ReviewCurrent opinion in cell biology2009
Substrate-specific mediators of ER associated degradation (ERAD).
Review in Current opinion in cell biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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.
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
55 citing papers in PubMed.
- COPII cage assembly factor Sec13 integrates information flow regulating endomembrane function in response to human variation.Scientific reports · 2024Article
- Heterologous expression of influenza haemagglutinin leads to early and transient activation of the unfolded protein response in Nicotiana benthamiana.Plant biotechnology journal · 2024Article
- Article
- Noncanonical Form of ERAD Regulates Cardiac Hypertrophy.Circulation · 2023Article
- Article
- How Is the Fidelity of Proteins Ensured in Terms of Both Quality and Quantity at the Endoplasmic Reticulum? Mechanistic Insights into E3 Ubiquitin Ligases.International journal of molecular sciences · 2021Review
- Epsin-mediated degradation of IP3R1 fuels atherosclerosis.Nature communications · 2020Article
- Does Inter-Organellar Proteostasis Impact Yeast Quality and Performance During Beer Fermentation?Frontiers in genetics · 2020Article
- Proteostasis In The Endoplasmic Reticulum: Road to Cure.Cancers · 2019Review
- How to Avoid a No-Deal ER Exit.Cells · 2019Review
- HDAC inhibitors rescue multiple disease-causing CFTR variants.Human molecular genetics · 2019Article
- Folding and Misfolding of Human Membrane Proteins in Health and Disease: From Single Molecules to Cellular Proteostasis.Chemical reviews · 2019Article
- A personal retrospective on the mechanisms of antigen processing.Immunogenetics · 2019Review
- Protein Quality Control in the Endoplasmic Reticulum and Cancer.International journal of molecular sciences · 2018Review
- "Mallostery"-ligand-dependent protein misfolding enables physiological regulation by ERAD.The Journal of biological chemistry · 2018Article
- A Proteomic Variant Approach (ProVarA) for Personalized Medicine of Inherited and Somatic Disease.Journal of molecular biology · 2018Article
- Correcting the F508del-CFTR variant by modulating eukaryotic translation initiation factor 3-mediated translation initiation.The Journal of biological chemistry · 2018Article
- Lost in Translation: Ribosome-Associated mRNA and Protein Quality Controls.Frontiers in genetics · 2018Review
- Article
- Unfolded Protein Response of the Endoplasmic Reticulum in Tumor Progression and Immunogenicity.Oxidative medicine and cellular longevity · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Approximately one-third of newly synthesized eukaryotic proteins are targeted to the secretory pathway, which is composed of an organellar network that houses the enzymes and maintains the chemical environment required for the maturation of secreted and membrane proteins. Nevertheless, this diverse group of proteins may fail to achieve their native states and are consequently selected for ER associated degradation (ERAD). Over the past few years, significant effort has been made to dissect the components of the core ERAD machinery that is responsible for the destruction of most ERAD substrates. Interestingly, however, some ERAD substrates associate with dedicated chaperone-like proteins that target them for proteolysis or protect them from destruction. Other substrates fold and function normally but can be selected for ERAD by protein adaptors that identify and transmit regulatory cues.
Indexed as
Identifiers
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.