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PubMed · 12019562

Actin dynamics in platelets.

E L Bearer·J M Prakash·Z Li
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Abstract

The human blood platelet circulates in the blood as a non-adherent disk. Upon receiving signals of blood vessel damage, the platelet reorganizes its actin cytoskeleton which transforms it into a spiky dynamic adherent glue. This transformation involves a temporal sequence of four morphologically distinct steps which is reproducible in vitro. The actin dynamics underlying these shape changes depend on a large number of actin-binding proteins. Maintenance of the discoid shape requires actin-binding proteins that inhibit these reorganizations, whereas transformation involves other proteins, some to disassemble old filaments and others to polymerize new ones. F-Actin-affinity chromatography identified a large set of actin-binding proteins including VASP, Arp2 and 2E4/kaptin. Recent discoveries show that VASP inhibits filament disassembly and Arp2/3 is required to polymerize new filaments. Morphological analysis of the distribution of these actin-binding proteins in spread platelets together with biochemical measurements of their interactions with actin lead to a model of interactions with actin that mediate shape change.

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ActinsAnimalsBlood PlateletsCalciumCytoplasmHumansPlatelet ActivationTime FactorsJournal ArticleReview

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BibTeXRIS

E L Bearer, J M Prakash, Z Li. 2002. Actin dynamics in platelets.. https://doi.org/10.1016/s0074-7696(02)17014-8

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