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Filamin A in platelets: Bridging the (signaling) gap between the plasma membrane and the actin cytoskeleton

期刊

出版社

FRONTIERS MEDIA SA
DOI: 10.3389/fmolb.2022.1060361

关键词

platelets; filamin A; cytoskeleton; cell signaling; actin

资金

  1. Canadian Institutes of Health Research (CIHR) [PJT-156341]
  2. Michael Smith Foundation for Health Research (MSFHR) Scholar Award
  3. National Heart, Lung, and Blood Institute (NHLBI) [HL126743]
  4. Research Training Studentship from the Canadian Venous Thromboembolism Research Network (CanVECTOR)
  5. UBC Centre for Blood Research
  6. Arthritis Society [19-0491]

向作者/读者索取更多资源

This mini-review summarizes how FLNA transduces critical cell signals to the platelet cytoskeleton.
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.

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