Mechanotransduction in striated muscle via focal adhesion kinase
Mechanotransduction in striated muscle via focal adhesion kinase
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DOI：
10.1042/bst0351312
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发表时间：
2007-11-01
影响因子：
3.9
通讯作者：
Flueck, M.
中科院分区：
文献类型：
--
作者：
Durieux, A. C.;Desplanches, D.;Flueck, M.
收缩组织表现出明显的能力，以重塑其组成，以应对机械挑战。描述性证据表明，上游参与磷酸转移酶FAK（粘着斑激酶）的分子控制负荷依赖性肌肉可塑性。因此，FAK作为机械信号的肌细胞换能器向肌纤维中的下游转录表达进化。体细胞基因治疗的最新进展现在允许探索这种酶在完整肌肉中机械转导的功能参与。
Contractile tissues demonstrate a pronounced capacity to remodel their composition in response to mechanical challenges. Descriptive evidence suggests the upstream involvement of the phosphortransfer enzyme FAK (focal adhesion kinase) in the molecular control of load-dependent muscle plasticity. Thereby FAK evolves as a myocellular transducer of mechanical signals towards downstream transcript expression in myofibres. Recent advances in somatic gene therapy now allow the exploration of the functional involvement of this enzyme in mechanotransduction in intact muscle.