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EGF leads to the phosphorylation of EIF4EBP1. 30 / 31
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"Inhibition of PI-3 kinase blocked NGF- and EGF-induced PHAS-I phosphorylation in PC12 cells."
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"We determined that EGF activates phosphorylation of Akt, mTOR, p70S6 kinase, ribosomal protein S6, eIF4E and 4E-BP1 in a PI-3-kinase dependent manner, and PI-3-kinase activation may prevent lactogenic differentiation in HC11 mammary epithelial cells by regulating the synthesis of proteins."
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"Effect of rapamycin on NGF- and EGF-induced PHAS-I and MAPK phosphorylation."
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"In summary, this paper provides evidence that PI-3 kinase, PKC, as well as FRAP are involved in the regulation of NGF- and EGF-induced PHAS-I phosphorylation in PCI2 cells."
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"EGF induced a rapid phosphorylation of Akt, tuberin, p70S6K and 4E-BP1 ( xref )."
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"Biochemical analyses confirmed that CC214-1 successfully inhibited mTORC1 dependent 4E-BP1 and S6 phosphorylation in EGFRvIII-expressing GBM cells ( xref and xref , xref ), as well as blocked EGF-induced 4E-BP1 and S6 phosphorylation in GBM cells overexpressing wild type EGFR ( xref )."
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"It was found in the present study that ascofuranone significantly inhibits the EGF-induced phosphorylation of p70S6K and 4E-BP1."
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"PC12 cells were used to study the signal transduction pathway leading to phosphorylation of PHAS-I. Both EGF and NGF induced phosphorylation of PHAS-I. Wortmannin, a PI-3 kinase inhibitor, staurosporine, a PKC inhibitor, and rapamycin, a FRAP inhibitor all blocked the phosphorylation of PHAS-I. Of the three inhibitors, only wortmannin was able to inhibit MAPK phosphorylation."
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"In H28V cells, both S6K and 4EBP1 are markedly phosphorylated in response to EGF treatment, higher than in H28T7 cells, with S6K exhibiting a more transient response as compared with 5AT1; while that of 4EBP1 showed a similar pattern in these two sets of cells (XREF_FIG)."
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"EGF induced a rapid phosphorylation of Akt, tuberin, p70S6K and 4E-BP1 (XREF_FIG)."
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"This excludes a role for MAPK in NGF- and EGF-induced PHAS-I phosphorylation in PC12 cells."
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"Collectively, these results suggest that AR inhibition prevents EGF induced PDCD4 and 4E-BP1 phosphorylation via regulation of mTOR/Raptor/S6K pathway."
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"We highlighted that 4E-BP1 phosphorylation was not activated by epidermal growth factor (EGF) but was under an insulin regulation mechanism through a PI3K-FRAP and mTOR activation that could account for the permissive role of insulin on hepatocyte proliferation."
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"PC12 cells were used to study the signal transduction pathway leading to phosphorylation of PHAS-I. Both EGF and NGF induced phosphorylation of PHAS-I. Wortmannin, a PI-3 kinase inhibitor, staurosp[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"This excludes a role for MAPK in NGF- and EGF-induced PHAS-I phosphorylation in PC12 cells."
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"Treatment of HT29 cells with AR inhibitor, fidarestat, prevented the EGF-induced phosphorylation of mTOR, Raptor, eIF4E, S6K and 4E-BP1 and increased the phosphorylation of AMPK."
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"Both EGF and NGF induced phosphorylation of PHAS-I."
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"The growth of A + cells requires EGF supplementation, which also markedly increased 4EBP1 phosphorylation, which should lead to dissociation from eIF4E and consequent translation."
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"In rat skeletal muscle, EGF markedly increased MAP kinase activity, but did not increase the phosphorylation of PHAS-I (24)."
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"Both EGF and NGF induced phosphorylation of PHAS-I."
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"Both EGF and NGF induced phosphorylation of PHAS-I, which released eIF4E from PHAS-I, mak- ing eIF4E available for translation [5,13]."
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"We highlighted that 4E-BP1 phosphorylation was not activated by epidermal growth factor (EGF) but was under an insulin-regulation mechanism through a PI3K-FRAP/mTOR activation that could account for the permissive role of insulin on hepatocyte proliferation."
12395317
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"Effect of staurosporine on NGF- and EGF-induced PHAS-I and MAPK phosphorylation."
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"Since mTOR causes the phosphorylation of downstream targets such as eIF4E, S6K and 4E-BP1, we next examined the affect of AR inhibition on EGF-induced phosphorylation of eIF4E, S6K and 4E-BP1 in HT-29 cells."
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"NGF- and EGF-induced PHAS-I phosphorylation was also studied in the presence of the PI-3 kinase inhibitor wortman- nin, the PKC inhibitor staurosporine, and the FRAP inhibitor rapamycin, to determi[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Although wortmannin also inhibited MAPK phosphorylation partially, the results with staurosporine and rapamycin showed that MAPK activation is not involved in the NGF- and EGF-induced PHAS-I phosph[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"As shown in xref , EGF-induced phosphorylation of mTOR, 4E-BP1, and P70S6K was significantly decreased in SiNUAK1/H1299 cells compared with Scr/H1299 cells."
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"Both EGF and NGF induced phosphorylation of PHAS-I (Fig. 1), which released eIF4E from PHAS-I (Fig. 2A), mak- ing eIF4E available for translation [5,13]."
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"Collectively, these results suggest that AR inhibition prevents EGF-induced PDCD4 and 4E-BP1 phosphorylation via regulation of mTOR/Raptor/S6K pathway."
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"Hormones (insulin, angiotensin), growth factors (EGF, PDGF, NGF, IGFI, IGFII), cytokines (IL-3, GMCSF+ steel factor), mitogens (TPA), G protein coupled receptor ligands (gastrin), and adenovirus infec[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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