| Literature DB >> 26519113 |
Xiping Cheng1, Xiaoli Zhang2, Lu Yu2, Haoxing Xu3.
Abstract
Resealing allows cells to mend damaged membranes rapidly when plasma membrane (PM) disruptions occur. Models of PM repair mechanisms include the "lipid-patch", "endocytic removal", and "macro-vesicle shedding" models, all of which postulate a dependence on local increases in intracellular Ca(2+) at injury sites. Multiple calcium sensors, including synaptotagmin (Syt) VII, dysferlin, and apoptosis-linked gene-2 (ALG-2), are involved in PM resealing, suggesting that Ca(2+) may regulate multiple steps of the repair process. Although earlier studies focused exclusively on external Ca(2+), recent studies suggest that Ca(2+) release from intracellular stores may also be important for PM resealing. Hence, depending on injury size and the type of injury, multiple sources of Ca(2+) may be recruited to trigger and orchestrate repair processes. In this review, we discuss the mechanisms by which the resealing process is promoted by vesicular Ca(2+) channels and Ca(2+) sensors that accumulate at damage sites.Entities:
Keywords: Ca(2+); Calcium sensor; Lysosomal exocytosis; Membrane repair; TRPML1
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Year: 2015 PMID: 26519113 PMCID: PMC4681278 DOI: 10.1016/j.semcdb.2015.10.031
Source DB: PubMed Journal: Semin Cell Dev Biol ISSN: 1084-9521 Impact factor: 7.727