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BCL10 — JUN
Text-mined interactions from Literome
Jazirehi et al., Mol Cancer Ther 2004
(Lymphoma, Non-Hodgkin...) :
Inhibition of Bcl-x ( L ) expression by resveratrol was due to the inhibition of the extracellular signal regulated kinase 1/2 ( ERK1/2 ) pathway and diminished
activator protein-1 dependent
Bcl-x ( L ) expression
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
Takeuchi et al., FEBS J 2006
(Adenocarcinoma...) :
These results indicate that
AP1 mediated upregulation of
Bcl-X ( L ) expression is critical for protection of TMK-1 cells against ADR induced apoptosis
Yao et al., J Neurosci 2007
:
In the presence of toxic levels of Abeta, we observe that E2 attenuates indices of neuronal apoptosis :
c-Jun N-terminal kinase (JNK) dependent downregulation of
Bcl-w and upregulation of Bim, mitochondrial release of cytochrome c and Smac, and cell death
Jeong et al., Biol Pharm Bull 2008
(Brain Neoplasms...) :
Here, we confirmed that stable expression of
B-cell lymphoma-xL ( Bcl-xL ) in N18TG neuroglioma cells could
suppress c-Jun N-terminal protein kinase (JNK) activation, nuclear fragmentation, and cell death caused by etoposide treatment
Jacobs-Helber et al., Mol Cell Biol 1998
:
A dominant negative
AP1 mutant rendered these cells resistant to apoptosis induced by EPO withdrawal and
blocked the downregulation of
Bcl-XL