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Showing COPS5 — CSN5 is a alias.

COPS5

COP9 signalosome complex subunit 5 · UniProt Q92905

Length
334 aa
Mass
37.6 kDa
Annotated
2026-06-09
100 papers in source corpus 54 papers cited in narrative 54 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

COPS5 (CSN5/JAB1) is the catalytic subunit of the COP9 signalosome (CSN) and the cell's principal deneddylase for cullin-RING E3 ubiquitin ligases, thereby acting as a master regulator of protein stability across proliferation, DNA repair, and metabolism (PMID:12183637, PMID:20974137). Its enzymatic activity is encoded by a JAMM-motif metalloprotease that cleaves Nedd8 from Cul1; metal chelation or active-site mutation abolishes this activity without disrupting complex assembly (PMID:12183637). In the free monomer this isopeptidase is autoinhibited by the Ins-1 segment occluding the substrate site, and a single Ins-1 mutation restores activity (PMID:23288897); productive catalysis is unlocked upon assembly into the CSN, where an MPN-MPN interaction between CSN5 and CSN6 within a CSN4-5-6-7 module activates the enzyme, though that module alone is insufficient for efficient CRL deneddylation (PMID:25144743, PMID:23086934). Genetic loss of CSN5 disrupts the entire CSN, leaving cullins hyper-neddylated and causing accumulation of CRL substrates such as p27, p53, and cyclin E, with consequent cell-cycle arrest, senescence, endoreduplication, and embryonic lethality (PMID:15299027, PMID:20974137). Beyond the canonical deneddylase function, CSN5 acts as a CRM1-dependent nuclear-export adaptor through a leucine-rich NES — exemplified by driving nuclear export and proteasomal degradation of p27 — and serves as a substrate-specific stabilizing or destabilizing factor for diverse proteins including Smad4, Smad7, RUNX3, PD-L1, HK2, ZEB1, and NCoR, frequently through control of their ubiquitination and proteasomal turnover (PMID:11704659, PMID:11818334, PMID:14993265, PMID:27866850, PMID:27375289, PMID:31991125). Through these activities CSN5 modulates TGF-β/Smad signaling, DNA repair via a p53→Rad51 axis, p21- and CDK2/cyclin E-dependent senescence, and a metabolic program that suppresses autophagic degradation of Mtch2 to favor glycolysis and limit ROS-driven DNA damage (PMID:11818334, PMID:14993265, PMID:20802511, PMID:23316279, PMID:34874913, PMID:31964807). CSN5 itself is regulated by transcriptional induction downstream of NF-κB and STAT3 and is targeted for degradation by the CUL4B E3 ligase (PMID:27866850, PMID:23357576, PMID:21689417). Its potentiation of MYC and CRL-dependent substrate turnover makes CSN5 isopeptidase activity rate-limiting for oncogenic transformation in vivo (PMID:18199546).

Mechanistic history

Synthesis pass · year-by-year structured walk · 18 steps
  1. 2000 Medium

    Established an early non-deneddylase role for JAB1 as a transcriptional coactivator, framing CSN5 as more than a CRL regulator.

    Evidence Yeast/mammalian two-hybrid, GST pulldown, and reporter assays mapping JAB1 binding to PR and SRC-1

    PMID:10722692

    Open questions at the time
    • No structural basis for coactivation defined
    • Relationship to CSN holocomplex not addressed
  2. 2001 High

    Defined a CSN-independent mechanism by which CSN5 controls substrate fate, identifying it as a CRM1 nuclear-export adaptor for p27.

    Evidence LMB inhibition, NES mutagenesis, dominant-negative truncation, fractionation, and Co-IP identifying a cytoplasmic CSN4-8 shuttle subcomplex

    PMID:11704659

    Open questions at the time
    • Whether export adaptor function requires isopeptidase activity not resolved
    • Subcomplex composition only partially defined
  3. 2002 High

    Identified the JAMM metalloprotease motif as the molecular basis of CSN deneddylase activity, defining CSN5's core catalytic function.

    Evidence In vitro isopeptidase assays with active-site mutagenesis and metal chelation, plus genetic rescue in yeast and Drosophila

    PMID:12183637

    Open questions at the time
    • Did not explain how monomeric CSN5 is kept inactive
    • Substrate repertoire beyond Cul1 not mapped
  4. 2002 Medium

    Connected CSN5 to TGF-β signaling by showing it destabilizes Smad4, establishing it as an antagonist of this pathway.

    Evidence Co-IP, overexpression, proteasome inhibitors, and TGF-β reporter assays

    PMID:11818334

    Open questions at the time
    • E3 ligase mediating Smad4 ubiquitination not identified
    • Dependence on CSN holocomplex untested
  5. 2004 Medium

    Demonstrated CSN5 also targets the inhibitory Smad7 for export and degradation, showing it can both promote and antagonize TGF-β signaling depending on substrate.

    Evidence Reciprocal Co-IP, siRNA, immunofluorescence, FRAP, and phosphorylation assays

    PMID:14993265

    Open questions at the time
    • Reconciliation of opposing Smad4 vs Smad7 effects unresolved
    • Context determining substrate choice unknown
  6. 2004 High

    Established the essentiality of CSN5 in vivo and tied its loss to CRL-substrate accumulation and a deneddylase-independent subcomplex defect.

    Evidence Jab1 knockout and heterozygous mice with p27/p53/cyclin E and neddylated Cul1 readouts in MEFs

    PMID:15299027

    Open questions at the time
    • Distinct contributions of subcomplex vs holocomplex not fully separated
    • Direct substrate vs indirect effects not delineated
  7. 2006 Medium

    Linked CSN5 to apoptotic control via E2F1 and p53, broadening its role beyond proliferation into cell-death decisions.

    Evidence Y2H, Co-IP, shRNA depletion, and apoptosis/p53 assays mapping E2F1 marked-box binding

    PMID:16481464

    Open questions at the time
    • Mechanism of p53 accumulation downstream of E2F1-Jab1 unclear
    • Catalytic requirement untested
  8. 2008 High

    Showed CSN5 isopeptidase activity is rate-limiting for oncogenic transformation, establishing therapeutic rationale for targeting its catalysis.

    Evidence Isopeptidase-dead mutant in primary human cells plus MYC/RAS transgenic mouse breast cancer model

    PMID:18199546

    Open questions at the time
    • Direct CRL substrate driving transformation not pinpointed
    • Mechanism of MYC potentiation not molecularly defined
  9. 2010 High

    Confirmed the JAMM/deneddylase domain is essential for proliferation and linked CSN5 loss to p53-independent senescence and genome instability.

    Evidence Conditional MEF knockout with JAMM-domain rescue and DNA-repair/ChIP analysis of a p53→Rad51 axis

    PMID:20802511 PMID:20974137

    Open questions at the time
    • How CSN5 controls p53 levels mechanistically not fully resolved
    • Direct vs CRL-mediated DNA repair role unclear
  10. 2013 High

    Resolved the structural basis of catalytic autoinhibition, explaining why monomeric CSN5 is inactive.

    Evidence X-ray crystallography of inactive monomer, MD simulation, AUC, and Ins-1 mutagenesis restoring activity

    PMID:23288897

    Open questions at the time
    • Conformational change upon holocomplex assembly not captured at high resolution
    • Physiological trigger of monomer-dimer equilibrium unknown
  11. 2013 High

    Defined the CSN4-5-6-7 architecture and the CSN5-CSN6 MPN-MPN interface that positions the catalytic module within the complex.

    Evidence Bacterial reconstitution, pulldown, SEC, and ITC mapping pairwise and combinatorial interactions

    PMID:23086934

    Open questions at the time
    • Full holocomplex assembly intermediates not all defined
    • How assembly relieves Ins-1 autoinhibition not shown structurally
  12. 2013 High

    Identified CUL4B as the E3 ligase that degrades CSN5, closing a feedback loop in which CSN5 regulates CRLs and a CRL regulates CSN5.

    Evidence siRNA, in vitro and in vivo ubiquitination assays, and CUL4B-null MEFs with BMP reporter

    PMID:23357576

    Open questions at the time
    • Conditions selecting CUL4B-mediated turnover unknown
    • Whether degradation targets monomer or complexed CSN5 unclear
  13. 2014 High

    Demonstrated that CSN5-CSN6 MPN association is necessary but not sufficient for efficient CRL deneddylation, refining the activation model.

    Evidence Hybrid structural modeling, cross-linking mass spectrometry, and heterodimer reconstitution isopeptidase assays

    PMID:25144743

    Open questions at the time
    • Which additional subunits complete activation not identified
    • Quantitative activation mechanism unresolved
  14. 2016 High

    Established CSN5 as a stabilizer of PD-L1 downstream of inflammatory signaling, linking it to tumor immune evasion.

    Evidence Co-IP, ubiquitination assay, NF-κB reporter, siRNA, and in vivo mouse tumor model

    PMID:27866850

    Open questions at the time
    • Whether stabilization is via deneddylation or direct deubiquitination unclear
    • E3 ligase counteracted not defined
  15. 2016 High

    Showed CSN5 isopeptidase-dependent degradation of NCoR drives endocrine-therapy resistance, with catalytic inhibition restoring sensitivity.

    Evidence Co-IP, ubiquitination assay, isopeptidase-dead mutant, and in vitro/in vivo breast cancer models

    PMID:27375289

    Open questions at the time
    • Direct vs CRL-mediated NCoR ubiquitination not separated
  16. 2019 High

    Placed CSN5-mediated p53 degradation under upstream control by Asrij/OCIAD1 sequestration, defining a regulatory brake in stem-cell homeostasis.

    Evidence Asrij knockout mice, Co-IP, polyubiquitination assays, and Nutlin-3 rescue with transplantation

    PMID:30952670

    Open questions at the time
    • Structural basis of OCIA-domain sequestration unknown
    • Whether sequestration blocks catalysis or interaction unclear
  17. 2020 High

    Integrated CSN5 into a metabolism-genome-stability axis by showing it suppresses Mtch2 autophagy to favor glycolysis and limit ROS-driven DNA damage in ESCs.

    Evidence Inducible CRISPR KO ESCs with metabolic, ROS, comet, DDR, and autophagy/Mtch2 readouts

    PMID:31964807

    Open questions at the time
    • Mechanism by which CSN5 restrains Mtch2 autophagy not molecularly defined
    • Relationship to deneddylase activity unclear
  18. 2022 High

    Defined CSN5's tissue-specific requirement in myelinating glia, linking its loss to DNA-damage-induced, p21-dependent senescence and neuroinflammation.

    Evidence Oligodendrocyte-specific conditional KO mice with DNA-damage markers and p21 vs p16 genetic epistasis

    PMID:34874913

    Open questions at the time
    • Direct DNA-repair substrate of CSN5 in glia unknown
    • Why p21 rather than p16 is selected unresolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • How CSN5 selects between its CSN-dependent deneddylase activity and its many CSN-independent substrate-specific and adaptor functions in a given cellular context remains unresolved.
  • No unified model distinguishing holocomplex vs monomer/subcomplex substrate routing
  • Direct deubiquitinase vs CRL-mediated effects rarely separated for individual substrates
  • Structural transition from autoinhibited monomer to active holocomplex not captured

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140096 catalytic activity, acting on a protein 5 GO:0016787 hydrolase activity 3 GO:0098772 molecular function regulator activity 3 GO:0140110 transcription regulator activity 3 GO:0060090 molecular adaptor activity 2
Localization
GO:0005634 nucleus 3 GO:0005829 cytosol 2
Pathway
R-HSA-392499 Metabolism of proteins 4 R-HSA-162582 Signal Transduction 3 R-HSA-1640170 Cell Cycle 3 R-HSA-73894 DNA Repair 3 R-HSA-168256 Immune System 2 R-HSA-8953897 Cellular responses to stimuli 2
Partners
CDK2CSN6CUL4BMIFP27PD-L1RANBP9SMAD7
Complex memberships
COP9 signalosome (CSN)CSN4-5-6-7 subcomplex

Evidence

Reading pass · 54 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2002 The JAMM (JAB1/MPN domain metalloenzyme) motif in the CSN5/Jab1 subunit underlies the COP9 signalosome's Nedd8 isopeptidase (deneddylase) activity. Metal chelators and point mutations within JAMM abolished CSN-dependent cleavage of Nedd8 from Cul1, yet had little effect on CSN complex assembly. In vitro isopeptidase assays, active-site mutagenesis, metal chelation; genetic rescue in yeast and Drosophila Science High 12183637
2001 Jab1/CSN5 functions as an adaptor between p27(Kip1) and CRM1 to drive CRM1-dependent nuclear export of p27 and its subsequent proteasomal degradation. Jab1/CSN5 contains a leucine-rich NES through which CRM1 binds; mutation of NES leucines abolishes CRM1 interaction, nuclear export, and p27 degradation. A cytoplasmic ~100 kDa sub-complex (CSN4-8, lacking CSN1-3) exists and is the shuttle form. Leptomycin B inhibition, NES mutagenesis, dominant-negative Jab1 truncation, cell fractionation, glycerol gradient sedimentation, Co-IP Journal of Biological Chemistry High 11704659
2002 Jab1/CSN5 directly interacts with Smad4 and induces its ubiquitination and proteasomal degradation, thereby antagonizing TGF-β signaling; ectopic Jab1 expression decreases endogenous Smad4 and inhibits TGF-β-induced gene transcription. Co-immunoprecipitation, ectopic overexpression, proteasome inhibitors (lactacystin, MG132), transcriptional reporter assays EMBO Reports Medium 11818334
2004 Jab1/CSN5 constitutively associates with Smad7 and promotes its translocation from nucleus to cytoplasm and proteasomal degradation, thereby releasing Smad7-mediated suppression of TGF-β signaling and enhancing Smad2 phosphorylation. siRNA knockdown of Jab1 stabilizes Smad7. Co-immunoprecipitation, overexpression, siRNA knockdown, immunofluorescence localization, FRAP, phosphorylation assays Molecular and Cellular Biology Medium 14993265
2013 Crystal structure of CSN5 in its catalytically inactive monomeric form reveals that the Ins-1 segment obstructs access to the substrate-binding site. A single mutation in Ins-1 is sufficient to restore isopeptidase activity. A dynamic monomer-dimer equilibrium exists both in vitro and in vivo and is functionally relevant for catalytic activation. X-ray crystallography, molecular dynamics simulation, in vitro isopeptidase assay, Ins-1 mutagenesis, analytical ultracentrifugation Proceedings of the National Academy of Sciences High 23288897
2014 Association of the CSN5 and CSN6 MPN domains activates CSN5 isopeptidase activity; CSN5 alone is inactive due to an auto-inhibited catalytic domain conformation. The CSN5/CSN6 module is insufficient for efficient CRL deneddylation, indicating further subunits are required. The C-termini of CSN subunits likely form a helical bundle at the core, positioning the MPN catalytic module. Structural hybrid modeling, cross-linking/mass spectrometry, in vitro isopeptidase assay with CSN5/CSN6 heterodimer reconstitution PloS One High 25144743
2012 A CSN4-5-6-7 subcomplex was biochemically reconstituted; CSN5 associates with the CSN4-6-7 heterotrimer via MPN-MPN interaction between CSN5 and CSN6. PCI-PCI interactions between CSN4 and CSN7, and CSN6 C-terminus interactions with CSN4 and CSN7 further stabilize the subcomplex. Bacterial co-expression reconstitution, in vitro pulldown, biochemical and biophysical characterization (SEC, ITC) Journal of Biological Chemistry High 23086934
2016 CSN5, induced by NF-κB p65 downstream of TNF-α, inhibits ubiquitination and proteasomal degradation of PD-L1, thereby stabilizing PD-L1 on cancer cells and suppressing anti-tumor T-cell immunity. Co-immunoprecipitation, ubiquitination assay, siRNA knockdown, NF-κB reporter, in vivo mouse tumor model Cancer Cell High 27866850
2008 CSN5 isopeptidase activity is required for breast epithelial transformation; CSN5 potentiates MYC transcriptional activity in a manner dependent on assembly of the full COP9 signalosome. Transgenic inhibition of CSN5 isopeptidase activity blocks MYC/RAS-driven breast cancer progression in vivo. Isopeptidase-dead mutant expression, oncogene transformation assays in primary human cells, transgenic mouse model Cancer Research High 18199546
2016 COPS5 overexpression, through its isopeptidase activity, leads to ubiquitination and proteasomal degradation of NCoR (nuclear co-repressor for ERα), causing tamoxifen resistance. Genetic inhibition of COPS5 isopeptidase activity re-sensitizes resistant cells to tamoxifen. Co-immunoprecipitation, ubiquitination assay, isopeptidase-dead COPS5 mutant, genomic amplification analysis, in vitro and in vivo breast cancer models Nature Communications High 27375289
2004 Jab1-null embryos die shortly after implantation. Jab1-/- embryonic cells lack other CSN components and accumulate p27, p53, and cyclin E, resulting in impaired proliferation and accelerated apoptosis. In Jab1+/- MEFs, the Jab1-containing small subcomplex (not the CSN holocomplex) is selectively reduced, and G0-to-S phase progression is delayed via inefficient p27 down-regulation, while deneddylated Cul1 levels are unchanged. Jab1 knockout mice (homologous recombination), embryo analysis, MEF proliferation assays, western blotting for p27/p53/cyclin E/neddylated Cul1 Journal of Biological Chemistry High 15299027
2010 Conditional knockout of CSN5/Jab1 in MEFs ceases proliferation; the JAMM/deneddylase domain is essential for this function. Loss of CSN5 enhances neddylation of cullins 1 and 4, alters cyclin E and p53 levels, blocks cell cycle at multiple points, initiates p53-independent senescence, and increases cell ploidy (endoreduplication). CRE-lox conditional MEF knockout, cell cycle analysis, neddylation western blot, JAMM-domain rescue experiments FEBS Letters High 20974137
2010 Loss of Jab1 in mice causes early embryonic lethality due to accelerated apoptosis. Loss of Jab1 sensitizes cells to γ-radiation-induced apoptosis, increases spontaneous DNA damage, and causes homologous recombination (HR) defects correlated with reduced Rad51 and elevated p53 levels. Accumulated p53 binds the Rad51 promoter and suppresses its expression, representing the mechanistic link between Jab1 loss and HR deficiency. Jab1 knockout mice, γ-irradiation assays, comet assay, HR assay, chromatin immunoprecipitation for p53 on Rad51 promoter Oncogene High 20802511
2005 JAB1/CSN5 dual-regulates MIF-induced ERK signaling: JAB1 overexpression inhibits sustained (CD74-dependent) ERK phosphorylation by MIF, while JAB1 knockdown (siRNA) abolishes transient ERK activation by MIF. Transient MIF-ERK signaling requires a Src-type kinase upstream and minimum JAB1 levels. siRNA knockdown of JAB1, Src-deficient cells with Src re-expression, Src inhibitor PP2, genistein inhibition, ERK/Raf/MEK phosphorylation assays Cellular Signalling Medium 16122907
2005 The MPN domain of JAB1 (without requiring the JAMM catalytic motif) mediates direct binding to MIF. The MIF sequence MIF(50-65) and the MPN domain are sufficient for the MIF-JAB1 interaction, confirmed by endogenous Co-IP showing that MPN (via CSN6 as a proxy) mediates the interaction in mammalian cells. Yeast two-hybrid with domain deletions, in vitro CoIP, GST pulldown, MALDI-TOF mass spectrometry with nanobead affinity matrix FEBS Letters Medium 15757663
2006 Jab1 acts as a specificity factor for E2F1-induced apoptosis: Jab1 binds E2F1 specifically (not other E2Fs) via the E2F1 marked box region, and co-expression of Jab1+E2F1 synergistically induces apoptosis coincident with p53 accumulation. Jab1 depletion impairs both E2F1-induced apoptosis and p53 induction. Yeast two-hybrid screen, Co-IP, shRNA depletion, apoptosis and cell cycle assays, p53 western blot Genes & Development Medium 16481464
2008 CSN5 is a critical regulator of both p53 and MDM2: CSN5 interacts with p53, promotes MDM2-mediated p53 ubiquitination, facilitates p53 nuclear export, and stabilizes MDM2 by reducing its self-ubiquitination. CSN5 also antagonizes p53 transcriptional activity. Co-immunoprecipitation, ubiquitination assay, nuclear export assay, transcriptional reporter, curcumin (CSN-kinase inhibitor) treatment Journal of Cellular Biochemistry Medium 17879958
2004 Thioredoxin (Trx) directly interacts with and negatively regulates Jab1, competing with p27(Kip1) for Jab1 binding; Trx inhibits both AP-1 transcriptional activation and p27 degradation through this interaction. The negative effect on AP-1 is Jab1-dependent. FRET, Co-immunoprecipitation, antisense knockdown of Jab1, competition binding assay, AP-1 reporter assay Oncogene Medium 15480426
2009 CSN5-associated deubiquitinase activity (via its JAMM domain) regulates sorting of proteins into exosomes: CSN5 knockdown increases ubiquitinated and non-ubiquitinated exosomal proteins. JAMM-domain-deleted CSN5 increases ubiquitinated (but not non-ubiquitinated) exosomal Hsp70, and promotes HIV Gag sorting and HIV-1 release. siRNA knockdown, JAMM-deletion mutant expression, western blot of exosomal fractions, HIV-1 release assay American Journal of Pathology Medium 19246649
2004 JAB1 interacts with IRE1α in the absence of ER stress, and this interaction is decreased upon ER stress induction. A JAB1 mutant that binds IRE1α constitutively down-regulates UPR signaling, suggesting JAB1 modulates the choice between UPR and apoptosis via its association/dissociation with IRE1α. Yeast two-hybrid, Co-immunoprecipitation, UPR reporter assay, mutant JAB1 expression Neurochemistry International Low 15234121
2005 CSN5/Jab1 co-immunoprecipitates with ERα and overexpression of CSN5/Jab1 increases ligand-induced ERα proteasomal degradation. This requires CSN-associated kinase activity (blocked by curcumin) and nuclear export (blocked by leptomycin B) for estradiol-induced degradation. Co-immunoprecipitation, LMB/curcumin inhibition, proteasome inhibitor, ERα degradation assays Molecular and Cellular Biology Medium 15899841
2000 JAB1 interacts with both the progesterone receptor (PR) and steroid receptor coactivator 1 (SRC-1), stabilizing PR-SRC-1 complexes and potentiating the transcriptional activity of multiple SRC-1-associated transcription factors without altering PR or SRC-1 protein levels. Yeast two-hybrid, mammalian two-hybrid, GST pulldown, transcriptional reporter assays Journal of Biological Chemistry Medium 10722692
2002 Drosophila CSN5/JAB1, expressed in photoreceptor R cells, is required for lamina glial cell migration into the optic lobe target region. Missense mutations in CSN5 specifically disrupt R1-R6 axon targeting; protein-null alleles additionally impair R cell differentiation at an earlier stage. Drosophila genetic analysis, CSN5 missense and null alleles, immunostaining of optic lobe development Neuron High 11779478
2002 In Drosophila oogenesis, CSN5/JAB1 is required for meiotic progression and axis specification. CSN5 mutations reduce Gurken protein accumulation and cause Vasa modification, phenocopying spindle-class DNA-repair genes. The phenotype is suppressed by mutations in the DNA-damage checkpoint kinase mei-41 or by abolishing double-strand breaks (mei-W68), linking CSN5 to meiotic DNA repair checkpoint control of Gurken translation. Drosophila genetic epistasis (mei-41 and mei-W68 suppressors), immunostaining for Gurken and Vasa, oocyte axis analysis Development High 12397113
2013 CSN5, but not the CSN holocomplex, directly binds CDK2 in vivo and in vitro. CSN5 depletion enhances Akt-mediated CDK2 phosphorylation, causing cytoplasmic accumulation of CDK2/cyclin E and impaired Rb phosphorylation. Additional knockdown of CDK2 (reducing cyclin E) suppresses senescence in CSN5-depleted cells, and enforced cytoplasmic cyclin E alone induces premature senescence. Co-IP (in vivo and in vitro), siRNA double knockdown, cytoplasmic cyclin E overexpression, SA-β-gal senescence assay, Rb phosphorylation assay Scientific Reports Medium 23316279
2013 Jab1/CSN5 induces nuclear export and proteasomal degradation of RUNX3. The nuclear export is controlled by CSN-associated kinases, and cytoplasmic RUNX3 is rapidly degraded via the proteasome pathway. Co-immunoprecipitation, nuclear export assay (LMB inhibition), proteasome inhibitor, overexpression/knockdown Journal of Cellular Biochemistry Medium 19350572
2013 COPS5 interacts with RanBP9 (confirmed by Co-IP in neuronal and non-neuronal cells and mouse brain) and increases RanBP9 protein stability (half-life). Overexpression of COPS5 increases amyloid-β generation via increased sAPP-β, and siRNA knockdown of COPS5 reduces Aβ generation. Yeast two-hybrid, co-immunoprecipitation, siRNA knockdown, APP processing assays (ELISA for Aβ, western blot for sAPP-α/β), protein half-life assay Journal of Biological Chemistry Medium 23926111
2013 JAB1 interacts with unphosphorylated STAT3 in the nucleus (demonstrated by Co-IP from nuclear extract) and positively regulates its DNA-binding activity. JAB1 knockdown decreases unphosphorylated STAT3 DNA-binding and reduces expression of MDR1, NANOG, and VEGF (STAT3 target genes). Nuclear fractionation, Co-immunoprecipitation from nuclear extract, siRNA knockdown, STAT3 DNA-binding ELISA, qPCR of target genes Biochemical and Biophysical Research Communications Medium 23911788
2006 Jab1 directly interacts with the West Nile virus capsid protein (WNVCp) and promotes its CRM1-dependent nuclear export to the cytoplasm and subsequent proteasomal degradation, preventing WNVCp-induced G2 cell cycle arrest. The first 15 aa of WNVCp (including P5/P8) are required for interaction. Yeast two-hybrid, Co-IP, GST pulldown, immunofluorescence, LMB inhibition, deletion/point mutant analysis, flow cytometry Journal of Biological Chemistry Medium 16882664
2006 Jab1 directly interacts with and acts as a pro-apoptotic co-activator for BclGs (a BH3-only protein). Jab1 competes with Bcl-XL/Bcl-2 for BclGs binding, promotes Bax translocation to mitochondria, cytochrome c release, and caspase-3 activation. JAB1 knockdown reduces BclGs-induced apoptosis. Yeast two-hybrid, Co-IP, GST pulldown, competition binding assay, RNAi knockdown, apoptosis assays (caspase, cytochrome c) Cellular Signalling Medium 18006276
2013 CUL4B E3 ubiquitin ligase (as part of DDB1-CUL4B-ROC1 complex) targets Jab1/CSN5 for polyubiquitination and proteasomal degradation. RNAi depletion of CUL4B impairs Jab1 degradation; in vitro and in vivo ubiquitination assays confirm CUL4B promotes Jab1 polyubiquitination. This degradation is independent of CUL4A. In Cul4b-deficient mouse fibroblasts, Jab1 accumulates and BMP signaling is aberrantly activated. siRNA knockdown of CUL4B, in vitro ubiquitination assay, in vivo ubiquitination assay, CUL4B-null MEFs, BMP signaling reporter Biochimica et Biophysica Acta High 23357576
2013 Jab1/CSN5 is required for normal Schwann cell proliferation and axonal sorting. Loss of Jab1 in Schwann cells increases p27 levels causing cell cycle defects and aberrant differentiation; genetic reduction of p27 in Jab1-null Schwann cells rescues cell number, differentiation, axonal sorting, and dysmyelinating neuropathy. Schwann-cell-specific Jab1 conditional knockout mice, genetic epistasis with p27 knockout, nerve morphology, cell cycle analysis Journal of Experimental Medicine High 24344238
2022 Oligodendrocyte-specific deletion of JAB1/CSN5 causes DNA damage and defective DNA repair, leading to a p21CIP1-dependent senescence-like phenotype that triggers chronic neuroinflammation and oxidative stress. Deletion of p21CIP1 (but not p16INK4a) ameliorates the disease, linking CSN5 to senescence pathway selection in myelinating glia. Oligodendrocyte-specific Jab1 conditional KO mice, DNA damage markers, SA-β-gal, microglia inhibition, p21/p16 genetic epistasis Journal of Clinical Investigation High 34874913
2008 JAB1 overexpression in hematopoietic cells promotes myeloproliferative disease in vivo; stable JAB1 transgenic mice have larger stem cell populations with higher transplantable proliferative potential. JAB1 interacts with the histone methyltransferase SMYD3, and together they suppress p16(INK4a) transcription. Jab1 transgenic mice, bone marrow transplantation, Co-IP (JAB1-SMYD3), p16 promoter reporter assay Journal of Biological Chemistry Medium 18667426
2006 CSN5/Jab1 inhibits cardiac L-type Ca2+ channel (α1C subunit) activity through direct protein-protein interaction with the II-III linker of α1C. Silencing CSN5 with siRNA in COS7 cells activates L-type Ca2+ channel current. CSN5 and α1C co-immunoprecipitate from rat heart and co-localize in sarcolemmal membranes and transverse tubules. Yeast two-hybrid, co-immunoprecipitation from cardiac tissue, siRNA knockdown, electrophysiology (patch clamp), immunofluorescence co-localization Journal of Molecular and Cellular Cardiology Medium 16483597
2017 CSN5 directly binds ZEB1 and decreases its ubiquitination, enhancing ZEB1 protein stability. This promotes RCC cell EMT, migration, and invasion. Co-immunoprecipitation, ubiquitination assay, siRNA knockdown, in vitro migration/invasion, in vivo xenograft Biochemical and Biophysical Research Communications Medium 28479251
2016 Jab1/Csn5 mediates proteasome-dependent degradation of the CDK inhibitor p57(KIP2) through direct physical interaction in HCC cells, independently of Skp2 and Akt pathways. Co-immunoprecipitation, 26S proteasome inhibitor treatment, siRNA knockdown, in vitro interaction assay, in vivo xenograft Hepatology Medium 26606000
2019 Asrij/OCIAD1 sequesters CSN5 via its conserved OCIA domain, preventing CSN5-mediated p53 ubiquitination and degradation. Loss of Asrij in mouse HSCs leads to increased CSN5-mediated p53 ubiquitination, reduced p53 levels, and HSC over-proliferation; Nutlin-3 treatment restores p53 and normalizes HSC frequencies. Asrij knockout mice, Co-IP of Asrij-CSN5 interaction, polyubiquitination assays, Nutlin-3 rescue, transplantation studies Blood High 30952670
2013 CSN5 knockdown in HCC cells causes accumulation of neddylated Cullin 1, alters SKP2, p53, p27, and NF-κB protein levels, induces apoptosis, and inhibits cell cycle progression. Systemic delivery of CSN5 siRNA via lipid nanoparticles suppresses orthotopic HCC xenograft growth in vivo. siRNA knockdown, neddylation western blot, transcriptomic analysis, in vivo xenograft with siRNA nanoparticle delivery Oncogene Medium 21499307
2011 Stat3 and C/EBP-β transcriptionally regulate Jab1/CSN5 expression in breast cancer cells. Stat3 and C/EBP-β directly bind overlapping sites in the Jab1 promoter; Src/Stat3/IL-6 axis activates Jab1 transcription. Re-activation of Stat3 in normal mammary epithelial cells is sufficient to reactivate Jab1 expression. 5'-deletion reporter assays, mutational analysis of promoter binding sites, EMSA, ChIP, Stat3 and Src siRNA knockdown, IL-6 stimulation Breast Cancer Research Medium 21689417
2017 COPS5 and LASP1 synergistically interact (SH3 domain of LASP1 binds the MPN domain of COPS5, confirmed by GST pulldown) to promote ubiquitination and degradation of 14-3-3σ and activate PI3K/Akt signaling, driving CRC cell proliferation, migration, and invasion. Yeast two-hybrid, GST pulldown (domain mapping), Co-IP, siRNA knockdown, in vitro and in vivo functional assays International Journal of Cancer Medium 29226323
2020 CSN5 directly binds HK2 (hexokinase 2) and inhibits its ubiquitin-proteasome-mediated degradation, thereby stabilizing HK2 and promoting glycolysis. Silencing CSN5 decreases HK2 protein, glucose uptake, and glycolytic flux; HK2 re-expression rescues glycolysis in CSN5 knockdown cells. Co-immunoprecipitation, ubiquitination assay, siRNA knockdown, HK2 rescue overexpression, glycolysis assays, in vivo xenograft Experimental Cell Research Medium 31991125
2018 CSN5 directly binds survivin and decreases its ubiquitination, enhancing survivin protein stability in NSCLC cells; the tumor-promoting effects of CSN5 are at least partially mediated through this survivin stabilization. Co-immunoprecipitation, ubiquitination assay, siRNA knockdown, cell growth/apoptosis assays Biochemical and Biophysical Research Communications Low 29596838
2018 CSN5 directly binds FOXM1 and decreases its ubiquitination, enhancing FOXM1 protein stability and thereby promoting MMP2 expression to drive pancreatic cancer invasion and metastasis. Co-immunoprecipitation, ubiquitination assay, siRNA knockdown, in vitro/in vivo invasion assays Experimental Cell Research Low 30352219
2004 JAB1 directly binds the HLH domain of HAND2 and augments HAND2 transcriptional activity by enhancing HAND2 DNA binding rather than by recruiting a transcriptional activation domain. Yeast two-hybrid, Co-IP, domain-deletion mapping, transcriptional reporter assay, DNA-binding assay Journal of Neuroscience Research Medium 15139020
2005 p8 directly interacts with Jab1 (confirmed by His6-pulldown and Co-IP) and is required for Jab1-mediated nuclear-to-cytoplasmic translocation of p27 and its subsequent degradation. p8 knockdown strongly inhibits Jab1-induced p27 degradation. Yeast two-hybrid, His6-pulldown, Co-immunoprecipitation, siRNA knockdown of p8, p27 localization/degradation assay Biochemical and Biophysical Research Communications Medium 16300740
2006 NRBP (nuclear receptor binding protein) interacts with Jab1 in vivo and inhibits Jab1-induced c-Jun phosphorylation and AP-1 activation, acting as a negative regulator of Jab1-mediated transcription. Co-immunoprecipitation, AP-1 reporter assay, overexpression in mammalian cells FEBS Letters Low 17052710
2013 Jab1/CSN5 positively regulates Rad51 through a p53-dependent pathway, and elevated Rad51 confers cellular resistance to cisplatin and radiation in NPC cells. Jab1 knockdown reduces Rad51 and sensitizes cells to DNA-damaging agents. siRNA knockdown, Rad51 overexpression rescue, cisplatin/radiation survival assays, p53 pathway analysis Oncogene Medium 22797071
2014 CSN5 affects β-catenin signaling in CRC cells via regulation of the SIAH-1 E3 ubiquitin ligase: CSN5 promotes SIAH-1 degradation in a deNEDDylase-dependent manner, and β-catenin and SIAH-1 both form protein complexes with CSN5. Co-immunoprecipitation, siRNA knockdown, deNEDDylase inhibitor (MLN-4924), qPCR and western blot for SIAH-1 and β-catenin Cellular Signalling Medium 24882689
2010 5-HT6 receptor (5-HT6R) physically interacts with Jab1 (confirmed by GST pulldown, FRET, Co-IP). Jab1 siRNA decreases 5-HT6R cell membrane expression and 5-HT6R-mediated signaling. 5-HT6R activation induces Jab1 nuclear translocation and increased c-Jun phosphorylation. Yeast two-hybrid, GST pulldown, FRET, Co-immunoprecipitation, siRNA knockdown, immunocytochemistry Journal of Biological Chemistry Medium 20093369
2020 Cops5 is essential for genomic stability in mouse ESCs: it suppresses autophagic degradation of Mtch2 to direct cellular metabolism toward glycolysis, minimizing ROS and endogenous DNA damage. Independently, Cops5 is required for DNA damage repair (DDR) activities. Loss of Cops5 causes elevated ROS, DNA damage accumulation, p53-dependent G2/M arrest, and apoptosis. Inducible CRISPR/Cas9 Cops5 KO ESCs, metabolic assays, ROS measurement, comet assay, DDR marker analysis, autophagy/Mtch2 western blot Proceedings of the National Academy of Sciences High 31964807
2017 Jab1 interacts with and stabilizes Thioredoxin (Trx) protein; ectopic Jab1 expression increases Trx expression, while Jab1 silencing reduces it. Jab1 also transcriptionally regulates Trx. Co-immunoprecipitation, western blot, siRNA knockdown, ectopic overexpression, qRT-PCR for Trx mRNA Clinical Cancer Research Medium 28270496
2013 In endothelial cells, CSN5 forms a super-complex with IKK that dissociates upon TNF-α stimulation. CSN5 silencing enhances TNF-α-induced IκBα degradation and NF-κB activity, increases chemokine/adhesion molecule expression, and promotes monocyte arrest. CSN5 overexpression has reverse effects, indicating CSN5 is a negative regulator of NF-κB in endothelial cells. Co-immunoprecipitation (CSN-IKK super-complex), siRNA knockdown, luciferase NF-κB reporter, flow cytometry, monocyte adhesion assay Thrombosis and Haemostasis Medium 23636414
2019 CSN5i-3 (pharmacological CSN5 inhibitor) causes endothelial barrier disruption by activating NF-κB pathway, inducing RhoB (and to lesser extent RhoA) expression and activation, and consequent Rho/ROCK-dependent MLC activation and endothelial contraction. This establishes that sustained CRL neddylation (via CSN5 inhibition) drives NF-κB→RhoB axis in endothelial cells. CSN5i-3 pharmacological inhibition, RhoGTPase activity assays, NF-κB reporter, ROCK inhibitor, endothelial permeability assay in vitro and in vivo Scientific Reports Medium 31148579

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2016 Deubiquitination and Stabilization of PD-L1 by CSN5. Cancer cell 677 27866850
2002 Role of predicted metalloprotease motif of Jab1/Csn5 in cleavage of Nedd8 from Cul1. Science (New York, N.Y.) 604 12183637
2001 The cytoplasmic shuttling and subsequent degradation of p27Kip1 mediated by Jab1/CSN5 and the COP9 signalosome complex. The Journal of biological chemistry 252 11704659
2020 Berberine diminishes cancer cell PD-L1 expression and facilitates antitumor immunity via inhibiting the deubiquitination activity of CSN5. Acta pharmaceutica Sinica. B 198 33354502
2019 Macrophage-derived CCL5 facilitates immune escape of colorectal cancer cells via the p65/STAT3-CSN5-PD-L1 pathway. Cell death and differentiation 198 31802034
2005 Rapid and transient activation of the ERK MAPK signalling pathway by macrophage migration inhibitory factor (MIF) and dependence on JAB1/CSN5 and Src kinase activity. Cellular signalling 171 16122907
2001 JAB1/CSN5 and the COP9 signalosome. A complex situation. EMBO reports 152 11258719
2002 Jab1 antagonizes TGF-beta signaling by inducing Smad4 degradation. EMBO reports 141 11818334
2004 Multiple functions of Jab1 are required for early embryonic development and growth potential in mice. The Journal of biological chemistry 137 15299027
2022 Cuproptosis related genes associated with Jab1 shapes tumor microenvironment and pharmacological profile in nasopharyngeal carcinoma. Frontiers in immunology 126 36618352
2010 JAB1/CSN5: a new player in cell cycle control and cancer. Cell division 118 20955608
1987 Retroviruses and insertional mutagenesis in mice: proviral integration at the Mov 34 locus leads to early embryonic death. Genes & development 109 2824282
2004 Jab1/CSN5, a component of the COP9 signalosome, regulates transforming growth factor beta signaling by binding to Smad7 and promoting its degradation. Molecular and cellular biology 98 14993265
2000 JAB1 interacts with both the progesterone receptor and SRC-1. The Journal of biological chemistry 94 10722692
2002 Interaction and colocalization of PGP9.5 with JAB1 and p27(Kip1). Oncogene 93 12082530
2013 Insights into the regulation of the human COP9 signalosome catalytic subunit, CSN5/Jab1. Proceedings of the National Academy of Sciences of the United States of America 87 23288897
2002 Drosophila JAB1/CSN5 acts in photoreceptor cells to induce glial cells. Neuron 81 11779478
2005 CSN5/Jab1 is involved in ligand-dependent degradation of estrogen receptor {alpha} by the proteasome. Molecular and cellular biology 76 15899841
2004 JAB1 participates in unfolded protein responses by association and dissociation with IRE1. Neurochemistry international 73 15234121
2008 Roles for CSN5 in control of p53/MDM2 activities. Journal of cellular biochemistry 72 17879958
2012 Suppression of Jab1/CSN5 induces radio- and chemo-sensitivity in nasopharyngeal carcinoma through changes to the DNA damage and repair pathways. Oncogene 70 22797071
2012 Jab1/CSN5 negatively regulates p27 and plays a role in the pathogenesis of nasopharyngeal carcinoma. Cancer research 68 22350412
2011 Molecular targeting of CSN5 in human hepatocellular carcinoma: a mechanism of therapeutic response. Oncogene 63 21499307
2004 Thioredoxin modulates activator protein 1 (AP-1) activity and p27Kip1 degradation through direct interaction with Jab1. Oncogene 60 15480426
2009 COP9-associated CSN5 regulates exosomal protein deubiquitination and sorting. The American journal of pathology 59 19246649
2008 CSN5 isopeptidase activity links COP9 signalosome activation to breast cancer progression. Cancer research 59 18199546
2006 Jab1 mediates cytoplasmic localization and degradation of West Nile virus capsid protein. The Journal of biological chemistry 59 16882664
2010 Essential roles of Jab1 in cell survival, spontaneous DNA damage and DNA repair. Oncogene 57 20802511
2006 Jab1 is a specificity factor for E2F1-induced apoptosis. Genes & development 57 16481464
2017 Jab1/Csn5-Thioredoxin Signaling in Relapsed Acute Monocytic Leukemia under Oxidative Stress. Clinical cancer research : an official journal of the American Association for Cancer Research 54 28270496
2014 Emerging roles of Jab1/CSN5 in DNA damage response, DNA repair, and cancer. Cancer biology & therapy 54 24495954
2016 COPS5 amplification and overexpression confers tamoxifen-resistance in ERα-positive breast cancer by degradation of NCoR. Nature communications 53 27375289
2016 Stat3 contributes to cancer progression by regulating Jab1/Csn5 expression. Oncogene 50 27524414
2012 Targeting Jab1/CSN5 in nasopharyngeal carcinoma. Cancer letters 49 22867945
2010 Physical interaction of Jab1 with human serotonin 6 G-protein-coupled receptor and their possible roles in cell survival. The Journal of biological chemistry 49 20093369
2011 Stat3 and CCAAT/enhancer binding protein beta (C/EBP-beta) regulate Jab1/CSN5 expression in mammary carcinoma cells. Breast cancer research : BCR 48 21689417
2002 CSN5/Jab1 mutations affect axis formation in the Drosophila oocyte by activating a meiotic checkpoint. Development (Cambridge, England) 48 12397113
2016 Down-regulation of the cyclin-dependent kinase inhibitor p57 is mediated by Jab1/Csn5 in hepatocarcinogenesis. Hepatology (Baltimore, Md.) 47 26606000
2017 COPS5 and LASP1 synergistically interact to downregulate 14-3-3σ expression and promote colorectal cancer progression via activating PI3K/AKT pathway. International journal of cancer 44 29226323
2017 CSN5 promotes renal cell carcinoma metastasis and EMT by inhibiting ZEB1 degradation. Biochemical and biophysical research communications 43 28479251
2016 The emerging roles of Jab1/CSN5 in cancer. Medical oncology (Northwood, London, England) 40 27412572
2014 Plant COP9 signalosome subunit 5, CSN5. Plant science : an international journal of experimental plant biology 40 24908506
2004 Expression of cell cycle inhibitor p27Kip1 and its inactivator Jab1 in melanocytic lesions. Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc 40 15154004
2020 CSN5 upregulates glycolysis to promote hepatocellular carcinoma metastasis via stabilizing the HK2 protein. Experimental cell research 39 31991125
2013 CSN5 specifically interacts with CDK2 and controls senescence in a cytoplasmic cyclin E-mediated manner. Scientific reports 39 23316279
2005 Binding of JAB1/CSN5 to MIF is mediated by the MPN domain but is independent of the JAMM motif. FEBS letters 39 15757663
2009 Jab1/CSN5 induces the cytoplasmic localization and degradation of RUNX3. Journal of cellular biochemistry 38 19350572
1990 Molecular analysis of the Mov 34 mutation: transcript disrupted by proviral integration in mice is conserved in Drosophila. Development (Cambridge, England) 37 2209467
2013 Jab1 regulates Schwann cell proliferation and axonal sorting through p27. The Journal of experimental medicine 36 24344238
2022 Alpha5 nicotinic acetylcholine receptor mediated immune escape of lung adenocarcinoma via STAT3/Jab1-PD-L1 signalling. Cell communication and signaling : CCS 33 35971127
2017 CSN5/JAB1 suppresses the WNT inhibitor DKK1 in colorectal cancer cells. Cellular signalling 33 28229932
2010 Fank1 interacts with Jab1 and regulates cell apoptosis via the AP-1 pathway. Cellular and molecular life sciences : CMLS 33 20978819
2000 Characterization of the mouse JAB1 cDNA and protein. Gene 33 10721695
2020 α5-nAChR contributes to epithelial-mesenchymal transition and metastasis by regulating Jab1/Csn5 signalling in lung cancer. Journal of cellular and molecular medicine 32 31930655
2012 Role of CSN5/JAB1 in Wnt/β-catenin activation in colorectal cancer cells. FEBS letters 32 22668871
2021 PDIA6 promotes pancreatic cancer progression and immune escape through CSN5-mediated deubiquitination of β-catenin and PD-L1. Neoplasia (New York, N.Y.) 31 34325342
2006 Jab1 as a mediator of nuclear export and cytoplasmic degradation of p53. Molecules and cells 31 17085963
2019 Asrij/OCIAD1 suppresses CSN5-mediated p53 degradation and maintains mouse hematopoietic stem cell quiescence. Blood 30 30952670
2018 CSN5/Jab1 facilitates non-small cell lung cancer cell growth through stabilizing survivin. Biochemical and biophysical research communications 30 29596838
2018 Jab1/Cops5 contributes to chemoresistance in breast cancer by regulating Rad51. Cellular signalling 29 30244171
2013 JAB1 regulates unphosphorylated STAT3 DNA-binding activity through protein-protein interaction in human colon cancer cells. Biochemical and biophysical research communications 28 23911788
2008 Stable form of JAB1 enhances proliferation and maintenance of hematopoietic progenitors. The Journal of biological chemistry 28 18667426
2014 Structural and biochemical characterization of the Cop9 signalosome CSN5/CSN6 heterodimer. PloS one 27 25144743
2012 The organization of a CSN5-containing subcomplex of the COP9 signalosome. The Journal of biological chemistry 27 23086934
2007 JAB1 accelerates mitochondrial apoptosis by interaction with proapoptotic BclGs. Cellular signalling 27 18006276
2021 Overexpression of DAPK1-mediated inhibition of IKKβ/CSN5/PD-L1 axis enhances natural killer cell killing ability and inhibits tumor immune evasion in gastric cancer. Cellular immunology 26 35114597
2019 MicroRNA-17 acts as a tumor chemosensitizer by targeting JAB1/CSN5 in triple-negative breast cancer. Cancer letters 26 31473252
2005 Interaction of the stress protein p8 with Jab1 is required for Jab1-dependent p27 nuclear-to-cytoplasm translocation. Biochemical and biophysical research communications 26 16300740
2022 JAB1 deletion in oligodendrocytes causes senescence-induced inflammation and neurodegeneration in mice. The Journal of clinical investigation 25 34874913
2018 CSN5 promotes the invasion and metastasis of pancreatic cancer by stabilization of FOXM1. Experimental cell research 25 30352219
2018 The pivotal oncogenic role of Jab1/CSN5 and its therapeutic implications in human cancer. Gene 25 30468907
2013 Endothelial CSN5 impairs NF-κB activation and monocyte adhesion to endothelial cells and is highly expressed in human atherosclerotic lesions. Thrombosis and haemostasis 25 23636414
2010 Clinicopathological significance of expression of Tspan-1, Jab1 and p27 in human hepatocellular carcinoma. Journal of Korean medical science 25 20890423
2008 Jab1 is overexpressed in human breast cancer and is a downstream target for HER-2/neu. Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc 25 18246048
2022 SENP1 promotes triple-negative breast cancer invasion and metastasis via enhancing CSN5 transcription mediated by GATA1 deSUMOylation. International journal of biological sciences 24 35342335
2013 COPS5 (Jab1) protein increases β site processing of amyloid precursor protein and amyloid β peptide generation by stabilizing RanBP9 protein levels. The Journal of biological chemistry 24 23926111
2006 Depletion of Jab1 inhibits proliferation of pancreatic cancer cell lines. FEBS letters 24 17027978
2000 Differentiation-associated expression and intracellular localization of cyclin-dependent kinase inhibitor p27KIP1 and c-Jun co-activator JAB1 in neuroblastoma. International journal of oncology 24 10995887
2020 The crucial p53-dependent oncogenic role of JAB1 in osteosarcoma in vivo. Oncogene 23 32390003
2018 Let-7d Inhibits Growth and Metastasis in Breast Cancer by Targeting Jab1/Cops5. Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology 23 29975923
2010 CSN5/Jab1 controls multiple events in the mammalian cell cycle. FEBS letters 23 20974137
2015 Suppression of CSN5 promotes the apoptosis of gastric cancer cells through regulating p53-related apoptotic pathways. Bioorganic & medicinal chemistry letters 22 26048783
2014 The β-catenin E3 ubiquitin ligase SIAH-1 is regulated by CSN5/JAB1 in CRC cells. Cellular signalling 22 24882689
2001 JAB1/CSN5 interacts with the GAL4 DNA binding domain: a note of caution about two-hybrid interactions. Biochimie 22 11728635
2021 Jab1/Cops5: a promising target for cancer diagnosis and therapy. International journal of clinical oncology 21 34019195
2017 CSN5 Promotes Hepatocellular Carcinoma Progression by SCARA5 Inhibition Through Suppressing β-Catenin Ubiquitination. Digestive diseases and sciences 21 29189991
2019 COP9 Signalosome CSN4 and CSN5 Subunits Are Involved in Jasmonate-Dependent Defense Against Root-Knot Nematode in Tomato. Frontiers in plant science 20 31649695
2017 COPS5 inhibition arrests the proliferation and growth of serous ovarian cancer cells via the elevation of p27 level. Biochemical and biophysical research communications 20 28919423
2013 X-linked intellectual disability gene CUL4B targets Jab1/CSN5 for degradation and regulates bone morphogenetic protein signaling. Biochimica et biophysica acta 20 23357576
2004 JAB1 enhances HAND2 transcriptional activity by regulating HAND2 DNA binding. Journal of neuroscience research 20 15139020
2024 Berberine Derivative B68 Promotes Tumor Immune Clearance by Dual-Targeting BMI1 for Senescence Induction and CSN5 for PD-L1 Degradation. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 19 39721027
2019 MRPS30-DT Knockdown Inhibits Breast Cancer Progression by Targeting Jab1/Cops5. Frontiers in oncology 19 31788446
2016 JAB1 accelerates odontogenic differentiation of dental pulp stem cells. Journal of molecular histology 19 26989054
2011 Jab1/CSN5 mediates E2F dependent expression of mitotic and apoptotic but not DNA replication targets. Cell cycle (Georgetown, Tex.) 19 21937878
2019 CSN5 inhibition triggers inflammatory signaling and Rho/ROCK-dependent loss of endothelial integrity. Scientific reports 18 31148579
2015 CSN5 silencing inhibits invasion and arrests cell cycle progression in human colorectal cancer SW480 and LS174T cells in vitro. International journal of clinical and experimental pathology 18 26045788
2006 Adapter protein NRBP associates with Jab1 and negatively regulates AP-1 activity. FEBS letters 18 17052710
2019 The novel Jab1 inhibitor CSN5i-3 suppresses cell proliferation and induces apoptosis in human breast cancer cells. Neoplasma 17 30868895
2020 Cops5 safeguards genomic stability of embryonic stem cells through regulating cellular metabolism and DNA repair. Proceedings of the National Academy of Sciences of the United States of America 16 31964807
2006 CSN5/Jab1 inhibits cardiac L-type Ca2+ channel activity through protein-protein interactions. Journal of molecular and cellular cardiology 16 16483597

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