Journal
SCIENCE
Volume 314, Issue 5796, Pages 136-139Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1131920
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Funding
- NHLBI NIH HHS [R01 HL080706, R01 HL080706-10, R01 HL080706-11] Funding Source: Medline
- NIDDK NIH HHS [K08 DK02965, R01 DK25387] Funding Source: Medline
- NIGMS NIH HHS [R01 GM073823, R01 GM054597, R01 GM72002] Funding Source: Medline
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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 beta 2 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.
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