整合素β1通过FAK传导ly6d诱导的巨噬细胞增多症信号并介导诱导衰老的应激诱导液泡形成。

IF 3 4区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY
Keitaro Nakagawa, Taiki Nagano, Ryoko Katasho, Tetsushi Iwasaki, Shinji Kamada
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引用次数: 1

摘要

细胞衰老是由DNA损伤和各种细胞应激引起的高度稳定的细胞周期阻滞。最近,我们发现淋巴细胞抗原6复合体D位点(LY6D)通过诱导Src家族激酶(SFK)介导的巨噬细胞增多症(macropinocytosis),负责诱导衰老诱导的应激诱导液泡形成。然而,从胞外LY6D到胞质SFK的巨量胞饮信号转导的信号分子尚不清楚。在本研究中,我们通过蛋白质组学分析和共免疫沉淀分析确定了跨膜信号蛋白整合素β1是LY6D的相互作用物。抑制整合素β1可破坏ly6d诱导的巨噬细胞增多症,整合素β1通过黏附激酶激活SFK介导巨噬细胞增多症。这些结果表明,整合素β1是ly6d诱导的衰老细胞液泡形成的重要介质。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Integrin β1 transduces the signal for LY6D-induced macropinocytosis and mediates senescence-inducing stress-evoked vacuole formation via FAK.

Cellular senescence is a highly stable cell-cycle arrest induced by DNA damage and various cellular stresses. Recently, we have revealed that lymphocyte antigen 6 complex, locus D (LY6D) is responsible for senescence-inducing stress-evoked vacuole formation through induction of Src family kinase (SFK)-mediated macropinocytosis. However, the signaling molecule(s) transducing the macropinocytosis signal from extracellular LY6D to the cytoplasmic SFK are unknown. In this study, we identified integrin β1, a transmembrane signaling protein, as an interactor of LY6D by proteomic analysis and co-immunoprecipitation assays. Inhibition of integrin β1 impaired LY6D-induced macropinocytosis, and integrin β1 activated SFK through focal adhesion kinase to mediate macropinocytosis. These results indicate that integrin β1 is a crucial mediator of the LY6D-induced vacuole formation in senescent cells.

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来源期刊
FEBS Letters
FEBS Letters 生物-生化与分子生物学
CiteScore
6.60
自引率
2.90%
发文量
303
审稿时长
1 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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