磷脂酶
内质网
细胞生物学
翻转酶
磷脂
化学
细胞器
脂质双层
磷脂转移蛋白
磷脂酰丝氨酸
磷脂酰乙醇胺
生物化学
胞浆
膜蛋白
转运蛋白
脂滴
膜接触部位
心磷脂
C2域
生物
未折叠蛋白反应
酿酒酵母
血浆蛋白结合
易位
细胞膜
分泌物
膜脂
钙连接素
内体
溶酶体
脂质双层融合
蛋白质-脂质相互作用
脂质代谢
翻译(生物学)
第61节
外周膜蛋白
蛋白质结构域
植物脂质转运蛋白
整体膜蛋白
内膜
作者
Heitor Gobbi Sebinelli,Camille Syska,Hafez Razmazma,Véronique Albanèse,Ana Rita Dias Araújo,Cécile Hilpert,Cédric Montigny,Christine Jaxel,Manuella Tchamba,Karolina Belingar,Juan Martín D'Ambrosio,Luca Monticelli,Guillaume Lenoir,Alenka Čopič
标识
DOI:10.1083/jcb.202502112
摘要
Lipid scramblases allow passive flip-flop of phospholipids between bilayer leaflets, thereby promoting membrane symmetry. At the endoplasmic reticulum (ER), where phospholipid synthesis is restricted to one leaflet, scramblase activity should be essential for equilibrated membrane growth. The yeast protein Ist2 contains an ER domain and a cytosolic tail that binds the plasma membrane and participates in the transfer of phosphatidylserine. We show both in vitro and in silico that the ER domain of Ist2, which bears homology to the TMEM16 proteins, possesses a lipid scramblase activity that is not regulated by Ca2+. In cells, overexpression or deletion of the ER domain of Ist2 affects ER-related processes including COPII-mediated vesicular transport, lipid droplet homeostasis, and general phospholipid transport, with a specific contribution of residues implicated in lipid scrambling. The weak phenotypes can be augmented by the deletion of another putative scramblase, the protein insertase Get1, suggesting that the combined action of different proteins supports lipid scrambling at the ER.
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