ReviewMolecular neurobiology2012
E3 ubiquitin ligases in protein quality control mechanism.
Review in Molecular neurobiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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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.
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Who cites it
11 citing papers in PubMed.
- Deep mutational scanning reveals a correlation between degradation and toxicity of thousands of aspartoacylase variants.Nature communications · 2024Article
- LRSAM1 E3 ubiquitin ligase: molecular neurobiological perspectives linked with brain diseases.Cellular and molecular life sciences : CMLS · 2019Review
- E3 Ubiquitin Ligases Neurobiological Mechanisms: Development to Degeneration.Frontiers in molecular neuroscience · 2017Review
- Gp78 E3 Ubiquitin Ligase: Essential Functions and Contributions in Proteostasis.Frontiers in cellular neuroscience · 2017Review
- Autophagy coupling interplay: can improve cellular repair and aging?Molecular neurobiology · 2014Review
- Ubiquitin ligase ITCH recruitment suppresses the aggregation and cellular toxicity of cytoplasmic misfolded proteins.Scientific reports · 2014Article
- Targeting aldehyde dehydrogenase 2: new therapeutic opportunities.Physiological reviews · 2014Review
- The Not4 E3 ligase and CCR4 deadenylase play distinct roles in protein quality control.PloS one · 2014Article
- Protein quality control system in neurodegeneration: a healing company hard to beat but failure is fatal.Molecular neurobiology · 2013Review
- Misfolded proteins recognition strategies of E3 ubiquitin ligases and neurodegenerative diseases.Molecular neurobiology · 2013Review
- Mahogunin ring finger-1 (MGRN1) suppresses chaperone-associated misfolded protein aggregation and toxicity.Scientific reports · 2013Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In living cells, polypeptide chains emerging from ribosomes and preexisting polypeptide chains face constant threat of misfolding and aggregation. To prevent protein aggregation and to fulfill their biological activity, generally, protein must fold into its proper three-dimensional structure throughout their lifetimes. Eukaryotic cell possesses a quality control (QC) system to contend the problem of protein misfolding and aggregation. Cells achieve this functional QC system with the help of molecular chaperones and ubiquitin-proteasome system (UPS). The well-conserved UPS regulates the stability of various proteins and maintains all essential cellular function through intracellular protein degradation. E3 ubiquitin ligase enzyme determines specificity for degradation of certain substrates via UPS. New emerging evidences have provided considerable information that various E3 ubiquitin ligases play a major role in cellular QC mechanism and principally designated as QC E3 ubiquitin ligases. Nevertheless, very little is known about how E3 ubiquitin ligase maintains QC mechanism against abnormal proteins under various stress conditions. Here in this review, we highlight and discuss the functions of various E3 ubiquitin ligases implicated in protein QC mechanism. Improving our knowledge about such processes may provide opportunities to modulate protein QC mechanism in age-of-onset diseases that are caused by protein aggregation.
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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.