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BCL3 — EPHB2

Text-mined interactions from Literome

Azuma et al., Anticancer Res 2003 (Mammary Neoplasms, Experimental) : Selective cancer cell apoptosis induced by FTY720 ; evidence for a Bcl dependent pathway and impairment in ERK activity
Choi et al., J Biol Chem 2004 (MAP Kinase Signaling System) : Using the selective mitogen activated protein kinase kinase inhibitor PD98059, we found that Nef induced Erk signaling is essential for Bcl-XL up-regulation and cell survival ... These data suggest that Nef produces survival signals in myeloid cells through Erk mediated Bcl-XL induction, a pathway distinct from Nef survival pathways recently reported in T lymphocytes
Kataoka et al., J Gastroenterol 2005 : The inhibition of ERK phosphorylation by a specific inhibitor, PD98059, did not affect the increase in Bcl-xL expression level
Nakamura et al., J Biol Chem 2006 (MAP Kinase Signaling System) : We found that MNSFbeta.Bcl-G directly bound to ERKs and inhibited ERK activation by MEK1
Marzec et al., Oncogene 2007 (MAP Kinase Signaling System) : The U0126 mediated inhibition of ERK1/2 activation impaired proliferation and viability of the ALK+ TCL cells and expression of antiapoptotic factor Bcl-xL and cell cycle promoting CDK4 and phospho-RB
Wang et al., Cancer Res 2009 (Breast Neoplasms) : We conclude that CTGF expression could confer resistance to chemotherapeutic agents through augmenting a survival pathway through ERK1/2 dependent Bcl-xL/cIAP1 up-regulation
Wang et al., Cancer Lett 2010 (Ovarian Neoplasms) : Meanwhile, the further study demonstrates that the chemoresistance caused by IL-6 is associated with increased expression of both multidrug resistance related genes ( MDR1 and GSTpi ) and apoptosis inhibitory proteins ( Bcl-2, Bcl-xL and XIAP ), as well as activation of Ras/MEK/ERK and PI3K/Akt signaling
Gupta et al., Int J Oncol 2011 (Cerebellar Neoplasms...) : Intermittent hypoxia also inhibited expression of pro-anti-apoptotic proteins ( Bax and Bad ), and induced expression of anti-pro-apoptotic proteins ( Bcl2 and Bcl-xL ), and activation of ERK in medulloblastoma cells