Modulation of Cell Adhesion and Motility in the Immune System by Myo1f

著者: Sangwon V. Kim, Wajahat Z. Mehal, Xuemei Dong, Volkmar Heinrich, Marc Pypaert, Ira Mellman, Micah Dembo, Mark S. Mooseker, Dianqing Wu, Richard A. Flavell - Science 2006 被引用: 141

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 beta2 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.