Gene interactions and pathways from curated databases and text-mining

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BCL2 — CREB1

Pathways - manually collected, often from reviews:

Text-mined interactions from Literome

Freeland et al., Brain Res Mol Brain Res 2001 (Second Messenger Systems) : Despite the lack of cyclic AMP responsiveness, activation of the Bcl-2 promoter via the CRE in response to hypoxia requires the CREB transcription factor and is associated with the enhanced phosphorylation of CREB on serine 133 and enhanced transcriptional activation by the CREB binding protein, CBP, in response to hypoxia
Bellido et al., J Biol Chem 2003 (Bone Resorption) : Attenuation of apoptosis by PTH in cultured osteoblastic cells requires protein kinase A-mediated phosphorylation and inactivation of the pro-apoptotic protein Bad as well as transcription of survival genes, like Bcl-2 , mediated by CREB ( cAMP response element binding protein ) and Runx2
Saini et al., J Neurochem 2004 : Interestingly, the presence of a putative CREB binding site ( CRE ) in the Bcl-2 gene raised the possibility that CREB could also be involved in regulating Bcl-2 expression in the OLGs ... In addition, transient transfection experiments using various regions of the Bcl-2 promoter and mutation of the CRE site indicate a direct role of CREB in regulating Bcl-2 gene activity in response to NT-3
Das et al., Am J Physiol Heart Circ Physiol 2005 (Myocardial Infarction) : Pharmacological preconditioning with resveratrol : role of CREB dependent Bcl-2 signaling via adenosine A3 receptor activation
Meller et al., J Cereb Blood Flow Metab 2005 (Brain Ischemia) : CREB mediated Bcl-2 protein expression after ischemic preconditioning ... Because Bcl-2 expression is regulated by the transcription factor cyclic AMP response element binding protein ( CREB ), we investigated the role of CREB activation in two models of ischemic preconditioning : focal ischemic tolerance after middle cerebral artery occlusion ( MCAO ) and in vitro ischemic tolerance modeled by oxygen-glucose deprivation ( OGD ) ... Taken together, these data suggest that after ischemic preconditioning CREB activation regulates the expression of the prosurvival protein Bcl-2
Ryu et al., Cell Death Differ 2007 : We further found that P-cAMP response element binding protein ( CREB ), a positive regulator of Bcl-2 , decreased in stress induced apoptosis of young HDFs but not in senescent HDFs, and that Bcl-2 was markedly reduced in CREB small interfering RNA ( siRNA ), transfected senescent HDFs
O'Driscoll et al., J Neurochem 2007 : bFGF promotes photoreceptor cell survival in vitro by PKA mediated inactivation of glycogen synthase kinase 3beta and CREB dependent Bcl-2 up-regulation
Aggarwal et al., Cancer Res 2008 (Carcinoma, Non-Small-Cell Lung...) : Furthermore, treating H1734 NSCLC cells with an inhibitor of the CREB signaling pathway Ro-31-8220 inhibited CREB activation by blocking the activity of extracellular signal kinase and ribosomal s6 kinase, arrested the cell cycle at the G(2)-M phase, and subsequently induced apoptosis with the suppression of Bcl-2 and Bcl-xL expression
Lin et al., Eur J Pharmacol 2008 (Brain Ischemia) : These results suggest that preconditioning with glutamate conferred neuroprotection against subsequent OGD by inducing p-CREB mediated Bcl-2 expression
Yano et al., Yakugaku Zasshi 2008 (Kidney Diseases) : On the other hand, a prostacyclin analog beraprost prevented RCN in mice by the increase of endogenous cAMP and subsequent CREB phosphorylation resulted in enhancement of Bcl-2 expression
Suzuki et al., Cancer Chemother Pharmacol 2009 (Carcinoma, Squamous Cell...) : Suppression of 5-FU induced apoptosis by Zeb was not associated with increased Bcl-2 and Bcl-xL expressions dependent on transcription factor CREB , and with the expression level of thymidylate synthase ... Suppression of 5-FU induced apoptosis by Zeb was not associated with increased Bcl-2 and Bcl-xL expressions dependent on transcription factor CREB , and with the expression level of thymidylate synthase
Lu et al., Am J Physiol Lung Cell Mol Physiol 2009 : We noted that inhibition of ALK5 attenuated serum deprivation induced apoptosis, an effect that correlated with increased expression and activation of CREB and its potential target genes, Bcl-2 and cFLIP
Dittmer et al., J Cell Sci 2011 : TOX3 also interacts with native CREB and induces the CREB-responsive BCL-2 promoter, which can be inhibited by coexpression of CITED1
Nikitina et al., Zh Evol Biokhim Fiziol 2012 (MAP Kinase Signaling System) : Our data demonstrated that in vitro inhibition of Bcl-2 by HA14-1 prevented CREB translocation into the cell nuclei and significantly decreased vasopressin mRNA level and enhanced contents of vasopressin protein in magnocellular neurons in supraoptic nucleus
Shi et al., J Biol Chem 2012 (MAP Kinase Signaling System) : Furthermore, ectopic expression of active Rit stimulates CREB-Ser133 phosphorylation, induces expression of the anti-apoptotic Bcl-2 and Bcl ( XL ) proteins, and promotes cell survival ... Furthermore, ectopic expression of active Rit stimulates CREB-Ser133 phosphorylation, induces expression of the anti-apoptotic Bcl-2 and Bcl ( XL ) proteins, and promotes cell survival
Kim et al., J Cell Biochem 2013 : CREB mediated Bcl-2 expression contributes to RCAN1 protection from hydrogen peroxide induced neuronal death ... Furthermore, RCAN1 induced the expression of the CREB target gene, Bcl-2