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A single class II myosin modulates T cell motility and stopping, but not synapse formation
被引:167
作者:
Jacobelli, J
Chmura, SA
Buxton, DB
Davis, MM
Krummel, MF
机构:
[1] Univ Calif San Francisco, Dept Pathol, San Francisco, CA 93143 USA
[2] NHLBI, Mol Cardiol Lab, Bethesda, MD 20892 USA
[3] Stanford Univ, Dept Microbiol & Immunol, Sch Med, Stanford, CA 94305 USA
[4] Stanford Univ, Howard Hughes Med Inst, Stanford, CA 94305 USA
关键词:
D O I:
10.1038/ni1065
中图分类号:
R392 [医学免疫学];
Q939.91 [免疫学];
学科分类号:
100102 ;
摘要:
Upon encountering an antigen, motile T cells stop crawling, change morphology and ultimately form an 'immunological synapse'. Although myosin motors are thought to mediate various aspects of this process, the molecules involved and their exact roles are not defined. Here we show that nonmuscle myosin heavy chain IIA, or MyH9, is the only class II myosin expressed in T cells and is associated with the uropod during crawling. MyH9 function is required for maintenance of the uropod and for T cell motility but is dispensable for synapse formation. Phosphorylation of MyH9 in its multimerization domain by T cell receptor-generated signals indicates that inactivation of this motor may be a key step in the 'stop' response during antigen recognition.
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页码:531 / 538
页数:8
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