dAsap 在 S2R+ 细胞中通过 Arf6 依赖性肌动蛋白调节途径调节细胞突起。

IF 3.5 4区 生物学 Q1 Biochemistry, Genetics and Molecular Biology
Shikha Kushwaha, Bhagaban Mallik, Anjali Bisht, Zeeshan Mushtaq, Srikanth Pippadpally, Nitika Chandra, Subhradip Das, Girish Ratnaparkhi, Vimlesh Kumar
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引用次数: 0

摘要

膜突起是细胞迁移、粘附和通讯等功能的基础,依赖于细胞骨架的动态重组。Arf 蛋白依赖 GAP 的 GTP 水解调节肌动蛋白依赖的膜重塑。在这里,我们发现 dAsap 调节 S2R+ 细胞膜突起的机制主要依赖于其 ArfGAP 结构域以及肌动蛋白调节因子、SCAR 和 Ena 的重新定位。虽然我们的数据加强了 dAsap 在体外对 Arf1 GTP 水解的偏好,但我们证明了在 S2R+ 细胞中膜突起的诱导依赖于 Arf6 的失活。这项研究加深了我们对依赖于 dAsap 的 GTP 水解如何在 Arf6 的活性和非活性状态之间保持平衡以调节细胞形状的理解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

dAsap regulates cellular protrusions via an Arf6-dependent actin regulatory pathway in S2R+ cells

dAsap regulates cellular protrusions via an Arf6-dependent actin regulatory pathway in S2R+ cells

Membrane protrusions are fundamental to cellular functions like migration, adhesion, and communication and depend upon dynamic reorganization of the cytoskeleton. GAP-dependent GTP hydrolysis of Arf proteins regulates actin-dependent membrane remodeling. Here, we show that dAsap regulates membrane protrusions in S2R+ cells by a mechanism that critically relies on its ArfGAP domain and relocalization of actin regulators, SCAR, and Ena. While our data reinforce the preference of dAsap for Arf1 GTP hydrolysis in vitro, we demonstrate that induction of membrane protrusions in S2R+ cells depends on Arf6 inactivation. This study furthers our understanding of how dAsap-dependent GTP hydrolysis maintains a balance between active and inactive states of Arf6 to regulate cell shape.

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来源期刊
FEBS Letters
FEBS Letters 生物-生化与分子生物学
CiteScore
7.00
自引率
2.90%
发文量
303
审稿时长
1.0 months
期刊介绍: FEBS Letters is one of the world''s leading journals in molecular biology and is renowned both for its quality of content and speed of production. Bringing together the most important developments in the molecular biosciences, FEBS Letters provides an international forum for Minireviews, Research Letters and Hypotheses that merit urgent publication.
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