Gene interactions and pathways from curated databases and text-mining

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AKT3 — ERBB3

Text-mined interactions from Literome

Mattoon et al., BMC biology 2004 : We also demonstrate that tyrosine phosphorylation of ErbB3 may lead to recruitment and activation of PI-3 kinase and Akt in Gab1-/- MEFs
Engelman et al., Proc Natl Acad Sci U S A 2005 (Carcinoma, Non-Small-Cell Lung...) : Down-regulation of ErbB-3 by means of short hairpin RNA leads to decreased phospho-Akt levels in the gefitinib-sensitive NSCLC cell lines, Calu-3 ( WT EGFR ) and H3255 ( L858R EGFR ), but has no effect on Akt activation in the gefitinib-resistant cell lines, A549 and H522
Löbke et al., Proteomics 2008 (Breast Neoplasms) : Activation of ERK1/2 and AKT by ERBB1 ( EGFR ), ERRB2 ( HER2/neu ), and ERBB3-4 was monitored in a time resolved manner
Kawano et al., J Biol Chem 2009 : This interaction reduced the ligand induced, ErbB2 catalyzed tyrosine phosphorylation of ErbB3 and inhibited the consequent ErbB3 mediated activation of Rac and Akt , resulting in the inhibition of cancer cell movement and survival
Balko et al., Proc Natl Acad Sci U S A 2012 (MAP Kinase Signaling System) : ErbB3 harbors weak kinase activity, but strongly activates downstream phosphatidylinositol 3-kinase/Akt signaling through heterodimerization with and activation by other ErbB receptor tyrosine kinases ... We report here that ErbB3 loss in the luminal mammary epithelium of mice impaired Akt and MAPK signaling and reduced luminal cell proliferation and survival
Vaught et al., Cancer Res 2012 (Adenocarcinoma...) : In addition, loss of ErbB3 impaired Akt and p44/42 phosphorylation in preneoplastic HER2 overexpressing mammary glands and in tumors, decreased growth of preexisting HER2 overexpressing tumors, and improved tumor response to the HER2 tyrosine kinase inhibitor lapatinib
Fattore et al., Journal of translational medicine 2013 : In the present study we demonstrate that ErbB3 is the main RTK undergoing rapidly hyperphosphorylation upon either treatment with a BRAF inhibitor or with a MEK inhibitor in a panel of melanoma cell lines harboring a variety of V600BRAF mutations and that this results in a strong activation of phospho-AKT