Ca2+-Sensor Proteins in the Autophagic and Endocytic Traffic

被引:23
|
作者
Ghislat, Ghita
Knecht, Erwin
机构
[1] Ctr Invest Principe Felipe, Lab Biol Celular, Valencia 46012, Spain
[2] CIBERER, Valencia, Spain
关键词
Autophagy; calcium; endocytosis; lysosomes; membrane fusion; INOSITOL 1,4,5-TRISPHOSPHATE RECEPTOR; MUCOLIPIDOSIS TYPE-IV; ENDOPLASMIC-RETICULUM; MEMBRANE-FUSION; CELL-DEATH; SNARE COMPLEXES; CALCIUM-RELEASE; EARLY STEPS; BH3; DOMAIN; BECLIN;
D O I
10.2174/13892037112139990033
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Autophagy and endocytosis are two evolutionarily conserved catabolic processes that comprise vesicle trafficking events for the clearance of the sequestered intracellular and extracellular cargo. Both start differently but end in the same compartment, the lysosome. Mounting evidences from the last years have established the involvement of proteins sensitive to intracellular Ca2+ in the control of the early autophagic steps and in the traffic of autophagic, endocytic and lysosomal vesicles. However, this knowledge is based on dispersed outcomes that do not set up a consensus model of the Ca2+-dependent control of autophagy and endocytosis. Here, we will provide a critical synopsis of insights from the last decade on the involvement of Ca2+-sensor proteins in the activation of autophagy and in fusion events of endocytic vesicles, autophagosomes and lysosomes.
引用
收藏
页码:97 / 110
页数:14
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