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Cell:PKC依赖的新机制促进细胞损伤愈合

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6月21日,<em>Cell</em>杂志报道,科学家揭示一种PKC依赖的新机制可预防细胞损伤部位与极化细胞骨架之间的竞争,进而促进细胞愈合。</p>
细胞损伤的愈合作用,使细胞膜损伤得以修复,在真核生物中是普遍存在的。损伤愈合反应的一个重要方面是极化的细胞骨架和细胞内分泌机器朝向损伤位点的重新定向。

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虽然关于参与损伤愈合过程的保守蛋白的研究屡有进展,科学家一直没能将这些参与成员联系为一个连贯的反应机制。通过在芽殖酵母中使用激光损伤的方法,研究者证明,局部细胞壁/膜的损伤触发蛋白质从极性生长部位扩散,从而使这些蛋白在伤口部位积累。

研究者发现了一个蛋白激酶-C依赖的机制,可介导成形素蛋白Bni1(一组参与肌动蛋白聚合并与快速增长的肌动蛋白微丝末端相关的蛋白)和胞吐囊组件Sec3蛋白的降解。

这种蛋白降解对防止极化生长部位和细胞损伤部位之间的相互竞争构建的原材料是必不可少的。避免与预先存在的极化细胞骨架发生竞争,可能是高效的极化细胞损伤愈合的一般特征。

该研究,为众多细胞损伤相关疾病,如,心肌细胞、神经细胞损伤,肌肉萎缩等的研究提供了新的启示。 
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<a title="" href="http://dx.doi.org/10.1016/j.cell.2011.10.017" target="_blank">doi:</a><a title="" href="http://www.cell.com/abstract/S0092-8674(12)00651-4" target="_blank">10.1016/j.cell.2011.10.017</a>
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<br/><strong>Proteasomal Degradation Resolves Competition between Cell Polarization and Cellular Wound Healing</strong><br/>


Keiko Kono, Yasushi Saeki, Satoshi Yoshida, Keiji Tanaka, David Pellman

Cellular wound healing, enabling the repair of membrane damage, is ubiquitous in eukaryotes. One aspect of the wound healing response is the redirection of a polarized cytoskeleton and the secretory machinery to the damage site. Although there has been recent progress in identifying conserved proteins involved in wound healing, the mechanisms linking these components into a coherent response are not defined. Using laser damage in budding yeast, we demonstrate that local cell wall/membrane damage triggers the dispersal of proteins from the site of polarized growth, enabling their accumulation at the wound. We define a protein-kinase-C-dependent mechanism that mediates the destruction of the formin Bni1 and the exocyst component Sec3. This degradation is essential to prevent competition between the site of polarized growth and the wound. Mechanisms to overcome competition from a pre-existing polarized cytoskeleton may be a general feature of effective wound healing in polarized cells.

<br/>来源:生物谷

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