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    Mol Cell. 2009 Jun 12;34(5):627-33.

    EDEM1 recognition and delivery of misfolded proteins to the SEL1L-containing ERAD complex.

    Cormier JH, Tamura T, Sunryd JC, Hebert DN.

    Source

    Department of Biochemistry and Molecular Biology, University of Massachusetts, Amherst, MA 01003, USA.

    Abstract

    Terminally misfolded or unassembled secretory proteins are retained in the endoplasmic reticulum (ER) and subsequently cleared by the ER-associated degradation (ERAD) pathway. The degradation of ERAD substrates involves mannose trimming of N-linked glycans; however, the mechanisms of substrate recognition and sorting to the ERAD pathway are poorly defined. EDEM1 (ER degradation-enhancing alpha-mannosidase-like 1 protein) has been proposed to play a role in ERAD substrate signaling or recognition. We show that EDEM1 specifically binds nonnative proteins in a glycan-independent manner. Inhibition of mannosidase activity with kifunensine or disruption of the EDEM1 mannosidase-like domain by mutation had no effect on EDEM1 substrate binding but diminished its association with the ER membrane adaptor protein SEL1L. These results support a model whereby EDEM1 binds nonnative proteins and uses its mannosidase-like domain to target aberrant proteins to the ER membrane dislocation and ubiquitination complex containing SEL1L.

    PMID:
    19524542
    [PubMed - indexed for MEDLINE]
    PMCID:
    PMC2740909
    Free PMC Article

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