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BCL10 — EPHB2
Text-mined interactions from Literome
Bryckaert et al., Oncogene 1999
:
Thus, FGF2 induced cell survival is a progressive adaptive phenomenon involving ERK2 activation by excreted FGF1 and
ERK2 dependent
Bcl-x production
Song et al., Zhonghua Xue Ye Xue Za Zhi 2002
(Multiple Myeloma) :
In addition, the expression of gp130 on cell surface, the
activation of protein kinase
ERK and the expression of Bcl-2 and
Bcl-x ( L ) were all down regualted in IFNalpha stimulated Sko-007 cells
Miranda et al., Leukemia 2003
:
Moreover,
Bcl-X ( L ) upregulation was
dependent on
MEK/ERK signaling
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
Tian et al., Blood 2005
(Lymphoma, B-Cell) :
Induction of
Bcl10 activity
caused rapid activation of nuclear factor-kappaB (NF-kappaB) and c-Jun N-terminal kinase (JNK), but not activation of extracellular signal regulated kinase (
ERK ) or p38 mitogen activated protein ( MAP ) kinases
Ríos-Muñoz et al., J Neurochem 2005
(MAP Kinase Signaling System...) :
FGF-2 treatment caused an
ERK dependent increase in Bcl-2 and an ERK independent increase in
Bcl-x ( L )
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