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Role of EDEM in the Release of Misfolded Glycoproteins from the Calnexin Cycle

Molinari, Maurizio, Calanca, Verena, Galli, Carmela, Lucca, Paola, Paganetti, Paolo·2003·Science

Abstract

The mechanisms that determine how folding attempts are interrupted to target folding-incompetent proteins for endoplasmic reticulum–associated degradation (ERAD) are poorly defined. Here the α-mannosidase I–like protein EDEM was shown to extract misfolded glycoproteins, but not glycoproteins undergoing productive folding, from the calnexin cycle. EDEM overexpression resulted in faster release of folding-incompetent proteins from the calnexin cycle and earlier onset of degradation, whereas EDEM down-regulation prolonged folding attempts and delayed ERAD. Up-regulation of EDEM during ER stress may promote cell recovery by clearing the calnexin cycle and by accelerating ERAD of terminally misfolded polypeptides.

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Metadata

Authors
Molinari, M., Calanca, V., Galli, C., Lucca, P., & Paganetti, P.
Venue
Science
Published
2003-02-28
Volume
299
Issue
5611
Pages
1397-1400
ISSN
  • 0036-8075 (ISSN-L)
  • 1095-9203
OpenAlex
W1964706050
Cited by
470
References
2
FWCI
15.41
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: Role of EDEM in the Release of Misfolded Glycoproteins from the Calnexin Cycle. https://app.cochat.ai/papers/10.1126/science.1079474
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Molinari, M., Calanca, V., Galli, C., Lucca, P., & Paganetti, P. (2003). Role of EDEM in the Release of Misfolded Glycoproteins from the Calnexin Cycle. Science. https://doi.org/10.1126/science.1079474

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.