Absence of platelet phenotype in mice lacking the motor protein myosin Va

Matthew T Harper, Marion T J van den Bosch, Ingeborg Hers, Alastair W Poole

Research output: Contribution to journalArticle (Academic Journal)peer-review

4 Citations (Scopus)

Abstract

The motor protein myosin Va plays an important role in the trafficking of intracellular vesicles. Mutation of the Myo5a gene causes Griscelli syndrome type 1 in humans and the dilute phenotype in mice, which are both characterised by pigment dilution and neurological defects as a result of impaired vesicle transport in melanocytes and neuroendocrine cells. The role of myosin Va in platelets is currently unknown. Rab27 has been shown to be associated with myosin Va cargo vesicles and is known to be important in platelet dense granule biogenesis and secretion, a crucial event in thrombus formation. Therefore, we hypothesised that myosin Va may regulate granule secretion or formation in platelets.
Original languageEnglish
Pages (from-to)e53239
JournalPLoS ONE
Volume8
Issue number1
DOIs
Publication statusPublished - 2013

Keywords

  • Phenotype
  • Secretory Vesicles
  • Animals
  • Blood Platelets
  • Platelet Glycoprotein GPIIb-IIIa Complex
  • Myosin Type V
  • Myosin Heavy Chains
  • Mice
  • Cell Shape
  • Male
  • Female
  • Calcium Signaling

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