ArticleMolecular biology of the cell2013
Golgi-situated endoplasmic reticulum α-1, 2-mannosidase contributes to the retrieval of ERAD substrates through a direct interaction with γ-COP.
Article in Molecular biology of the cell, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 55 citations in OpenAlex.
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- Organellar quality control crosstalk in aging-related disease: Innovation to pave the way.Aging cell · 2025Review
- Trafficking and localization of Golgi-residentFrontiers in plant science · 2025Review
- The Essential Functions of Molecular Chaperones and Folding Enzymes in Maintaining Endoplasmic Reticulum Homeostasis.Journal of molecular biology · 2024Review
- Tracing genetic diversity captures the molecular basis of misfolding disease.Nature communications · 2024Article
- Expression of the Z Variant of α1-Antitrypsin Suppresses Hepatic Cholesterol Biosynthesis in Transgenic Zebrafish.International journal of molecular sciences · 2023Article
- Trafficking-defective mutant PROKR2 cycles between endoplasmic reticulum and Golgi to attenuate endoplasmic reticulum stress.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Critical Determinants in ER-Golgi Trafficking of Enzymes Involved in Glycosylation.Plants (Basel, Switzerland) · 2022Review
- Golgi Alpha1,2-Mannosidase IA Promotes Efficient Endoplasmic Reticulum-Associated Degradation of NKCC2.Cells · 2021Article
- A Genome-Wide Association Study on Liver Stiffness Changes during Hepatitis C Virus Infection Cure.Diagnostics (Basel, Switzerland) · 2021Article
- Article
- Unconventional p97/VCP-Mediated Endoplasmic Reticulum-to-Endosome Trafficking of a Retroviral Protein.Journal of virology · 2021Article
- Differential Effects of STCH and Stress-Inducible Hsp70 on the Stability and Maturation of NKCC2.International journal of molecular sciences · 2021Article
- The cytoplasmic tail of human mannosidase Man1b1 contributes to catalysis-independent quality control of misfolded alpha1-antitrypsin.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- The Crucial Role of Demannosylating Asparagine-Linked Glycans in ERADicating Misfolded Glycoproteins in the Endoplasmic Reticulum.Frontiers in plant science · 2020Review
- A Peptide-Lectin Fusion Strategy for Developing a Glycan Probe for Use in Various Assay Formats.Chemosensors (Basel, Switzerland) · 2019Article
- How to Avoid a No-Deal ER Exit.Cells · 2019Review
- A signal motif retains Arabidopsis ER-α-mannosidase I in the cis-Golgi and prevents enhanced glycoprotein ERAD.Nature communications · 2019Article
- Chaperoning Endoplasmic Reticulum-Associated Degradation (ERAD) and Protein Conformational Diseases.Cold Spring Harbor perspectives in biology · 2019Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Endoplasmic reticulum (ER) α-1, 2-mannosidase (ERManI) contributes to ER-associated protein degradation (ERAD) by initiating the formation of degradation signals on misfolded N-linked glycoproteins. Despite its inferred intracellular location, we recently discovered that the mammalian homologue is actually localized to the Golgi complex. In the present study, the functional role of Golgi-situated ERManI was investigated. Mass spectrometry analysis and coimmunoprecipitation (co-IP) identified a direct interaction between ERManI and γ-COP, the gamma subunit of coat protein complex I (COPI) that is responsible for Golgi-to-ER retrograde cargo transport. The functional relationship was validated by the requirement of both ERManI and γ-COP to support efficient intracellular clearance of the classical ERAD substrate, null Hong Kong (NHK). In addition, site-directed mutagenesis of suspected γ-COP-binding motifs in the cytoplasmic tail of ERManI was sufficient to disrupt the physical interaction and ablate NHK degradation. Moreover, a physical interaction between NHK, ERManI, and γ-COP was identified by co-IP and Western blotting. RNA interference-mediated knockdown of γ-COP enhanced the association between ERManI and NHK, while diminishing the efficiency of ERAD. Based on these findings, a model is proposed in which ERManI and γ-COP contribute to a Golgi-based quality control module that facilitates the retrieval of captured ERAD substrates back to the ER.
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