Novel insights into mechanisms for Pak1-mediated regulation of cardiac Ca(2+) homeostasis.
Novel insights into mechanisms for Pak1-mediated regulation of cardiac Ca(2+) homeostasis.
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DOI:
10.3389/fphys.2015.00076
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发表时间:
2015
影响因子:
4
通讯作者:
Lei M
中科院分区:
文献类型:
--
作者:
Wang Y;Tsui H;Bolton EL;Wang X;Huang CL;Solaro RJ;Ke Y;Lei M
A series of recent studies report novel roles for Pak1, a key member of the highly conserved family of serine-threonine protein kinases regulated by Ras-related small G-proteins, Cdc42/Rac1, in cardiac physiology and cardioprotection. Previous studies had identified Pak1 in the regulation of hypertrophic remodeling that could potentially lead to heart failure. This article provides a review of more recent findings on the roles of Pak1 in cardiac Ca2+ homeostasis. These findings identified crucial roles for Pak1 in cardiomyocyte Ca2+ handling and demonstrated that it functions through unique mechanisms involving regulation of the post-transcriptional activity of key Ca2+-handling proteins, including the expression of Ca2+-ATPase SERCA2a, along with the speculative possibility of an involvement in the maintenance of transverse (T)-tubular structure. They highlight important regulatory functions of Pak1 in Ca2+ homeostasis in cardiac cells, and identify novel potential therapeutic strategies directed at manipulation of Pak1 signaling for the management of cardiac disease, particularly heart failure.
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影响因子:
37.8
作者:
Liu W;Zi M;Naumann R;Ulm S;Jin J;Taglieri DM;Prehar S;Gui J;Tsui H;Xiao RP;Neyses L;Solaro RJ;Ke Y;Cartwright EJ;Lei M;Wang X
通讯作者:
Wang X
影响因子:
4.4
作者:
Backes C;Rühle F;Stoll M;Haas J;Frese K;Franke A;Lieb W;Wichmann HE;Weis T;Kloos W;Lenhof HP;Meese E;Katus H;Meder B;Keller A
通讯作者:
Keller A
影响因子:
5.5
作者:
Santana, LF;Chase, EG;Greven, R
通讯作者:
Greven, R
影响因子:
64.8
作者:
MANSER, E;LEUNG, T;LIM, L
通讯作者:
LIM, L
DOI:
10.1161/circep.113.001198
发表时间:
2014-10
期刊:
Circulation. Arrhythmia and electrophysiology
影响因子:
--
作者:
Wang Y;Tsui H;Ke Y;Shi Y;Li Y;Davies L;Cartwright EJ;Venetucci L;Zhang H;Terrar DA;Huang CL;Solaro RJ;Wang X;Lei M
通讯作者:
Lei M