Gene interactions and pathways from curated databases and text-mining

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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