| First Author | Kim SV | Year | 2006 |
| Journal | Science | Volume | 314 |
| Issue | 5796 | Pages | 136-9 |
| PubMed ID | 17023661 | Mgi Jnum | J:113020 |
| Mgi Id | MGI:3664353 | Doi | 10.1126/science.1131920 |
| Citation | Kim SV, et al. (2006) Modulation of cell adhesion and motility in the immune system by Myo1f. Science 314(5796):136-9 |
| abstractText | 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. |
