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BCL2 — JUN
Text-mined interactions from Literome
Schwarz et al., Neuroreport 2002
(MAP Kinase Signaling System) :
Bcl-2 up-regulates ha-ras mRNA expression and
induces c-Jun phosphorylation at Ser73 via an ERK dependent pathway in PC 12 cells ... Here we demonstrate that inducible overexpression of the anti-apoptotic protein
Bcl-2 in a PC12 Tet-on- cell line up-regulates mRNA expression and
leads to phosphorylation of
c-Jun at Ser73 via the ERK pathway in a time and concentration dependent manner
Du et al., J Biol Chem 2004
:
In the presence of SP600125, mitotic progression was prolonged, and
c-Jun phosphorylation was
inhibited , but neither H1 nor
Bcl-2 phosphorylation was inhibited
Feng et al., Oncogene 2004
(MAP Kinase Signaling System) :
Inhibition of the activities of these kinases or the upstream activating kinases by pharmacological inhibitors or dominant negative mutants abolishes the
Bcl-2 mediated regulation of
AP-1 , LEDGF and their downstream genes
Choi et al., Cancer Res 2005
(Carcinoma, Non-Small-Cell Lung...) :
Reporter assays combined with deletion mutagenesis analysis and gel shift assays showed the
involvement of
activator protein 1 in the activation of MMP-2 promoter activity by
Bcl-2
Rosenzweig et al., Cancer Res 2006
(Astrocytoma...) :
We found that overexpression of RTVP-1 decreased the phosphorylation of
c-Jun-NH2-kinase and increased the expression of Bcl2 and that the protective effect of RTVP-1 was partially
mediated by
Bcl2
Tai et al., J Orthop Res 2007
:
This study shows that pretreatment with low NO can protect osteoblasts from high NO-induced cell insults via
JNK/c-Jun mediated regulation of
Bcl-2 gene expression and protein translocation
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
Murakami et al., J Biochem 2007
:
While the brefeldin A-treatment induced the phosphorylation of both
c-Jun N-terminal kinase (JNK) and p38 MAPK, overexpression of Bcl-x ( L ) or
Bcl-2 reduced the prolonged phosphorylation of JNK, but not of p38 MAPK
Wei et al., Mol Cell 2008
(Starvation) :
Furthermore, the stress activated signaling molecule,
c-Jun N-terminal protein kinase 1 (JNK1) , but not JNK2,
mediates starvation induced
Bcl-2 phosphorylation, Bcl-2 dissociation from Beclin 1, and autophagy activation
Ryu et al., Cell Death Differ 2008
:
Also, the level of antiapoptotic
B-cell lymphoma protein-2 (Bcl-2) was significantly reduced and the accumulation of
c-Jun increased in MVP knocked-down senescent HDFs
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
Marrero et al., Brain Res 2009
(Inflammation) :
In this study, we investigated the effects of inhibiting the alpha7 nAChR-JAK2 pro-survival cascade on the nicotine induced production of the survival factor
Bcl-2 and the transcriptional
activation of NF-kappaB,
AP-1 , STAT1, STAT3, and STAT5
Yang et al., Cell Res 2009
:
The decrease in the phosphorylation of
Bcl-2 at Ser70 upon exposure to palmitate is
mediated by inhibition of PKR and possibly by
c-Jun N-terminal kinase (JNK) , whereas the phosphorylation of Bcl-2 at Ser87 is unaffected by palmitate or PKR
Liu et al., Biomaterials 2010
(Necrosis) :
Silica nanoparticles also activated c-Jun N-terminal kinase (JNK),
c-Jun , p53, caspase-3 and NF-kappaB, increased Bax expression and
suppressed Bcl-2 protein
Geng et al., J Biol Chem 2011
(Urinary Bladder Neoplasms) :
We further showed that AITC induced
Bcl-2 phosphorylation was
caused by
c-Jun N-terminal kinase (JNK) , and AITC activates JNK
He et al., Diabetes 2013
(Diabetes Mellitus, Experimental...) :
Exposure of H9c2 cells to high glucose reduced AMPK activity,
inhibited Jun NH2-terminal kinase 1 (JNK1)-B-cell lymphoma 2 (Bcl-2) signaling, and promoted Beclin1 binding to
Bcl-2
Li et al., Neurosci Lett 2013
:
The
c-Jun N-terminal kinase (JNK) signaling can
regulate the expression of the
Bcl-2 family members that modulates mitochondrial membrane integrity
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
Lee et al., Mol Genet Metab 1998
:
Bcl-2 regulates nonapoptotic signal transduction : inhibition of
c-Jun N-terminal kinase (JNK) activation by IL-1 beta and hydrogen peroxide