Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Meller, R. et al.

Meller, Minami, Cameron, Impey, Chen, Lan, Henshall, Simon,

CREB- mediated Bcl-2 protein expression after ischemic preconditioning.

Bcl-2 plays a pivotal role in the control of cell death and is upregulated by ischemic tolerance. 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). After preconditioning ischemia (30 minutes MCAO or 30 minutes OGD), phosphorylation of CREB was increased, and there was an increased interaction between the bcl-2 cyclic AMP-responsive element (CRE) promoter and nuclear proteins after preconditioning ischemia in vivo and in vitro. Chromatin immunoprecipitation revealed an increased interaction between CREB-binding protein and the bcl-2 CRE rather than CREB, after preconditioning ischemia. Ischemic tolerance was blocked by a CRE decoy oligonucleotide, which also blocked Bcl-2 expression. The protein kinase A inhibitor H89, the calcium/calmodulin kinase inhibitor KN62, and the MEK inhibitor U0126 blocked ischemic tolerance, but not the phosphatidylinositol 3-kinase inhibitor LY294002. H89, KN62, and U0126 reduced CREB activation and Bcl-2 expression. Taken together, these data suggest that after ischemic preconditioning CREB activation regulates the expression of the prosurvival protein Bcl-2.[1]

References

CREB-mediated Bcl-2 protein expression after ischemic preconditioning. Meller, R., Minami, M., Cameron, J.A., Impey, S., Chen, D., Lan, J.Q., Henshall, D.C., Simon, R.P. J. Cereb. Blood Flow Metab. (2005) [Pubmed]

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