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Alpha-arrestins Aly1/Art6 and Aly2/Art3 regulate trafficking of the glycerophosphoinositol transporter Git1 and impact phospholipid homeostasis
Biology of the Cell ( IF 2.4 ) Pub Date : 2021-09-25 , DOI: 10.1111/boc.202100007
Benjamin P Robinson 1 , Sarah Hawbaker 2 , Annette Chiang 2 , Eric M Jordahl 2 , Sanket Anaokar 1 , Alexiy Nikiforov 1 , Ray W Bowman 1, 2 , Philip Ziegler 1 , Ceara K McAtee 2 , Jana Patton-Vogt 1 , Allyson F O'Donnell 1, 2
Affiliation  

Phosphatidylinositol (PI) is an essential phospholipid, critical to membrane bilayers. The complete deacylation of PI by B-type phospholipases produces intracellular and extracellular glycerophosphoinositol (GPI). Extracellular GPI is transported into the cell via Git1, a member of the Major Facilitator Superfamily of transporters at the yeast plasma membrane. Internalized GPI is degraded to produce inositol, phosphate and glycerol, thereby contributing to these pools. GIT1 gene expression is controlled by nutrient balance, with phosphate or inositol starvation increasing GIT1 expression to stimulate GPI uptake. However, less is known about control of Git1 protein levels or localization.

中文翻译:

α-arrestins Aly1/Art6 和 Aly2/Art3 调节甘油磷酸肌醇转运蛋白 Git1 的运输并影响磷脂稳态

磷脂酰肌醇 (PI) 是一种必需的磷脂,对膜双层至关重要。B 型磷脂酶对 PI 的完全脱酰基产生细胞内和细胞外甘油磷酸肌醇 (GPI)。细胞外 GPI 通过 Git1 转运到细胞中,Git1 是酵母质膜转运蛋白的主要促进子超家族的成员。内化的 GPI 被降解以产生肌醇、磷酸盐和甘油,从而有助于这些池。GIT1基因表达受营养平衡控制,磷酸盐或肌醇饥饿增加GIT1表达以刺激 GPI 摄取。然而,对 Git1 蛋白水平或定位的控制知之甚少。
更新日期:2021-09-25
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