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Inhibition of SHP2-mediated dephosphorylation of Ras suppresses oncogenesis
Ras is phosphorylated on a conserved tyrosine at position 32 within the switch I region via Src kinase. This phosphorylation inhibits the binding of effector Raf while promoting the engagement of…
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Suppression of hath1 gene expression directly regulated by hes1 via notch signaling is associated with goblet cell depletion in ulcerative colitis
TLDR
The present study suggests that Hes1 is essential for Hath1 gene suppression via Notch signaling, and the suppression of Hath1 is associated with goblet cell depletion in UC.
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Src promotes GTPase activity of Ras via tyrosine 32 phosphorylation
TLDR
It is shown that Y32 phosphorylation inhibits Raf binding to Ras and concomitantly promotes GAP association and GTP hydrolysis, thereby ensuring unidirectionality to the Ras GTPase cycle.
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Tyrosyl phosphorylation of KRAS stalls GTPase cycle via alteration of switch I and II conformation
Deregulation of the RAS GTPase cycle due to mutations in the three RAS genes is commonly associated with cancer development. Protein tyrosine phosphatase SHP2 promotes RAF-to-MAPK signaling pathway…
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Hes1 promotes the IL-22-mediated antimicrobial response by enhancing STAT3-dependent transcription in human intestinal epithelial cells.
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The acquisition of malignant potential in colon cancer is regulated by the stabilization of Atonal homolog 1 protein.
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Supplementary movie S1
Atonal homolog 1 protein stabilized by tumor necrosis factor α induces high malignant potential in colon cancer cell line
TLDR
The inflammation associated with carcinogenesis may preserve the differentiation system of intestinal epithelial cell (IEC), resulting in the acquisition of both the mucinous phenotype and high malignant potential associated with the enrichment of cancer stem cell.
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New structural and functional insight into the regulation of Ras.
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NRAS Status Determines Sensitivity to SHP2 Inhibitor Combination Therapies Targeting the RAS–MAPK Pathway in Neuroblastoma
TLDR
Inhibition of growth and downstream RAS–MAPK signaling in neuroblastoma cells in response to treatment with the SHP2 inhibitors SHP099, II-B08, and RMC-4550 suggest that conventional therapy–resistant, relapsed neuroblastomas may be effectively treated via combined inhibition of SHP1 and MEK or ERK of the RAS-MAPK pathway.
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