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  2. c-Met inhibitor - Wikipedia

    en.wikipedia.org/wiki/C-Met_inhibitor

    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]

  3. Receptor tyrosine kinase - Wikipedia

    en.wikipedia.org/wiki/Receptor_tyrosine_kinase

    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.

  4. Hepatocyte growth factor receptor - Wikipedia

    en.wikipedia.org/wiki/Hepatocyte_growth_factor...

    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.

  5. Epithelial–mesenchymal transition - Wikipedia

    en.wikipedia.org/wiki/Epithelial–mesenchymal...

    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 ...

  6. Mesenchymal–epithelial transition - Wikipedia

    en.wikipedia.org/wiki/Mesenchymal–epithelial...

    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.

  7. Proto-oncogene tyrosine-protein kinase Src - Wikipedia

    en.wikipedia.org/wiki/Proto-oncogene_tyrosine...

    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.

  8. ErbB - Wikipedia

    en.wikipedia.org/wiki/ErbB

    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 ...

  9. Mouse models of breast cancer metastasis - Wikipedia

    en.wikipedia.org/wiki/Mouse_models_of_breast...

    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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