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RNF139

E3 ubiquitin-protein ligase RNF139 · UniProt Q8WU17

Length
664 aa
Mass
76.0 kDa
Annotated
2026-06-10
38 papers in source corpus 17 papers cited in narrative 17 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 5/5 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

RNF139 (TRC8) is an ER-resident, multi-membrane-spanning RING-H2 E3 ubiquitin ligase that couples sterol sensing to protein turnover and serves as a central node in ER-associated degradation (ERAD) (PMID:9689122, PMID:12032852). Through a putative sterol-sensing domain it acts as a lipid-responsive regulator of cholesterol homeostasis: it cooperates with gp78 and binds Insig-1/2 to drive sterol-induced ubiquitination and proteasomal degradation of HMG-CoA reductase (PMID:22143767), and it suppresses SREBP processing by assembling a TRC8·SREBP-2·SCAP complex that blocks SCAP–Sec24 (COPII) interaction and thereby prevents ER-to-Golgi transport and cleavage of SREBP-2, a function independent of its ligase activity (PMID:19706601). Its RING-H2 ligase activity drives degradation of additional ER substrates, including heme oxygenase-1, ATF6 (ubiquitinated at K152), and the misfolded hERG channel, and operates in quality-control degradation of soluble misfolded reporters redundantly with MARCH6 and in concert with signal peptide peptidase (PMID:22689053, PMID:41406921, PMID:27998983, PMID:29519897). RNF139 receives ubiquitin from the membrane-anchored E2 enzyme UBE2J2 in a lipid-packing-sensitive ERAD cascade [PMID:bio_10.1101_2025.07.22.666085], and its own abundance is sterol-responsive and controlled by auto-ubiquitination and DEPTOR-promoted self-degradation (PMID:19706601, PMID:32916025). The ligase is co-opted by HCMV US2 to dislocate and degrade MHC class I and LMAN2L from the ER (PMID:19720873, PMID:38687323), and via its RING domain it enforces cell-cycle arrest, apoptosis, and tumor suppression, with its disruption linked to hereditary t(3;8) renal carcinoma (PMID:9689122, PMID:17016439).

Mechanistic history

Synthesis pass · year-by-year structured walk · 15 steps
  1. 1998 Medium

    Established the molecular identity of TRC8/RNF139 as an ER protein bearing both a sterol-sensing domain and a RING finger, and linked it to renal cancer, framing it as a candidate sterol-responsive regulator and tumor suppressor.

    Evidence Molecular cloning, sequence/domain analysis, and t(3;8) breakpoint characterization

    PMID:9689122

    Open questions at the time
    • No enzymatic activity demonstrated
    • No substrates identified
    • Functional consequence of sterol-sensing domain untested
  2. 2002 High

    Demonstrated that TRC8 is an active ER-localized ubiquitin ligase with in vivo genetic partners, moving it from a sequence-predicted RING protein to a functional E3.

    Evidence In vitro ubiquitin ligase assay, GST-pulldown/Co-IP with DVhl and CSN-5/JAB1, and Drosophila genetic epistasis

    PMID:12032852

    Open questions at the time
    • Physiological ubiquitination substrate not defined
    • Relevance of VHL/CSN5 interactions to mammalian function unclear
  3. 2006 High

    Tied TRC8 ligase activity to a defined cellular outcome by showing RING-dependent cell-cycle arrest, apoptosis, and tumor suppression operating through repression of SREBP target genes.

    Evidence RING mutagenesis, cell-cycle/apoptosis assays, nude mouse xenograft, and SREBP-1a rescue epistasis

    PMID:17016439

    Open questions at the time
    • Direct molecular link between TRC8 and SREBP not yet defined
    • Mechanism of SREBP-target repression unresolved
  4. 2009 High

    Resolved how TRC8 controls SREBP-2: it sequesters SREBP-2·SCAP and blocks COPII-dependent ER exit, a ligase-independent mechanism, while clarifying that TRC8 stability is itself sterol- and proteasome-regulated.

    Evidence Co-IP of ternary complex, RING mutagenesis distinguishing ligase-independent function, proteasome inhibition, and SREBP-2 processing assays

    PMID:19706601

    Open questions at the time
    • Stoichiometry and structure of the TRC8·SREBP-2·SCAP complex unknown
    • How sterol status switches TRC8 stability not mechanistically defined
  5. 2009 High

    Established TRC8 as a host ERAD factor hijacked by viruses, required for US2-mediated MHC I ubiquitination and dislocation within an ER complex containing SPP.

    Evidence siRNA functional screen, Co-IP of MHC I/US2/SPP complex, flow cytometry for surface MHC I, ubiquitination immunoblot

    PMID:19720873

    Open questions at the time
    • Direct vs indirect recognition of MHC I substrate unresolved
    • Role of SPP catalytic activity in the dislocation step undefined
  6. 2011 High

    Defined TRC8 as a partially redundant ERAD ligase for HMG-CoA reductase acting with gp78 and Insig, quantifying its contribution to sterol-regulated reductase degradation.

    Evidence Reciprocal RNAi, Co-IP with Insig-1/2, quantitative ubiquitination and pulse-chase degradation assays

    PMID:22143767

    Open questions at the time
    • E2 partner for reductase ubiquitination by TRC8 not specified here
    • Basis for functional split between TRC8 and gp78 unclear
  7. 2012 High

    Expanded the TRC8 substrate repertoire to heme oxygenase-1, linking TRC8-mediated HO-1 degradation to suppression of cancer cell growth and invasion.

    Evidence Co-IP, ubiquitination assay, viability/invasion assays, siRNA epistasis placing HO-1 downstream of TRC8

    PMID:22689053

    Open questions at the time
    • Role of intramembrane processing in HO-1 degradation not yet addressed
    • Recognition determinants on HO-1 undefined
  8. 2016 High

    Demonstrated TRC8 functions in misfolded-protein quality control, degrading the disease-associated misfolded hERG channel via its transmembrane region with Ube2g2, with chaperone choice (Bag1) routing substrates to TRC8.

    Evidence siRNA screen, transmembrane-domain Co-IP, electrophysiology, pharmacological stabilization, ubiquitination assay

    PMID:27998983

    Open questions at the time
    • How TRC8 discriminates misfolded from native transmembrane substrates unknown
    • Generality beyond hERG untested in this study
  9. 2016 High

    Showed intramembrane proteolysis gates TRC8 substrate access, with SPP cleavage protecting HCV core from TRC8-dependent degradation and combined SPP/TRC8 loss triggering ER stress.

    Evidence SPP knockout/inhibitor combined with TRC8 siRNA, ubiquitination assay, ER stress markers

    PMID:27142248

    Open questions at the time
    • Direct interaction between TRC8 and immature core not fully mapped
    • Coupling between SPP cleavage and TRC8 engagement mechanistically undefined
  10. 2018 High

    Generalized TRC8's quality-control role: it acts redundantly with MARCH6 and alongside SPP to degrade hydrophobic misfolded substrates (mCherry-CL1) routed through the ER membrane.

    Evidence Haploid forward genetic screen, CRISPR double knockout, quantitative turnover proteomics, Co-IP with SPP

    PMID:29519897

    Open questions at the time
    • Substrate features that partition between TRC8 and MARCH6 not defined
    • Structural basis of SPP–ligase coupling unknown
  11. 2018 Medium

    Implicated TRC8 in restriction of HIV-1 Gag, revealing a lysosomal degradation route distinct from its proteasomal handling of HMGCR.

    Evidence Pseudovirus assays, knockouts, proteasome vs lysosome inhibitors, co-localization

    PMID:30563842

    Open questions at the time
    • Single study, single lab
    • Mechanism directing substrates to lysosome vs proteasome unresolved
  12. 2020 Medium

    Identified DEPTOR as a regulator of TRC8 abundance, showing DEPTOR promotes TRC8 auto-ubiquitination/degradation to limit ER stress and chondrocyte apoptosis.

    Evidence Proteomics, Co-IP, DEPTOR knockout mouse, adenoviral TRC8 overexpression, ER stress markers

    PMID:32916025

    Open questions at the time
    • Whether DEPTOR acts directly on TRC8 or via another factor unclear
    • Single study, single lab
  13. 2024 Medium

    Added LMAN2L as an HCMV pUS2-directed TRC8 substrate, connecting TRC8-mediated ER degradation to downstream plasma-membrane trafficking of integrin alpha-6.

    Evidence Co-IP, siRNA/CRISPR knockdown, plasma-membrane proteomics, viral expression assays

    PMID:38687323

    Open questions at the time
    • Single study, single lab
    • Direct vs adaptor-mediated recognition of LMAN2L undefined
  14. 2025 Medium

    Placed RNF139 within a defined ERAD enzymatic cascade as a ligase receiving ubiquitin from the membrane E2 UBE2J2 in a lipid-packing-sensitive manner, providing a biochemical link between membrane lipid state and ubiquitin transfer.

    Evidence Reconstituted in vitro ubiquitination with purified factors and proteoliposomes (preprint)

    PMID:bio_10.1101_2025.07.22.666085

    Open questions at the time
    • Preprint, single lab, no mutagenesis confirmation
    • Physiological relevance of UBE2J2–RNF139 pairing in cells not shown
  15. 2025 Medium

    Demonstrated transcriptional and substrate-level regulation of the ER stress axis by RNF139, which is activated via NR4A3/KLF2/KLF4 and ubiquitinates ATF6 at K152 to limit ER stress in bladder cancer.

    Evidence Co-IP, site-specific (K152) ubiquitination mutagenesis, cycloheximide chase, transcriptional reporters, xenograft

    PMID:41406921

    Open questions at the time
    • Single study, single lab
    • Generality of ATF6 regulation beyond bladder cancer untested

Open questions

Synthesis pass · forward-looking unresolved questions
  • How RNF139 selects and discriminates among its diverse substrates, and how its sterol-sensing domain mechanistically transduces lipid status into substrate engagement and ligase activity, remains unresolved.
  • No structural model of the sterol-sensing domain or substrate-binding interface
  • Determinants partitioning substrates between TRC8 and partner ligases (gp78, MARCH6) undefined
  • Mechanism coupling sterol sensing to ligase activity vs ligase-independent SREBP sequestration unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140096 catalytic activity, acting on a protein 4 GO:0016740 transferase activity 3 GO:0016874 ligase activity 2 GO:0140299 molecular sensor activity 2 GO:0140313 molecular sequestering activity 1
Localization
GO:0005783 endoplasmic reticulum 5 GO:0005768 endosome 1
Pathway
R-HSA-392499 Metabolism of proteins 5 R-HSA-1430728 Metabolism 3 R-HSA-1643685 Disease 3 R-HSA-168256 Immune System 2 R-HSA-8953897 Cellular responses to stimuli 2
Partners
AMFRATF6INSIG1INSIG2MARCH6SCAPSREBP-2UBE2J2
Complex memberships
TRC8·MHC I·US2·SPP ER dislocation complexTRC8·SREBP-2·SCAP complex

Evidence

Reading pass · 17 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1998 TRC8 (RNF139) encodes a 664-amino acid multi-membrane spanning ER protein with similarity to patched, containing a putative sterol-sensing domain and a RING finger motif. The hereditary t(3;8) translocation disrupts TRC8 within its sterol-sensing domain, and an acquired TRC8 mutation was identified in sporadic renal carcinomas. Molecular cloning, sequence analysis, breakpoint characterization Proceedings of the National Academy of Sciences of the United States of America Medium 9689122
2002 TRC8 protein localizes to the endoplasmic reticulum, encodes a RING-H2 finger with in vitro ubiquitin ligase activity, physically interacts with DVhl (Drosophila VHL) as shown by GST-pulldown and co-immunoprecipitation, and both DTrc8 and DVhl loss-of-function produce an identical ventral midline defect in Drosophila. DTrc8 also physically interacts with CSN-5/JAB1. GST-pulldown, co-immunoprecipitation, in vitro ubiquitin ligase assay, subcellular fractionation/localization, Drosophila genetic epistasis Oncogene High 12032852
2005 TRC8-induced growth suppression in Drosophila is dependent on CSN5/JAB1 and CSN6 (COP9 signalosome subunits): haploinsufficiency of CSN5 or specific point mutations (T100I) relieved DTrc8-dependent growth suppression, consistent with yeast two-hybrid interaction strengths. DTrc8 overexpression elevated levels of CSN5, CSN7, and the CSN holocomplex. Drosophila genetic epistasis, yeast two-hybrid, immunoblot Oncogene Medium 15735686
2006 TRC8 causes G2/M arrest, decreased DNA synthesis, increased apoptosis, and tumor suppression in a nude mouse model, all dependent on the RING-H2 ubiquitin ligase domain. TRC8 represses SREBP target genes (cholesterol/fatty acid biosynthesis), and expression of activated SREBP-1a partially restores growth of TRC8-inhibited cells. RING domain mutagenesis, flow cytometry, BrdU incorporation, nude mouse xenograft, gene expression analysis, epistasis via SREBP-1a rescue Oncogene High 17016439
2009 TRC8 is required for US2-mediated MHC class I ubiquitination and dislocation from the ER. TRC8 forms a multiprotein ER complex containing MHC I, US2, and signal peptide peptidase (SPP). Depletion of TRC8 prevents MHC I ubiquitination and dislocation and restores cell surface MHC I. siRNA library functional screen, co-immunoprecipitation (complex formation), flow cytometry (cell surface MHC I), immunoblot for ubiquitination The Journal of cell biology High 19720873
2009 TRC8 binds both SREBP-2 and SCAP, forming a TRC8·SREBP-2·SCAP complex at the ER that blocks SCAP interaction with Sec24 (a COPII component), thereby preventing ER-to-Golgi transport of SREBP-2 and reducing SREBP-2 cleavage/activation. This inhibition of SREBP-2 processing is independent of TRC8 E3 ligase activity. TRC8 undergoes auto-ubiquitination and is destabilized by the proteasome; its stability is increased under sterol-depleted conditions. Co-immunoprecipitation, RING domain mutagenesis, proteasome inhibitor treatment, lipoprotein depletion, SREBP-2 cleavage/processing assays The Journal of biological chemistry High 19706601
2010 TRC8 protein levels are sterol-responsive; TRC8 binds INSIG and stimulates INSIG ubiquitylation. TRC8 overexpression destabilizes precursor forms of SREBP-1 and SREBP-2 in a RING-dependent, proteasome-dependent manner. TRC8 physically interacts with eIF3 subunits (eIF3f and eIF3h) as confirmed by co-immunoprecipitation, and TRC8 overexpression suppresses polysome profiles and generates ubiquitylated proteins in eIF3 immunoprecipitates. Co-immunoprecipitation, RING domain mutagenesis, polysome profiling, immunoblot, Drosophila genetic interaction Molecular cancer research : MCR Medium 20068067
2011 TRC8 and gp78 are both RING-finger E3 ubiquitin ligases that cooperate in sterol-induced ubiquitination and proteasomal degradation of HMG-CoA reductase. Both Insig-1 and Insig-2 bind TRC8. TRC8 knockdown inhibits sterol-induced reductase ubiquitination and degradation by 50-60%; combined knockdown of gp78 and TRC8 produces >90% inhibition. Knockdown of gp78 increases TRC8 and Insig-1 protein levels three- to fourfold. RNAi knockdown, co-immunoprecipitation, ubiquitination assay, pulse-chase degradation assay Proceedings of the National Academy of Sciences of the United States of America High 22143767
2012 TRC8 targets heme oxygenase-1 (HO-1) for ubiquitination and proteasomal degradation at the ER. Ectopic TRC8 suppresses HO-1-induced cancer cell growth and migration/invasion; HO-1 depletion reduces the tumorigenic and invasive capacities caused by TRC8 knockdown, placing HO-1 downstream of TRC8. Co-immunoprecipitation, ubiquitination assay, cell viability/invasion assays, siRNA epistasis Oncogene High 22689053
2016 TRC8 is required for proteasomal degradation of the immature (uncleaved) HCV core protein. SPP cleavage of immature core prevents TRC8-mediated degradation; in SPP-knockout or SPP-inhibitor-treated cells, the uncleaved immature core is rapidly degraded via TRC8-dependent ubiquitin-proteasome pathway. Loss of both SPP and TRC8 causes ER stress. SPP knockout/inhibitor, TRC8 siRNA knockdown, ubiquitination assay, ER stress markers, immunoblot Nature communications High 27142248
2016 TRC8 interacts through its transmembrane region with misfolded hERG potassium channel and mediates its ubiquitin-proteasome degradation together with E2-conjugating enzyme Ube2g2. The co-chaperone Bag1 shifts hERG degradation from CHIP-dependent to TRC8-dependent machinery. TRC8 also mediates degradation of the misfolded hERG-G601S disease mutant, and pharmacological stabilization of mutant structure prevents TRC8-mediated degradation. siRNA screen, co-immunoprecipitation (transmembrane interaction), electrophysiology (functional expression), pharmacological stabilization, ubiquitination assay The Journal of biological chemistry High 27998983
2018 TRC8 and MARCH6 are both ER-resident E3 ligases required for proteasome-mediated degradation of the misfolded soluble reporter mCherry-CL1, which is routed via the ER membrane in a substrate-hydrophobicity-dependent manner. Complete stabilization of mCherry-CL1 requires double knockout of both MARCH6 and TRC8. TRC8 and MARCH6 also associate with signal peptide peptidase (SPP) and facilitate degradation of the tail-anchored protein heme oxygenase-1 (HO-1) following intramembrane proteolysis. Forward genetic screen (haploid human cells), CRISPR double knockout, quantitative mass spectrometry (turnover), co-immunoprecipitation with SPP EMBO reports High 29519897
2018 INSIG1 coordinates with TRC8 to promote HIV-1 Gag protein degradation through the lysosome pathway (distinct from HMGCR degradation which uses gp78/AMFR and the proteasome). This degradation occurs at intracellular membrane sites including ER and endosomes. Pseudovirus production assay, protein overexpression and gene knockout, pathway inhibitors (proteasome vs lysosome), co-localization The Journal of biological chemistry Medium 30563842
2020 DEPTOR promotes TRC8 auto-ubiquitination and degradation by the ubiquitin-proteasome system in chondrocytes. Loss of DEPTOR leads to TRC8 accumulation, excessive ER stress, and chondrocyte apoptosis. Adenovirus-mediated TRC8 overexpression in chondrocytes exacerbates ER stress. Proteomics, co-immunoprecipitation, DEPTOR knockout mouse model, adenoviral overexpression, ER stress markers Journal of bone and mineral research Medium 32916025
2024 HCMV pUS2 co-opts TRC8 to degrade the ER-resident protein LMAN2L. pUS2 expression is both necessary and sufficient for LMAN2L downregulation in a TRC8-dependent manner. LMAN2L loss impairs trafficking of integrin alpha-6 (ITGA6) to the plasma membrane. Co-immunoprecipitation, siRNA/CRISPR knockdown, proteomic plasma membrane profiling, viral expression assays The Journal of general virology Medium 38687323
2025 RNF139 (TRC8) functions as an E3 ligase downstream of the membrane-anchored E2 enzyme UBE2J2 in the ERAD ubiquitination cascade. In reconstituted systems with purified factors, UBE2J2 activity (which is modulated by membrane lipid packing) directs ubiquitin transfer to RNF139 as well as to squalene monooxygenase substrate. Reconstituted in vitro ubiquitination assay with purified ERAD components, proteoliposome systems bioRxivpreprint Medium bio_10.1101_2025.07.22.666085
2025 NR4A3 transcriptionally activates RNF139 via KLF2 and KLF4. RNF139 directly interacts with ATF6 and mediates its ubiquitination at lysine 152, promoting ATF6 degradation and inhibiting ER stress in bladder cancer cells. Co-immunoprecipitation, ubiquitination assay with site-specific mutagenesis (K152), cycloheximide chase, transcriptional reporter assays, xenograft Pathology, research and practice Medium 41406921

Source papers

Stage 0 corpus · 38 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2011 Sterol-induced degradation of HMG CoA reductase depends on interplay of two Insigs and two ubiquitin ligases, gp78 and Trc8. Proceedings of the National Academy of Sciences of the United States of America 139 22143767
1998 The hereditary renal cell carcinoma 3;8 translocation fuses FHIT to a patched-related gene, TRC8. Proceedings of the National Academy of Sciences of the United States of America 128 9689122
2009 The TRC8 E3 ligase ubiquitinates MHC class I molecules before dislocation from the ER. The Journal of cell biology 123 19720873
1997 Control of G1 in the developing Drosophila eye: rca1 regulates Cyclin A. Genes & development 93 9000053
2018 MARCH6 and TRC8 facilitate the quality control of cytosolic and tail-anchored proteins. EMBO reports 67 29519897
2010 The TRC8 ubiquitin ligase is sterol regulated and interacts with lipid and protein biosynthetic pathways. Molecular cancer research : MCR 64 20068067
2009 The sterol-sensing endoplasmic reticulum (ER) membrane protein TRC8 hampers ER to Golgi transport of sterol regulatory element-binding protein-2 (SREBP-2)/SREBP cleavage-activated protein and reduces SREBP-2 cleavage. The Journal of biological chemistry 61 19706601
1995 Mutations in RCA1 and AFG3 inhibit F1-ATPase assembly in Saccharomyces cerevisiae. FEBS letters 55 7589436
2012 TRC8 suppresses tumorigenesis through targeting heme oxygenase-1 for ubiquitination and degradation. Oncogene 53 22689053
1993 The pde2 gene of Saccharomyces cerevisiae is allelic to rca1 and encodes a phosphodiesterase which protects the cell from extracellular cAMP. FEBS letters 53 8391474
2016 TRC8-dependent degradation of hepatitis C virus immature core protein regulates viral propagation and pathogenesis. Nature communications 46 27142248
2002 The TRC8 hereditary kidney cancer gene suppresses growth and functions with VHL in a common pathway. Oncogene 46 12032852
1996 Three genes for mitochondrial proteins suppress null-mutations in both Afg3 and Rca1 when over-expressed. Current genetics 44 8753648
2012 Identification and functional characterization of Rca1, a transcription factor involved in both antifungal susceptibility and host response in Candida albicans. Eukaryotic cell 43 22581526
2006 RING-dependent tumor suppression and G2/M arrest induced by the TRC8 hereditary kidney cancer gene. Oncogene 36 17016439
2005 Recognition factors of Ricinus communis agglutinin 1 (RCA(1)). Molecular immunology 36 16288808
1999 Neural cell fate in rca1 and cycA mutants: the roles of intrinsic and extrinsic factors in asymmetric division in the Drosophila central nervous system. Mechanisms of development 34 10534619
2007 A constitutional balanced t(3;8)(p14;q24.1) translocation results in disruption of the TRC8 gene and predisposition to clear cell renal cell carcinoma. Genes, chromosomes & cancer 31 17539022
1998 The Neurospora rca-1 gene complements an Aspergillus flbD sporulation mutant but has no identifiable role in Neurospora sporulation. Genetics 27 9539422
2016 Bag1 Co-chaperone Promotes TRC8 E3 Ligase-dependent Degradation of Misfolded Human Ether a Go-Go-related Gene (hERG) Potassium Channels. The Journal of biological chemistry 25 27998983
2015 A transcriptomic analysis of Neurospora crassa using five major crop residues and the novel role of the sporulation regulator rca-1 in lignocellulase production. Biotechnology for biofuels 22 25691917
2010 Characterization of harpy/Rca1/emi1 mutants: patterning in the absence of cell division. Developmental dynamics : an official publication of the American Association of Anatomists 21 20146251
2009 The tumor suppressor gene TRC8/RNF139 is disrupted by a constitutional balanced translocation t(8;22)(q24.13;q11.21) in a young girl with dysgerminoma. Molecular cancer 20 19642973
2023 Salvianolic acid A alleviates atherosclerosis by inhibiting inflammation through Trc8-mediated 3-hydroxy-3-methylglutaryl-coenzyme A reductase degradation. Phytomedicine : international journal of phytotherapy and phytopharmacology 17 36804757
2006 Molecular dissection of the APC/C inhibitor Rca1 shows a novel F-box-dependent function. EMBO reports 15 17099689
2020 DEPTOR Prevents Osteoarthritis Development Via Interplay With TRC8 to Reduce Endoplasmic Reticulum Stress in Chondrocytes. Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research 13 32916025
2016 Propyl gallate sensitizes human lung cancer cells to cisplatin-induced apoptosis by targeting heme oxygenase-1 for TRC8-mediated degradation. European journal of pharmacology 13 27375080
2005 Growth suppression induced by the TRC8 hereditary kidney cancer gene is dependent upon JAB1/CSN5. Oncogene 10 15735686
2017 E3 ubiquitin ligase, RNF139, inhibits the progression of tongue cancer. BMC cancer 9 28662643
2015 Glioblastomas with copy number gains in EGFR and RNF139 show increased expressions of carbonic anhydrase genes transformed by ENO1. BBA clinical 9 27051584
2018 Insulin-induced gene 1 (INSIG1) inhibits HIV-1 production by degrading Gag via activity of the ubiquitin ligase TRC8. The Journal of biological chemistry 6 30563842
2021 An E3 Ubiquitin Ligase RNF139 Serves as a Tumor-Suppressor in Glioma. Journal of molecular neuroscience : MN 5 34106407
2015 TRC8 downregulation contributes to the development of non-alcoholic steatohepatitis by exacerbating hepatic endoplasmic reticulum stress. Biochimica et biophysica acta 4 26319415
2024 HCMV US2 co-opts TRC8 to degrade the endoplasmic reticulum-resident protein LMAN2L. The Journal of general virology 2 38687323
2026 Arnicolide C induces ferroptosis in liver cancer through modulation of the HMOX1-TRC8 axis. Phytomedicine : international journal of phytotherapy and phytopharmacology 0 41579588
2025 Targeting the NR4A3-RNF139-ATF6 pathway as a therapeutic and diagnostic strategy in bladder cancer. Pathology, research and practice 0 41406921
2019 A Novel RNF139 Mutation in Hemangioblastomas: Case Report. Frontiers in neurology 0 31031691
1996 Analysis of the N-glycosylation of the serum glycoproteins defined by Con A, PHA-E, RCA1 and WGA in Chinese patients with gastrointestinal diseases. Chinese medical sciences journal = Chung-kuo i hsueh k'o hsueh tsa chih 0 9206117

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