Possible role of cortactin phosphorylation by protein kinase Cα in actin-bundle formation at growth cone.
Possible role of cortactin phosphorylation by protein kinase Cα in actin-bundle formation at growth cone.
复制标题
蛋白激酶 Cα 导致的皮质蛋白磷酸化在生长锥肌动蛋白束形成中的可能作用。
DOI：
10.1111/boc.201500032
复制
发表时间：
2015
影响因子：
2.7
通讯作者：
Takei K.
中科院分区：
文献类型：
--
作者：
Yamada H;Kikuchi T;Masumoto T;Wei FY;Abe T;Takeda T;Nishiki T;Tomizawa K;Watanabe M;Matsui H;Takei K.
背景信息Corbyn通过与发动蛋白形成环状复合物，机械地捆绑和稳定F‐actin，从而促进生长锥的形态发生。然而，调节机制coronin action是知之甚少。ResultsProtein kinase C（PKC）α colocalises与coronin在生长锥丝状伪足在SH‐ SY 5 Y神经母细胞瘤细胞。佛波醇12-肉豆蔻酸酯13-乙酸酯激活PKC可导致coronin磷酸化、丝状伪足收缩和F-肌动蛋白束丢失。此外，PKCα直接磷酸化cortactinin vitroat S135/T145/S172，减轻cortactinin的肌动蛋白结合和肌动蛋白交联活性，而细胞表达的磷酸化模拟cortactinin突变体阻碍丝状伪足的形成与actin bundle.ConclusionsOur的结果表明，PKC介导的cortactinin磷酸化可能与生长锥的维持有关。
Background InformationCortactin contributes to growth cone morphogenesis by forming with dynamin, ring‐shaped complexes that mechanically bundle and stabilise F‐actin. However, the regulatory mechanism of cortactin action is poorly understood.ResultsImmunofluorescence microscopy revealed that protein kinase C (PKC) α colocalises with cortactin at growth cone filopodia in SH‐SY5Y neuroblastoma cells. PKC activation by phorbol 12‐myristate 13‐acetate causes cortactin phosphorylation, filopodial retraction and F‐actin‐bundle loss. Moreover, PKCα directly phosphorylates cortactinin vitroat S135/T145/S172, mitigating both cortactin's actin‐binding and actin‐crosslinking activity, whereas cellular expression of a phosphorylation‐mimetic cortactin mutant hinders filopodial formation with a significant decrease of actin bundles.ConclusionsOur results indicate that PKC‐mediated cortactin phosphorylation might be implicated in the maintenance of growth cone.