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  • 1
    Publication Date: 2006-10-07
    Description: 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.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Sangwon V -- Mehal, Wajahat Z -- Dong, Xuemei -- Heinrich, Volkmar -- Pypaert, Marc -- Mellman, Ira -- Dembo, Micah -- Mooseker, Mark S -- Wu, Dianqing -- Flavell, Richard A -- K08 DK02965/DK/NIDDK NIH HHS/ -- R01 DK25387/DK/NIDDK NIH HHS/ -- R01 GM054597/GM/NIGMS NIH HHS/ -- R01 GM073823/GM/NIGMS NIH HHS/ -- R01 GM72002/GM/NIGMS NIH HHS/ -- R01 HL080706/HL/NHLBI NIH HHS/ -- R01 HL080706-10/HL/NHLBI NIH HHS/ -- R01 HL080706-11/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2006 Oct 6;314(5796):136-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17023661" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism ; Animals ; Antigens, CD18/metabolism ; *Cell Adhesion ; Cell Degranulation ; *Cell Movement ; Chemotaxis, Leukocyte ; Colony Count, Microbial ; Cytoplasmic Granules/metabolism ; Exocytosis ; *Immunity, Innate ; Ligands ; Listeria monocytogenes/growth & development ; Listeriosis/*immunology/microbiology ; Mice ; Mice, Knockout ; Myosin Type I/deficiency/genetics/*physiology ; N-Formylmethionine Leucyl-Phenylalanine ; Neutrophil Activation ; Neutrophils/immunology/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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