ArticleScientific reports2016
Genome-wide identification and gene expression profiling of ubiquitin ligases for endoplasmic reticulum protein degradation.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 77 citations in OpenAlex.
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- Hypertonicity-induced RNF183 targets NKCC1 to protect kidney collecting duct cells but induces apoptosis in colon cells.Communications biology · 2026Article
- Candidate Genes Associated with Survival Following Highly Pathogenic Avian Influenza Infection in Chickens.International journal of molecular sciences · 2024Article
- The ubiquitin codes in cellular stress responses.Protein & cell · 2024Review
- Application of PROTACs in Target Identification and Target Validation.Acta materia medica · 2024Article
- RNF185 Control of COL3A1 Expression Limits Prostate Cancer Migration and Metastatic Potential.Molecular cancer research : MCR · 2024Article
- Role of the Mitochondrial E3 Ubiquitin Ligases as Possible Therapeutic Targets in Cancer Therapy.International journal of molecular sciences · 2023Review
- Revolutionizing Drug Targeting Strategies: Integrating Artificial Intelligence and Structure-Based Methods in PROTAC Development.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Mechanisms of substrate processing during ER-associated protein degradation.Nature reviews. Molecular cell biology · 2023Review
- Novel gene-intergenic fusion involving ubiquitin E3 ligase UBE3C causes distal hereditary motor neuropathy.Brain : a journal of neurology · 2023Article
- The Endoplasmic Reticulum and the Fidelity of Nascent Protein Localization.Cold Spring Harbor perspectives in biology · 2023Review
- ATP13A1 prevents ERAD of folding-competent mislocalized and misoriented proteins.Molecular cell · 2022Article
- Improper Proteostasis: Can It Serve as Biomarkers for Neurodegenerative Diseases?Molecular neurobiology · 2022Review
- Knockdown of RNF183 suppressed proliferation of lung adenocarcinoma cellsCell cycle (Georgetown, Tex.) · 2022Article
- FromCells · 2022Review
- A structurally conserved site in AUP1 binds the E2 enzyme UBE2G2 and is essential for ER-associated degradation.PLoS biology · 2021Article
- Review
- Divalent Metal Transporter 1 Knock-Down Modulates IL-1β Mediated Pancreatic Beta-Cell Pro-Apoptotic Signaling Pathways through the Autophagic Machinery.International journal of molecular sciences · 2021Article
- Drugging the "Undruggable" MYCN Oncogenic Transcription Factor: Overcoming Previous Obstacles to Impact Childhood Cancers.Cancer research · 2021Review
- Elevated post-ischemic ubiquitination results from suppression of deubiquitinase activity and not proteasome inhibition.Cellular and molecular life sciences : CMLS · 2021Article
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endoplasmic reticulum (ER)-associated degradation (ERAD) is a mechanism by which unfolded proteins that accumulate in the ER are transported to the cytosol for ubiquitin-proteasome-mediated degradation. Ubiquitin ligases (E3s) are a group of enzymes responsible for substrate selectivity and ubiquitin chain formation. The purpose of this study was to identify novel E3s involved in ERAD. Thirty-seven candidate genes were selected by searches for proteins with RING-finger motifs and transmembrane regions, which are the major features of ERAD E3s. We performed gene expression profiling for the identified E3s in human and mouse tissues. Several genes were specifically or selectively expressed in both tissues; the expression of four genes (RNFT1, RNF185, CGRRF1 and RNF19B) was significantly upregulated by ER stress. To determine the involvement of the ER stress-responsive genes in ERAD, we investigated their ER localisation, in vitro autoubiquitination activity and ER stress resistance. All were partially localised to the ER, whereas CGRRF1 did not possess E3 activity. RNFT1 and RNF185, but not CGRRF1 and RNF19B, exhibited significant resistance to ER stressor in an E3 activity-dependent manner. Thus, these genes are possible candidates for ERAD E3s.
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Registered trials
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