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Pre-sorting endosomal transport of the GPI-anchored protein, CD59, is regulated by EHD1

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    SYSNO ASEP0358085
    Document TypeJ - Journal Article
    R&D Document TypeJournal Article
    Subsidiary JČlánek ve WOS
    TitlePre-sorting endosomal transport of the GPI-anchored protein, CD59, is regulated by EHD1
    Author(s) Cai, B. (US)
    Katafiasz, D. (US)
    Hořejší, Václav (UMG-J) RID
    Naslavsky, N. (US)
    Source TitleTraffic. - : Wiley - ISSN 1398-9219
    Roč. 12, č. 1 (2011), s. 102-120
    Number of pages19 s.
    Languageeng - English
    CountryDK - Denmark
    Keywordscanine kidney cells ; recycling compartment ; receptor
    Subject RIVEB - Genetics ; Molecular Biology
    CEZAV0Z50520514 - UMG-J (2005-2011)
    UT WOS000285206500010
    DOI10.1111/j.1600-0854.2010.01135.x
    AnnotationThe potential role of EHD1 in regulating the family of glycosylphosphatidylinositol-anchored proteins (GPI-APs) has not been determined. Here we demonstrate a novel role for EHD1 in regulating the trafficking of CD59, an endogenous GPI-AP, at early stages of trafficking through the endocytic pathway. EHD1 displays significant colocalization with newly internalized CD59. Upon EHD1 depletion, there is a rapid Rab5-independent coalescence of CD59 in the ERC region. However, expression of an active Arf6 mutant (Q67L), which traps internalized pre-sorting endosomal cargo in phosphatidylinositol(4,5)-bisphosphate enriched vacuoles, prevents this coalescence. It is of interest that sustained PKC activation leads to a similar coalescence of CD59 at the ERC, and treatment of EHD1-depleted cells with a PKC inhibitor (Go6976) blocked this rapid relocation of CD59. However, unlike sustained PKC activation, EHD1 depletion does not induce the translocation of PKC alpha to ERC.
    WorkplaceInstitute of Molecular Genetics
    ContactNikol Škňouřilová, nikol.sknourilova@img.cas.cz, Tel.: 241 063 217
    Year of Publishing2011
Number of the records: 1  

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