actin-independent behavior and membrane deformation exhibited by the four-transmembrane protein m6aactin-independent行为和m6a four-transmembrane膜变形表现出的蛋白质.pdfVIP

actin-independent behavior and membrane deformation exhibited by the four-transmembrane protein m6aactin-independent行为和m6a four-transmembrane膜变形表现出的蛋白质.pdf

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actin-independent behavior and membrane deformation exhibited by the four-transmembrane protein m6aactin-independent行为和m6a four-transmembrane膜变形表现出的蛋白质

Actin-Independent Behavior and Membrane Deformation Exhibited by the Four-Transmembrane Protein M6a 1¤ 2 3 1 1 Yasufumi Sato , Naoki Watanabe , Nanae Fukushima , Sakura Mita , Tatsumi Hirata * 1 Division of Brain Function, National Institute of Genetics, Graduate University for Advanced Studies (Sokendai), Mishima, Shizuoka, Japan, 2 Laboratory of Single- Molecule Cell Biology, Tohoku University Graduate School of Life Sciences, Sendai, Miyagi, Japan, 3 Department of Anatomy, Shinshu University School of Medicine, Matsumoto, Nagano, Japan Abstract M6a is a four-transmembrane protein that is abundantly expressed in the nervous system. Previous studies have shown that over-expression of this protein induces various cellular protrusions, such as neurites, filopodia, and dendritic spines. In this detailed characterization of M6a-induced structures, we found their varied and peculiar characteristics. Notably, the M6a- induced protrusions were mostly devoid of actin filaments or microtubules and exhibited free random vibrating motion. Moreover, when an antibody bound to M6a, the membrane-wrapped protrusions were suddenly disrupted, leading to perturbation of the surrounding membrane dynamics involving phosphoinositide signaling. During single-molecule analysis, M6a exhibited cytoskeleton-independent movement and became selectively entrapped along the cell perimeter in an actin-independent manner. These observations highlight the unusual characteristics of M6a, which may have a significant yet unappreciated role in biological systems. Citation: Sato Y, Watanabe N, Fukushima N, Mita S, Hirata T (2011) Actin-Independent Behavior an

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