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自噬(autophagy)是一种在真核生物中十分保守的溶酶体依赖性降解途径,它通过形成双层膜结构包裹胞内堆积的蛋白质和受损细胞器并将其运送到溶酶体中进行降解。在实验中发现,一型磷脂酰肌醇4-磷酸5-激酶C亚型(type I phosphatidylinositol 4-phosphate 5-kinase isoform C,PIP5KIC)会参与到自噬过程中。在哺乳动物细胞中,敲低一型磷脂酰肌醇4-磷酸5-激酶C亚型会造成欧米茄体(omegasome)的形状异常,进而造成自噬水平的降低。同样,在酵母中敲掉其同源物磷脂酰肌醇5-激酶Mss4后也会导致类似的现象。因此,推测一型磷脂酰肌醇4-磷酸5-激酶C亚型在自噬体的生成中起着很重要的作用。
Autophagy is a very lysosomal-dependent degradation pathway in eukaryotes that wraps intracellularly packed proteins and damaged organelles and transports them into lysosomes by forming a bilayer membrane structure Degradation. It was found in experiments that type I phosphatidylinositol 4-phosphate 5-kinase isoform C (PIP5KIC) is involved in autophagy. In mammalian cells, knockdown of type I phosphatidylinositol 4-phosphate 5-kinase C isoform causes abnormal omegasome shape, resulting in decreased levels of autophagy. Likewise, knocking out its homolog Phosphatidylinositol 5-kinase Mss4 in yeast also results in a similar phenomenon. Therefore, it is speculated that type I phosphatidylinositol 4-phosphate 5-kinase C subtype plays a very important role in the production of autophagosomes.