Septin 7 reduces nonmuscle myosin IIA activity in the SNAP23 complex and hinders GLUT4 storage vesicle docking and fusion

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• 作者：Anita A. Wasik^a ; Vincent Dumont^a ; Jukka Tienari^b ; Tuula A. Nyman^c ; Christopher L. Fogarty^e ; ^f ; ^g ; Carol Forsblom^e ; ^f ; ^g ; Markku Lehto^e ; ^f ; ^g ; Eero Lehtonen^a ; ^d ; Per-Henrik Groop^e ; ^f ; ^g ; ^h ; Sanna Lehtonen^a ; ^{sanna.h.lehtonen@helsinki.fi}
• 关键词：DN ; diabetic nephropathy ; GLUT4 ; glucose transporter 4 ; GSV ; GLUT4 storage vesicle ; NM-IIA ; nonmuscle myosin IIA ; NMHC-IIA ; nonmuscle myosin heavy chain IIA ; pp-RLC ; phosphorylated myosin regulatory light chain ; SNAP23 ; synaptosome-associated protein ; 23  ; kDa ; SNARE ; N-ethylmaleimide&ndash ; sensitive fusion protein attachment protein receptor ; VAMP2 ; vesicle-associated membrane protein 2
• 刊名：Experimental Cell Research
• 出版年：2017
• 出版时间：15 January 2017
• 年：2017
• 卷：350
• 期：2
• 页码：336-348
• 全文大小：2005 K
• 卷排序：350

文摘

Septin 7, nonmuscle myosin heavy chain IIA (NMHC-IIA) and SNAP23 form a complex. Knockdown of septin 7 increases NM-IIA activity in the SNAP23 complex. Insulin decreases septin 7 level and increases NM-IIA activity in the SNAP23 complex. Septin 7 hinders GSV docking/fusion by reducing NM-IIA activity in the SNAP23 complex.