Truncated CASK does not alter skeletal muscle or protein interactors.
Truncated CASK does not alter skeletal muscle or protein interactors.
复制标题
截短的 CASK 不会改变骨骼肌或蛋白质相互作用因子。
DOI：
10.1002/mus.20993
复制
发表时间：
2008
期刊：
影响因子：
3.4
通讯作者：
Rafael-Fortney,JillA
中科院分区：
文献类型：
--
作者：
Sanford,JamieL;Mays,TessilyA;Varian,KennethD;Wilson,JoannaB;Janssen,PaulML;Rafael-Fortney,JillA
CASK(Ca~(2+)，钙调蛋白相关丝氨酸/苏氨酸激酶)是哺乳动物细胞连接蛋白，也是果蝇神经肌肉突触的关键蛋白。我们已经证明在哺乳动物骨骼肌中，CASK存在于神经肌肉接头的突触后膜上。CASK与中央突触的通道以生物化学的方式相互作用，在培养细胞中的研究导致了对CASK的功能的提出。然而，GASK在骨骼肌中的体内功能仍不清楚。为了验证木桶功能的假说，我们产生了两个转基因小鼠系，它们在骨骼肌中过表达全长和截短的木桶蛋白。广泛的分析表明，CASK蛋白的过度表达不会影响骨骼肌的形态或生理、神经肌肉连接的形态，也不会影响蛋白质相互作用的水平或分布。这些结果与以前的细胞培养实验相比，强调了体内蛋白质功能分析的重要性。肌肉神经，2008
CASK (Ca2+, calmodulin‐associated serine/threonine kinase) is an essential mammalian cell junction protein and is also crucial atDrosophilaneuromuscular synapses. We have shown that CASK is present in mammalian skeletal muscle at the postsynaptic membrane of the neuromuscular junction. CASK interacts biochemically with channels at central synapses, and studies in cultured cells have led to proposed functions for CASK. However, in vivo functions of CASK in skeletal muscle remain unknown. To test hypotheses of CASK functions, we generated two lines of transgenic mice, which overexpress full‐length and truncated CASK protein in skeletal muscle. Extensive analyses showed that overexpression of CASK protein did not affect the morphology or physiology of skeletal muscle, the morphology of the neuromuscular junction, or the levels or distribution of protein interactors. These results contrast with previous cell culture experiments and emphasize the importance of in vivo analysis of protein function. Muscle Nerve, 2008