The mAKAP signalosorne and cardiac myocyte hypertrophy

被引:31
作者
Bauman, Andrea L.
Michel, Jennifer J. Carlisle
Henson, Edward
Dodge-Kafka, Kimberly L.
Kapiloff, Michael S.
机构
[1] Oregon Hlth & Sci Univ, Dept Pediat, Dept Cell & Dev Biol, Heart Res Ctr, Portland, OR 97239 USA
[2] Univ Connecticut, Ctr Hlth, Calhoun Ctr Cardiol, Farmington, CT USA
关键词
mAKAP; ryanodine receptor; calcineurin; hypertrophy; NFATc; PKA; ERK5; Epac1; heart; PDE4D3;
D O I
10.1080/15216540701358593
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
Cardiac hypertrophy is regulated by a large intracellular signal transduction network. Each of the many signaling pathways in this network contributes uniquely to the control of cell growth. In the last few years, it has become apparent that multimolecular signaling complexes or 'signalosomes' are important for mediating crosstalk between different signaling pathways. These complexes integrate upstream signals and control downstream effectors. In the cardiac myocyte, the protein mAKAP beta serves as a scaffold for a large signalosome that is responsive to upstream cAMP, Ca2+, and mitogen-activated protein kinase signaling. The mAKAP beta signalosome is important for the control of NFATc transcription factor activity and for the overall induction of myocyte hypertrophy.
引用
收藏
页码:163 / 169
页数:7
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