IndraLab

Statements


EGF leads to the phosphorylation of RB1. 10 / 10
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"EGF alone increased the amount of hyperphosphorylated (inactive) pRB; TGF beta blocked EGF-induced pRB phosphorylation, maintaining pRB in the active form."

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"As expected, EGF treatment of low-density cells increased Akt activation, caused Rb hyperphosphorylation, and decreased p27 levels when compared to untreated cells."

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"We report that EGCG inhibits EGF induced MCF10A cell proliferation accompanied by increased p21 CIP1/WAF1/SDI1 expression, decreased cyclin D1 associated pRB kinase activity, decreased pRB phosphoryla[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

"EGF induced the Rb hyperphosphorylation in time dependent manner."

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"This direct antiproliferative effect of acid is associated with inhibition of EGF-induced phosphorylation of the retinoblastoma protein (pRB), which maintains pRB activity and inhibits cell cycle progression from G1 to S phase."

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"TGF-beta converts EGF-induced hyperplasia to hypertrophy and inhibits EGF-induced pRB phosphorylation."

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"Inhibition of AR prevents EGF-induced phosphorylation of Rb."

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"Furthermore, when GSK3β was pharmacologically inhibited, EGF induced pRb hyperphosphorylation, cyclin D1 expression, p27 degradation and E2F4 nuclear translocation, four events associated with G1/S phase transition."

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"Treatment of HT29 cells with AR inhibitor, sorbinil or zopolrestat prevented EGF- and bFGF induced DNA binding activity of E2F-1 and phosphorylation of retinoblastoma protein."

"In addition, IFN-gamma decreased activation of cdk2 and expression of cyclin E, upstream signaling molecules responsible for Rb hyperphosphorylation in the late G1 phase."