Medical College of Wisconsin
CTSICores SearchResearch InformaticsREDCap

Filamin A in platelets: Bridging the (signaling) gap between the plasma membrane and the actin cytoskeleton. Front Mol Biosci 2022;9:1060361

Date

01/07/2023

Pubmed ID

36605989

Pubmed Central ID

PMC9808056

DOI

10.3389/fmolb.2022.1060361

Scopus ID

2-s2.0-85145466782 (requires institutional sign-in at Scopus site)   2 Citations

Abstract

Platelets are anucleate cells that are essential for hemostasis and wound healing. Upon activation of the cell surface receptors by their corresponding extracellular ligands, platelets undergo rapid shape change driven by the actin cytoskeleton; this shape change reaction is modulated by a diverse array of actin-binding proteins. One actin-binding protein, filamin A (FLNA), cross-links and stabilizes subcortical actin filaments thus providing stability to the cell membrane. In addition, FLNA binds the intracellular portion of multiple cell surface receptors and acts as a critical intracellular signaling scaffold that integrates signals between the platelet's plasma membrane and the actin cytoskeleton. This mini-review summarizes how FLNA transduces critical cell signals to the platelet cytoskeleton.

Author List

De Silva E, Hong F, Falet H, Kim H

Author

Herve Falet PhD Associate Professor in the Cell Biology, Neurobiology and Anatomy department at Medical College of Wisconsin