CREB-binding protein (CBP) regulates β-adrenoceptor (β-AR) - mediated apoptosis

被引：39

作者：

Lee, Y. Y. ^{[1
]}

Moujalled, D. ^{[1
]}

Doerflinger, M. ^{[1
]}

Gangoda, L. ^{[1
]}

Weston, R. ^{[1
]}

Rahimi, A. ^{[1
]}

de Alboran, I. ^{[2
]}

Herold, M. ^{[3
]}

Bouillet, P. ^{[3
]}

Xu, Q. ^{[4
]}

Gao, X. ^{[4
]}

Du, X-J ^{[4
]}

Puthalakath, H. ^{[1
]}

机构：

[1] La Trobe Univ, La Trobe Inst Mol Sci, Dept Biochem, Bundoora, Vic 3086, Australia

[2] CNB CSIC, Natl Biotechnol Ctr, Dept Immunol & Oncol, Madrid, Spain

[3] Royal Melbourne Hosp, Walter & Eliza Hall Inst Med Res, Mol Genet Canc Div, Parkville, Vic 3050, Australia

[4] Baker IDI Heart & Diabet Inst, Expt Cardiol Lab, Melbourne, Vic, Australia

来源：

CELL DEATH AND DIFFERENTIATION | 2013年 / 20卷 / 07期

基金：

澳大利亚国家健康与医学研究理事会; 澳大利亚研究理事会;

关键词：

apoptosis; beta-adrenoceptor; Bim; cyclic AMP; protein kinase A; FAMILY-MEMBER BIM; KINASE-A; BETA(2)-ADRENERGIC RECEPTORS; CELL-DEATH; STRESS; ACTIVATION; STIMULATION; EXPRESSION; MUTATIONS; GENE;

D O I：

10.1038/cdd.2013.29

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Catecholamines regulate the beta-adrenoceptor/cyclic AMP-regulated protein kinase A (cAMP/PKA) pathway. Deregulation of this pathway can cause apoptotic cell death and is implicated in a range of human diseases, such as neuronal loss during aging, cardiomyopathy and septic shock. The molecular mechanism of this process is, however, only poorly understood. Here we demonstrate that the beta-adrenoceptor/cAMP/PKA pathway triggers apoptosis through the transcriptional induction of the pro-apoptotic BH3-only Bcl-2 family member Bim in tissues such as the thymus and the heart. In these cell types, the catecholamine-mediated apoptosis is abrogated by loss of Bim. Induction of Bim is driven by the transcriptional co-activator CBP (CREB-binding protein) together with the proto-oncogene c-Myc. Association of CBP with c-Myc leads to altered histone acetylation and methylation pattern at the Bim promoter site. Our findings have implications for understanding pathophysiology associated with a deregulated neuroendocrine system and for developing novel therapeutic strategies for these diseases.

引用

页码：941 / 952

页数：12

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