Modulation of cell adhesion and motility in the immune system by Myo1f

Sangwon V. Kim, Wajahat Z. Mehal, Xuemei Dong, Volkmar Heinrich, Marc Pypaert, Ira Mellman, Micah Dembo, Mark S. Mooseker, Dianqing Wu, Richard A. Flavell

Research output: Contribution to journalArticlepeer-review

73 Scopus citations


Although class I myosins are known to play a wide range of roles, the physiological function of long-tailed class I myosins in vertebrates remains elusive. We demonstrated that one of these proteins, Myo1f, is expressed predominantly in the mammalian immune system. Cells from Myo1f-deficient mice exhibited abnormally increased adhesion and reduced motility, resulting from augmented exocytosis of β2 integrin-containing granules. Also, the cortical actin that co-localizes with Myo1f was reduced in Myo1f-deficient cells. In vivo, Myo1f-deficient mice showed increased susceptibility to infection by Listeria monocytogenes and an impaired neutrophil response. Thus, Myo1f directs immune cell motility and innate host defense against infection.

Original languageEnglish (US)
Pages (from-to)136-139
Number of pages4
Issue number5796
StatePublished - Oct 6 2006

ASJC Scopus subject areas

  • General


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