Evidence map›Paper›PMID 18573918›Full record

ArticleThe Journal of cell biology2008

Role of Sec61p in the ER-associated degradation of short-lived transmembrane proteins.

Daniel C Scott, Randy Schekman

Abstract read
In one paragraph

Article in The Journal of cell biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

52 citing papers in PubMed.

  1. Review
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  4. Hidden Relationships betweenInternational journal of molecular sciences · 2022
    Review
  5. Article
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  7. Review
  8. Article
  9. Article
  10. PINK1 Content in Mitochondria is Regulated by ER-Associated Degradation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  11. Article
  12. Article
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  15. Article
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  19. Article
  20. Glycosylation-directed quality control of protein folding.Nature reviews. Molecular cell biology · 2015
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Daniel C ScottDepartment of Molecular and Cell Biology and Howard Hughes Medical Institute, University of California, Berkeley, Berkeley, CA 94720, USA.
Randy Schekman

Funding

Howard Hughes Medical Institute
6 · The paper itself

Abstract

Misfolded proteins in the endoplasmic reticulum (ER) are identified and degraded by the ER-associated degradation pathway (ERAD), a component of ER quality control. In ERAD, misfolded proteins are removed from the ER by retrotranslocation into the cytosol where they are degraded by the ubiquitin-proteasome system. The identity of the specific protein components responsible for retrotranslocation remains controversial, with the potential candidates being Sec61p, Der1p, and Doa10. We show that the cytoplasmic N-terminal domain of a short-lived transmembrane ERAD substrate is exposed to the lumen of the ER during the degradation process. The addition of N-linked glycan to the N terminus of the substrate is prevented by mutation of a specific cysteine residue of Sec61p, as well as a specific cysteine residue of the substrate protein. We show that the substrate protein forms a disulfide-linked complex to Sec61p, suggesting that at least part of the retrotranslocation process involves Sec61p.

Indexed as

Protein Processing, Post-TranslationalCysteineDisulfidesElectrophoresisEndoplasmic ReticulumGlycosylationIntramolecular TransferasesMembrane ProteinsMembrane Transport ProteinsModels, BiologicalMutant ProteinsMutationProtein TransportSaccharomyces cerevisiae ProteinsSEC Translocation ChannelsSubstrate SpecificityCysteineDEG1 protein, S cerevisiaeDisulfidesIntramolecular TransferasesMembrane ProteinsMembrane Transport ProteinsMutant ProteinsSaccharomyces cerevisiae ProteinsSEC61 protein, S cerevisiaeSEC Translocation Channels

Identifiers

PMID18573918
PMCPMC2442213

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.