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Showing RNF123 — KPC1 is a alias.

RNF123

E3 ubiquitin-protein ligase RNF123 · UniProt Q5XPI4

Length
1314 aa
Mass
148.5 kDa
Annotated
2026-06-10
30 papers in source corpus 20 papers cited in narrative 20 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

RNF123 (KPC1) is a RING-finger E3 ubiquitin ligase that controls cell proliferation, NF-κB signaling, innate immunity, and tumor suppression through substrate-specific ubiquitination (PMID:25860612, PMID:19015242). Its founding activity is the limited proteasomal processing of NF-κB1 p105 to the p50 subunit: RNF123 binds the p105 ankyrin repeats through a seven-residue site (WILVRLW, residues 968–974) and ubiquitinates it, and excess p50 generation reprograms NF-κB transcription toward tumor suppression—downregulating PD-L1 and inducing CCL3/CCL4/CCL5 to recruit NK cells and macrophages (PMID:25860612, PMID:33168738, PMID:34873064). This processing activity is opposed by ADAR1-mediated A-to-I editing (p.M8V), which weakens p105 affinity and enhances oncogenic NF-κB signaling (PMID:36476255). Beyond p105, RNF123 ubiquitinates a broad substrate set for proteasomal degradation, including p27(Kip1) (linking it to G1/S cell-cycle control), the ETV6-NTRK3 oncoprotein, vimentin, ZEB1, Dvl2, the glycolytic enzymes PFKP and PKM2, and PRDX1, thereby restraining proliferation, migration, glycolysis, and oxidative stress across cancer and cardiomyocyte settings (PMID:19015242, PMID:29903916, PMID:39725718, PMID:39732122, PMID:41429767, PMID:33205477, PMID:41094513, PMID:42106994). In innate immunity RNF123 acts through two distinct mechanisms: an E3-ligase-independent inhibition of RIG-I/MDA5 signaling, in which its SPRY and coiled-coil domains compete with MAVS for CARD-domain binding to limit IFN-β (PMID:27312109), and a catalytic role generating unanchored K63-linked polyubiquitin that captures NEK7 to block NLRP3 inflammasome assembly, with the Crohn's-associated R854H variant aggravating colitis (PMID:41719337). RNF123 protein stability is itself regulated by the deubiquitinase USP19 and its expression is suppressed by miR-155 (PMID:19015242, PMID:21355095).

Mechanistic history

Synthesis pass · year-by-year structured walk · 11 steps
  1. 2008 High

    Established that RNF123/KPC1 protein abundance is itself ubiquitin-regulated, identifying USP19 as a stabilizing deubiquitinase that couples KPC1 levels to p27(Kip1) turnover and cell-cycle progression.

    Evidence Reciprocal Co-IP, RNAi depletion, proteasome inhibition, and cell-cycle rescue with KPC1 overexpression and p27-null cells

    PMID:19015242

    Open questions at the time
    • Did not map the USP19 cleavage sites on KPC1
    • Did not establish whether USP19 regulation extends to non-p27 substrates
  2. 2011 Medium

    Connected KPC1 to physiological proliferative contexts by showing its upregulation correlates inversely with p27(Kip1) in proliferating astrocytes, and that miR-155 represses KPC1 to control p27 in dendritic cells.

    Evidence Co-IP and IHC in a rat spinal-cord-injury model; miR-155 overexpression/silencing and knockout-mouse DCs with p27 Western blots

    PMID:21229311 PMID:21355095

    Open questions at the time
    • The SCI study is correlative with no direct ubiquitination assay
    • Functional consequence of the miR-155→KPC1 axis beyond DC apoptosis not defined
  3. 2012 High

    Identified an N-terminal PXVXL motif as a substrate-recognition element, showing RNF123 binds and degrades HP1α/β and links its activity to nuclear lamina state.

    Evidence Ectopic GFP-RNF123 expression, RNAi, PXVXL mutagenesis, and FRAP in HeLa cells

    PMID:23077635

    Open questions at the time
    • Ubiquitin-chain linkage on HP1 not determined
    • Physiological context beyond lamin A/C knockdown not explored
  4. 2015 High

    Defined RNF123's signature mechanism: it is the E3 ligase that ubiquitinates NF-κB1 p105 for limited proteasomal processing to p50, and excess p50 acts as a tumor suppressor by replacing the oncogenic p50-p65 dimer.

    Evidence Co-IP, in vitro ubiquitination, overexpression, and tumor xenograft models with transcript analysis

    PMID:25860612

    Open questions at the time
    • Did not define the minimal binding site on KPC1 (resolved later)
    • Mechanism distinguishing limited processing from full degradation not detailed
  5. 2016 High

    Revealed a non-catalytic function: RNF123 inhibits RIG-I/MDA5 antiviral signaling by competing with MAVS for CARD binding, independent of its RING domain.

    Evidence Endogenous and exogenous Co-IP, KO cells, domain-deletion mutants, and IFN-β reporter assays with SeV/EMCV

    PMID:27312109

    Open questions at the time
    • Structural basis of CARD competition not resolved
    • How viral infection induces the RNF123-CARD association is unknown
  6. 2018 High

    Extended RNF123's substrate range to an oncofusion protein, showing it ubiquitinates ETV6-NTRK3 and that IGF1R signaling shields the substrate from degradation.

    Evidence SILAC-MS interactomics, in vitro ubiquitination, knockdown rescue, and IGF1R inhibition across multiple cell lines

    PMID:29903916

    Open questions at the time
    • How IGF1R signaling protects EN mechanistically not defined
    • Ubiquitin-chain linkage type on EN not specified
  7. 2020 Medium

    Expanded the substrate repertoire and tumor-suppressive output: RNF123 degrades Bax (anti-apoptotic in cardiomyocytes) and Dvl2 (suppressing Wnt/PCP-JNK), and excess p50 downregulates PD-L1 while recruiting innate immune cells; the miR-155/RNF123/p50 axis modulates SerpinE1 in glioblastoma.

    Evidence Overexpression/knockdown with proteasome inhibition in H9c2 and I/R models; Co-IP and ubiquitination with siRNA rescue in trophoblasts; xenograft and immune-recruitment assays; RNA-seq and RPPA in glioblastoma lines

    PMID:31148189 PMID:32349217 PMID:33168738 PMID:33205477

    Open questions at the time
    • No direct ubiquitination assay for Bax
    • Whether these substrates are degraded in the same physiological setting unclear
  8. 2021 High

    Mapped the p105-binding determinant to a seven-residue stretch (WILVRLW, 968–974) sufficient for substrate recognition, enabling a minimal RING fusion and a PROTAC that drives p105 processing to p50.

    Evidence Domain deletion/mutagenesis, in vitro and cell-free ubiquitination/processing assays with PROTAC, and xenograft tumor model

    PMID:34873064

    Open questions at the time
    • Structural detail of the WILVRLW-ankyrin interaction not resolved
    • Whether this motif governs recognition of other substrates not tested
  9. 2022 Medium

    Demonstrated a post-transcriptional off-switch: ADAR1 A-to-I editing produces an M8V substitution that lowers KPC1 affinity for p105, reducing p50 generation and enhancing oncogenic NF-κB signaling in cholangiocarcinoma.

    Evidence Sanger validation of editing, binding-affinity and NF-κB signaling assays in iCCA cells with in vivo functional readouts

    PMID:36476255

    Open questions at the time
    • Editing frequency across tissues not established
    • Single-lab characterization of the affinity change
  10. 2024 Medium

    Tied RNF123 to metabolic and cytoskeletal control of tumor phenotypes by identifying PFKP and vimentin as degradation substrates, linking it to glycolytic suppression and anti-migratory effects.

    Evidence Co-IP and ubiquitination assays with overexpression/knockdown or CRISPR deletion plus glycolysis assays and xenograft/tumor mouse models

    PMID:39725718 PMID:39732122

    Open questions at the time
    • Ubiquitin-chain linkage on PFKP and vimentin not specified
    • Single-lab studies without reciprocal validation
  11. 2025 High

    Established RNF123 as a catalytic regulator of the NLRP3 inflammasome via unanchored K63 ubiquitin chains that capture NEK7, and defined disease-linked, oxidative, and EMT substrate axes (PRDX1, PKM2, ZEB1) plus the Crohn's-associated R854H variant.

    Evidence In vitro unanchored-chain and NEK7-capture assays, RNF123-deficient and R854H knock-in mice in colitis/endotoxemia/peritonitis models; LC-MS/MS plus site-specific K→R ubiquitination assays and KO mice for PRDX1; Co-IP/ubiquitination for PKM2 and ZEB1

    PMID:41094513 PMID:41429767 PMID:41719337 PMID:42106994

    Open questions at the time
    • How RNF123 switches between substrate-anchored and unanchored chain synthesis is unknown
    • Coordination among the many substrates within a single cell type not resolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • How RNF123 selects among its diverse substrates and switches between E3-ligase-dependent degradation, limited processing, unanchored-chain synthesis, and ligase-independent competition remains unresolved.
  • No structural model integrating the substrate-recognition motifs (WILVRLW, PXVXL, SPRY/coiled-coil)
  • No unifying account of how cellular context dictates which mechanism dominates
  • Upstream signals controlling RNF123 activity versus abundance incompletely defined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140096 catalytic activity, acting on a protein 5 GO:0016874 ligase activity 4 GO:0098772 molecular function regulator activity 1
Localization
GO:0005829 cytosol 2 GO:0005634 nucleus 1
Pathway
R-HSA-162582 Signal Transduction 3 R-HSA-1643685 Disease 3 R-HSA-168256 Immune System 3 R-HSA-392499 Metabolism of proteins 3 R-HSA-1640170 Cell Cycle 2
Partners
DVL2NEK7NFKB1PFKPPKM2PRDX1SOCS1USP19

Evidence

Reading pass · 20 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2015 KPC1 (RNF123) is the E3 ubiquitin ligase that binds to the ankyrin repeats domain of NF-κB1 p105, ubiquitinates it, and mediates its limited proteasomal processing to the p50 active subunit both under basal conditions and following signaling. Overexpression of KPC1 inhibits tumor growth via excessive generation of p50, and the resulting p50 homodimer modulates transcription in place of the tumorigenic p50-p65 heterodimer. Co-immunoprecipitation, in vitro ubiquitination assay, overexpression studies, tumor xenograft models, transcript analysis Cell High 25860612
2008 USP19, a deubiquitinating enzyme, interacts with and stabilizes KPC1 protein by reversing its ubiquitination, thereby modulating p27(Kip1) levels and cell proliferation. Depletion of USP19 reduces KPC1 levels and causes G1/S accumulation that is rescued by KPC1 overexpression or p27 knockout. Co-immunoprecipitation, RNA interference, proteasome inhibitor treatment, cell cycle analysis, rescue experiments with KPC1 overexpression Molecular and cellular biology High 19015242
2012 RNF123 ubiquitin ligase binds HP1α and HP1β via a canonical PXVXL pentapeptide motif in its N-terminus and targets them for proteasomal degradation. In lamin A/C knockdown cells, RNF123 is upregulated and mediates degradation of HP1α and HP1β (but not HP1γ). Mutation of the PXVXL motif abolishes HP1 binding and degradation. GFP-tagged RNF123 ectopic expression, RNAi knockdown of RNF123, mutational analysis of PXVXL motif, FRAP analysis, Western blot in HeLa cells PloS one High 23077635
2016 RNF123 is a negative regulator of RIG-I and MDA5 antiviral signaling. RNF123 associates with the N-terminal CARD domains of RIG-I and MDA5 in a viral infection-inducible manner and competes with the downstream adaptor VISA/MAVS for CARD binding, thereby inhibiting IFN-β production. This inhibitory function requires the SPRY and coiled-coil domains of RNF123 but NOT the RING domain, indicating an E3 ligase-independent mechanism. Overexpression, knockdown and knockout of RNF123, endogenous and exogenous Co-immunoprecipitation, domain deletion mutant analysis, IFN-β reporter assays with SeV and EMCV EMBO reports High 27312109
2018 KPC1/RNF123 directly ubiquitinates the ETV6-NTRK3 (EN) chimeric oncoprotein in vitro, and its overexpression decreases EN protein levels. IGF1R signaling protects EN from KPC1/RNF123-mediated proteasomal degradation; blocking IGF1R promotes rapid EN ubiquitylation and degradation that is reversed by KPC1 knockdown. SILAC-based MS interactomics, in vitro ubiquitination assay, KPC1 overexpression and knockdown, IGF1R inhibitor treatment in fibroblast, breast epithelial, and leukemia cell lines The Journal of biological chemistry High 29903916
2020 KPC1 promotes proteasomal degradation of Bax and prevents Bax translocation to mitochondria, thereby reducing apoptosis in cardiomyocytes under hypoxia/reoxygenation. This effect is abolished by the proteasome inhibitor MG132, confirming a proteasome-dependent mechanism. KPC1 overexpression and shRNA knockdown in H9c2 cells and rat I/R model, Western blot for Bax protein, MMP assay, cytochrome c release, MG132 proteasome inhibition Journal of cellular physiology Medium 31148189
2020 RNF123 overexpression in IDH WT glioblastoma cells reduces NF-κB1 p50 levels and negatively regulates SerpinE1 expression downstream of the miR-155-5p/RNF123/NF-κB1-p50 axis, thereby reducing proliferation and invasion. RNF123 overexpression in GB cell lines, RNA-sequencing, reverse-phase protein arrays, in vitro functional assays, miR-155-5p overexpression Cancers Medium 32349217
2020 KPC1-generated excess p50 suppresses tumor growth via multiple mechanisms: (1) downregulation of PD-L1 expression (abrogated by p65 overexpression), and (2) upregulation of pro-inflammatory chemokines CCL3, CCL4, and CCL5, which recruit NK cells and macrophages into tumors. KPC1 overexpression in cancer cells and tumor xenograft models, p65 co-overexpression rescue, gene expression analysis, immune cell recruitment assays Proceedings of the National Academy of Sciences of the United States of America Medium 33168738
2021 The p105-binding site on KPC1 consists of a seven amino acid sequence (WILVRLW, residues 968–974). Attaching this short stretch to the RING-finger domain fragment was sufficient to bind p105, ubiquitinate it, and suppress tumor growth in vivo. Fusion of these seven amino acids to a pVHL-binding ligand created a PROTAC that stimulated p105 ubiquitination in cell-free systems and its processing to p50 in cells. Domain deletion and mutagenesis of KPC1, in vitro ubiquitination assay with PROTAC, cell-free processing assay, xenograft tumor model Proceedings of the National Academy of Sciences of the United States of America High 34873064
2022 ADAR1-mediated A-to-I RNA editing of KPC1 results in a methionine-to-valine substitution at residue 8 (p.M8V), which weakens the affinity of KPC1 for its substrate NF-κB1 p105, thereby reducing ubiquitination and proteasomal processing of p105 to p50 and enhancing oncogenic NF-κB signaling. Sanger sequencing validation of RNA editing, molecular interaction assays, in vitro and in vivo functional assays in iCCA cells, NF-κB signaling analysis Journal of experimental & clinical cancer research : CR Medium 36476255
2020 RNF123 interacts with Dvl2 and participates in CCNG2-induced polyubiquitination and proteasomal degradation of Dvl2, thereby suppressing JNK-dependent Wnt/PCP signaling in trophoblast cells. RNF123 siRNA reversed CCNG2-induced Dvl2 degradation and restored Wnt/PCP-JNK signaling. Co-immunoprecipitation, polyubiquitination assay, siRNA knockdown, Western blot, Wnt/PCP-JNK signaling readouts in HTR8/SVneo cells FASEB journal Medium 33205477
2023 RNF123 binds the SH2 domain of SOCS1 via its RING domain, facilitates K48-linked ubiquitination specifically at K114 and K137 residues of SOCS1, and promotes SOCS1 proteasomal degradation, thereby promoting TLR3- and IRF7-mediated type I IFN production during duck Tembusu virus infection. Co-immunoprecipitation, in vivo ubiquitination assay with site-specific lysine mutants (K114R, K137R), proteasome inhibitor treatment, IRF7/TLR3 reporter assays Journal of virology Medium 37014223
2024 RNF123 directly interacts with and ubiquitinates PFKP (6-Phosphofructo-2-kinase), leading to PFKP degradation and inhibition of glycolysis, which suppresses breast cancer cell viability, cell cycle progression, and colony formation. Co-immunoprecipitation, ubiquitination assay, lentiviral overexpression/knockdown, glycolysis assays (ECAR, lactate, ATP), xenograft tumor model Naunyn-Schmiedeberg's archives of pharmacology Medium 39725718
2024 KPC1 (RNF123) forms a complex with vimentin, ubiquitinates it, and promotes its degradation. KPC1 overexpression in HEK293T cells downregulates vimentin, while KPC1 deletion in HAP1 cells upregulates vimentin. Downregulation of vimentin mediates at least part of KPC1's anti-migratory and anti-tumorigenic effects. Co-immunoprecipitation, in vitro ubiquitination assay, KPC1 overexpression in HEK293T, CRISPR-based KPC1 deletion in HAP1 cells, tumor model in mice Biochemical and biophysical research communications Medium 39732122
2025 RNF123 catalyzes unanchored K63-linked ubiquitination of NEK7, which prevents NEK7-mediated dissociation of inactive cage-like NLRP3 aggregates and subsequent NLRP3 inflammasome assembly. The Crohn's disease-associated variant RNF123-R854H aggravates colitis through the NLRP3-dependent pathway. K63-linked polyubiquitin chains can be captured by NEK7 in vitro and inhibit NEK7-licensed NLRP3 inflammasome assembly. In vitro ubiquitination assay with unanchored polyubiquitin chain analysis, Co-immunoprecipitation, RNF123-deficient mice, R854H knock-in mouse model, DSS colitis, LPS endotoxemia, Alum peritonitis models, in vitro NEK7 capture assay Proceedings of the National Academy of Sciences of the United States of America High 41719337
2025 KPC1 (RNF123) binds ZEB1 and promotes its ubiquitination and proteasomal degradation, thereby suppressing cadherin switching and cell motility in melanoma. Loss of KPC1 prevents ZEB1 proteasomal degradation and increases mesenchymal marker expression and cell migration. Co-immunoprecipitation, ubiquitination assay, KPC1 knockdown/overexpression, single-cell transcriptomic analyses, migration assays Cell death & disease Medium 41429767
2025 RNF123 targets PKM2 for ubiquitination in high-glucose-stimulated Müller cells, promoting PKM2 degradation and thereby reducing glycolysis and Müller cell activation. HG-induced downregulation of RNF123 is mediated upstream by ALKBH5 and IGF2BP1 via m6A modification, which is itself controlled by histone lactylation. Co-immunoprecipitation, ubiquitination assay, RNF123 overexpression and knockdown in MIO-M1 cells, ALKBH5/IGF2BP1 modulation, diabetic rat in vivo model Journal of translational medicine Medium 41094513
2025 RNF123 directly binds the N-terminal domain of PRDX1 and adds a K48-linked ubiquitin chain at the K7 site of PRDX1, promoting its proteasomal degradation. RNF123-mediated PRDX1 degradation increases ROS levels in cardiomyocytes, driving pathological cardiac hypertrophy. RNF123 deficiency mitigates Ang II- and TAC-induced cardiac hypertrophy and dysfunction in mice. LC-MS/MS combined with Co-IP to identify PRDX1, K48-linkage-specific ubiquitination assay with K7R mutant, RNF123 knockout mice, Ang II infusion and TAC surgery models, NRVMs KD/OE Acta physiologica (Oxford, England) High 42106994
2011 Following spinal cord injury, KPC1 is upregulated predominantly in astrocytes, and increased interaction between KPC1 and p27(Kip1) was detected by co-immunoprecipitation 4 days post-injury. KPC1 upregulation correlates inversely with p27(Kip1) and is associated with astrocyte proliferation, as demonstrated in LPS-stimulated astrocytes in vitro. Co-immunoprecipitation, Western blot, immunohistochemistry, immunofluorescence in rat SCI model and LPS-stimulated astrocytes Neurochemical research Low 21229311
2011 miR-155 targets KPC1 (Kip1 ubiquitination-promoting complex 1) as a functional target and indirectly regulates p27(Kip1) protein levels by reducing KPC1 expression in dendritic cells, thereby contributing to DC apoptosis. miRNA overexpression and silencing in human DCs, miR-155 knockout mice DCs, Western blot for p27(Kip1) and KPC1 protein levels Blood Medium 21355095

Source papers

Stage 0 corpus · 30 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2001 Novel carbapenem-hydrolyzing beta-lactamase, KPC-1, from a carbapenem-resistant strain of Klebsiella pneumoniae. Antimicrobial agents and chemotherapy 1300 11257029
2011 miR-221 and miR-155 regulate human dendritic cell development, apoptosis, and IL-12 production through targeting of p27kip1, KPC1, and SOCS-1. Blood 237 21355095
2015 KPC1-mediated ubiquitination and proteasomal processing of NF-κB1 p105 to p50 restricts tumor growth. Cell 93 25860612
2008 USP19 deubiquitinating enzyme supports cell proliferation by stabilizing KPC1, a ubiquitin ligase for p27Kip1. Molecular and cellular biology 80 19015242
2021 Genome-wide association study identifies RNF123 locus as associated with chronic widespread musculoskeletal pain. Annals of the rheumatic diseases 54 33926923
2017 Epigenetic Regulation of KPC1 Ubiquitin Ligase Affects the NF-κB Pathway in Melanoma. Clinical cancer research : an official journal of the American Association for Cancer Research 33 28389511
2020 Downregulation of the Ubiquitin-E3 Ligase RNF123 Promotes Upregulation of the NF-κB1 Target SerpinE1 in Aggressive Glioblastoma Tumors. Cancers 28 32349217
2020 Excess of the NF-ĸB p50 subunit generated by the ubiquitin ligase KPC1 suppresses tumors via PD-L1- and chemokines-mediated mechanisms. Proceedings of the National Academy of Sciences of the United States of America 24 33168738
2011 KPC1 expression and essential role after acute spinal cord injury in adult rat. Neurochemical research 21 21229311
2016 RNF123 has an E3 ligase-independent function in RIG-I-like receptor-mediated antiviral signaling. EMBO reports 19 27312109
2012 Ubiquitin ligase RNF123 mediates degradation of heterochromatin protein 1α and β in lamin A/C knock-down cells. PloS one 19 23077635
2019 KPC1 alleviates hypoxia/reoxygenation-induced apoptosis in rat cardiomyocyte cells though BAX degradation. Journal of cellular physiology 18 31148189
2023 The Tumor Suppressor Functions of Ubiquitin Ligase KPC1: From Cell-Cycle Control to NF-κB Regulator. Cancer research 15 36880841
2020 Cyclin G2 upregulation impairs migration, invasion, and network formation through RNF123/Dvl2/JNK signaling in the trophoblast cell line HTR8/SVneo, a possible role in preeclampsia. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 13 33205477
2018 Insulin-like growth factor 1 receptor stabilizes the ETV6-NTRK3 chimeric oncoprotein by blocking its KPC1/Rnf123-mediated proteasomal degradation. The Journal of biological chemistry 13 29903916
2023 RNF123 Mediates Ubiquitination and Degradation of SOCS1 To Regulate Type I Interferon Production during Duck Tembusu Virus Infection. Journal of virology 12 37014223
2022 The A-to-I editing of KPC1 promotes intrahepatic cholangiocarcinoma by attenuating proteasomal processing of NF-κB1 p105 to p50. Journal of experimental & clinical cancer research : CR 11 36476255
2021 A short binding site in the KPC1 ubiquitin ligase mediates processing of NF-κB1 p105 to p50: A potential for a tumor-suppressive PROTAC. Proceedings of the National Academy of Sciences of the United States of America 9 34873064
2023 The NF-ĸB p50 subunit generated by KPC1-mediated ubiquitination and limited proteasomal processing, suppresses tumor growth. Cancer cell international 6 37055826
2025 Lactylation-induced ALKBH5 targets RNF123 to worsen retinal Müller cell activation through PKM2-regulated Glycolysis in diabetic retinopathy. Journal of translational medicine 5 41094513
2024 RNF123 inhibits cell viability, cell cycle and colony formation of breast cancer by inhibiting glycolysis via ubiquitination of PFKP. Naunyn-Schmiedeberg's archives of pharmacology 4 39725718
2024 The kpc-1 3'UTR facilitates dendritic transport and translation efficiency of mRNAs for dendrite arborization of a mechanosensory neuron important for male courtship. PLoS genetics 2 39110773
2024 Vimentin is a ubiquitination and degradation substrate of the ubiquitin ligase KPC1. Biochemical and biophysical research communications 2 39732122
2022 E3 ubiquitin ligase RNF123-deficient mice exhibit reduced parasitemia and mortality in rodent malaria (Plasmodium yoelii 17XL) infection. Parasitology international 2 35063657
2020 Preliminary study on the inhibitory effect of tumor suppressor gene KPC1 on the proliferation in gastric carcinoma cell. Annals of translational medicine 1 32355787
2026 The Crohn's disease-related RNF123 prevents NLRP3 inflammasome assembly by catalyzing unanchored K63-linked ubiquitination on NEK7. Proceedings of the National Academy of Sciences of the United States of America 0 41719337
2026 The E3 Ubiquitin Ligase RNF123 Mediates Pathological Cardiac Hypertrophy by Ubiquitinating PRDX1 and Upregulating Oxidative Stress in Cardiomyocytes. Acta physiologica (Oxford, England) 0 42106994
2026 E3 Ligase KPC1 promotes sepsis-induced liver injury via ubiquitination and processing of NF-κB1 p105 in kupffer cells. Tissue & cell 0 42224868
2025 Tanshinone IIA targets RNF123 to inhibit non-small cell lung cancer cell proliferation, migration and invasion via KAT2B-mediated H3K18ac modification. Oncology letters 0 41415475
2025 Ubiquitin E3 ligase KPC1 governs mesenchymal metastatic melanoma reprogramming via proteasomal degradation of ZEB1. Cell death & disease 0 41429767

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