ErbB/integrin signaling interactions in regulation of myocardial cell-cell and cell-matrix interactions.
ErbB/integrin signaling interactions in regulation of myocardial cell-cell and cell-matrix interactions.
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DOI:
10.1016/j.bbamcr.2012.12.007
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发表时间:
2013-04
期刊:
影响因子:
--
通讯作者:
Sawyer DB
中科院分区:
文献类型:
--
作者:
Pentassuglia L;Sawyer DB
Neuregulin(Nrg)/ErbB and integrin signaling pathways are critical for the normal function of the embryonic and adult heart. Both systems activate several downstream signaling pathways, with different physiological outputs: cell survival, fibrosis, excitation-contraction coupling, myofilament structure, cell-cell and cell-matrix interaction. Activation of ErbB2 by Nrg1β in cardiomycytes or its overexpression in cancer cells induces phosphorylation of FAK (Focal Adhesion Kinase) at specific sites with modulation of survival, invasion and cell-cell contacts. FAK is also a critical mediator of integrin receptors, converting extracellular matrix alterations into intracellular signaling. Systemic FAK deletion is lethal and is associated with left ventricular non-compaction whereas cardiac restriction in adult hearts is well tolerated. Never the less, these hearts are more susceptible to stress conditions like trans-aortic constriction, hypertrophy, and ischemic injury. As FAK is both downstream and specifically activated by integrins and Nrg-1β, here we will explore the role of FAK in the heart as a protective factor and as possible mediator of the crosstalk between the ErbB and Integrin receptors.
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DOI:
10.1083/jcb.200911110
发表时间:
2010-07-26
期刊:
The Journal of cell biology
影响因子:
--
作者:
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通讯作者:
Kunz J
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DOI:
10.1152/ajpheart.00534.2001
发表时间:
2002-02-01
影响因子:
4.8
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Domingos, PP;Fonseca, PM;Franchini, KG
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Franchini, KG
DOI:
10.1152/ajpheart.1999.277.5.h2026
发表时间:
1999-11-01
影响因子:
4.8
作者:
Baliga, RR;Pimental, DR;Kelly, RA
通讯作者:
Kelly, RA
DOI:
10.1161/atvbaha.112.245134
发表时间:
2012-04
期刊:
Arteriosclerosis, thrombosis, and vascular biology
影响因子:
--
作者:
Cheng Z;DiMichele LA;Hakim ZS;Rojas M;Mack CP;Taylor JM
通讯作者:
Taylor JM