ArticlePLoS biology2011
Ubiquitylation in ERAD: reversing to go forward?
Article in PLoS biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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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.
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.
Who cites it
19 citing papers in PubMed, 31 citations in OpenAlex.
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- Molecular Regulation of Lysophosphatidic Acid Receptor 1 Maturation and Desensitization.Cell biochemistry and biophysics · 2021Review
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- Targeting protein quality control pathways in breast cancer.BMC biology · 2017Review
- Targeting p97 to Disrupt Protein Homeostasis in Cancer.Frontiers in oncology · 2016Review
- UBXN2A regulates nicotinic receptor degradation by modulating the E3 ligase activity of CHIP.Biochemical pharmacology · 2015Article
- Inhibitors of the AAA+ chaperone p97.Molecules (Basel, Switzerland) · 2015Review
- Ricin trafficking in cells.Toxins · 2015Review
- CHIP, a carboxy terminus HSP-70 interacting protein, prevents cell death induced by endoplasmic reticulum stress in the central nervous system.Frontiers in cellular neuroscience · 2014Article
- ERO1α-dependent endoplasmic reticulum-mitochondrial calcium flux contributes to ER stress and mitochondrial permeabilization by procaspase-activating compound-1 (PAC-1).Cell death & disease · 2013Article
- Identification of GABA(C) receptor protein homeostasis network components from three tandem mass spectrometry proteomics approaches.Journal of proteome research · 2013Article
- Decoupling the role of ubiquitination for the dislocation versus degradation of major histocompatibility complex (MHC) class I proteins during endoplasmic reticulum-associated degradation (ERAD).The Journal of biological chemistry · 2013Article
- Article
- Macrolide antibiotics block autophagy flux and sensitize to bortezomib via endoplasmic reticulum stress-mediated CHOP induction in myeloma cells.International journal of oncology · 2013Article
- Control of Tobacco mosaic virus movement protein fate by CELL-DIVISION-CYCLE protein48.Plant physiology · 2012Article
- Roles of p97-associated deubiquitinases in protein quality control at the endoplasmic reticulum.Current protein & peptide science · 2012Review
- The delicate balance between secreted protein folding and endoplasmic reticulum-associated degradation in human physiology.Physiological reviews · 2012Review
- Hormesis and Cellular Quality Control: A Possible Explanation for the Molecular Mechanisms that Underlie the Benefits of Mild Stress.Dose-response : a publication of International Hormesis Society · 2012Article
- Transmembrane domain determinants of CD4 Downregulation by HIV-1 Vpu.Journal of virology · 2012Article
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Authors and funding
2 authors at 1 institution in 2 countries.
Funding
Abstract
Proteins are co-translationally inserted into the endoplasmic reticulum (ER) where they undergo maturation. Homeostasis in the ER requires a highly sensitive and selective means of quality control. This occurs through ER-associated degradation (ERAD).This complex ubiquitin-proteasome–mediated process involves ubiquitin conjugating enzymes (E2) and ubiquitin ligases (E3),lumenal and cytosolic chaperones, and other proteins, including the AAA ATPase p97 (VCP; Cdc48 in yeast). Probing of processes involving proteasomal degradation has generally depended on proteasome inhibitors or knockdown of specific E2s or E3s. In this issue of PLoS Biology, Ernst et al. demonstrate the utility of expressing the catalytic domain of a viral deubiquitylating enzyme to probe the ubiquitin system. Convincing evidence is provided that deubiquitylation is integral to dislocation of ERAD substrates from the ER membrane. The implications of this work for understanding ERAD and the potential of expressing deubiquitylating enzyme domains for studying ubiquitin-mediated processes are discussed.
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What OpenQuestion holds
Registered trials
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.