| VIP36 is a target of ectodomain shedding and regulates phagocytosis in macrophage Raw 264.7 cells. | |
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MedLine Citation:
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PMID: 22016386 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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Ectodomain shedding is a posttranslational modification mechanism, which liberates extracellular domains of membrane proteins through juxtamembrane processing executed mainly by the ADAM (a disintegrin and metalloprotease) family of metalloproteases. Shedding is a unique and effective mechanism for inducing multifaceted effects through the soluble extracellular domains released and/or the remaining membrane-bound portions, however, the physiological functions of shedding are not yet fully understood. In this study, we performed unbiased proteomic screening for shedding targets in a lipopolysaccharide (LPS)-stimulated macrophage cell line to elucidate a new immunological function of shedding. We identified VIP36 (36 kDa vesicular integral membrane protein), a lectin domain-containing transmembrane protein postulated as a cargo receptor for Golgi-to-ER transport, as a new target for shedding and found that the shedding of VIP36 occurs mainly on the cell surface. In addition, we demonstrate that the amount of VIP36 precisely regulates phagocytosis in macrophages and that the shedding of VIP36 is required for this regulation. These results substantially expand our knowledge of the immunological and cell biological functions of both the shedding process and VIP36 itself. |
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Authors:
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Kyoko Shirakabe; Seisuke Hattori; Motoharu Seiki; Shigeo Koyasu; Yasunori Okada |
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Publication Detail:
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Type: JOURNAL ARTICLE Date: 2011-10-20 |
Journal Detail:
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Title: The Journal of biological chemistry Volume: - ISSN: 1083-351X ISO Abbreviation: - Publication Date: 2011 Oct |
Date Detail:
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Created Date: 2011-10-21 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 2985121R Medline TA: J Biol Chem Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Affiliation:
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Keio University School of Medicine, Japan; |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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