shows that the inhibitor binds a conformation that is distinct from published kinase structures. Tivantinib strongly inhibits c-Met autoactivation by selectively targeting the inactive form of the kinase between the N- and C- lobes and occupies the ATP binding site. [21]
An example of a vital signal transduction pathway involves the tyrosine kinase receptor, c-met, which is required for the survival and proliferation of migrating myoblasts during myogenesis. A lack of c-met disrupts secondary myogenesis and—as in LBX1—prevents the formation of limb musculature.
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.
The breast cancer bone metastasis has activated TGF-β signaling, which contributes to the formation of these lesions. [31] However, on the other hand, p53 , a well-known tumor suppressor, represses EMT by activating the expression of various microRNAs – miR-200 and miR-34 that inhibit the production of protein ZEB and SNAIL, and thus ...
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.
Elevated expression levels of c-Src were found in human breast cancer tissues compared to normal tissues. [29] [30] [31] Overexpression of Human Epidermal Growth Factor Receptor 2 (HER2), also known as erbB2, is correlated with a worse prognosis for breast cancer. [32] [33] Thus, c-Src plays a key role in the tumor progression of breast cancers.
In relation to breast tumors, somatic activating mutations in Akt and the p110α subunit of the PI3K have been detected in 3–5% and 20–25% of primary breast tumors, respectively. [27] Many breast tumors also have lower levels of PTEN, which is a lipid phosphatase that dephosphorylates phosphatidylinositol (3,4,5)-trisphosphate, thereby ...
Conditional ablation in MMTV-PyMT breast cancer cells has been done to reveal pro-metastatic actions of the angiogenic factors, Vascular endothelial growth factor A (VEGF-A). [50] The role of autocrine transforming growth factor beta 1(TGF-β1) signaling on motility and survival in PymT cells derived from an MMTV-PymT mouse mammary cancer. [51]
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