Affinage

TRIM41

E3 ubiquitin-protein ligase TRIM41 · UniProt Q8WV44

Length
630 aa
Mass
71.7 kDa
Annotated
2026-06-10
13 papers in source corpus 13 papers cited in narrative 13 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

TRIM41 (RINCK) is a TRIM-family RING E3 ubiquitin ligase that acts as a substrate-selective controller of protein abundance across antiviral defense, immune signaling, redox homeostasis, transcriptional control, and meiosis, with its E3 ligase activity required for these functions (PMID:17893151, PMID:29899090, PMID:35648791). It was first defined through its substrate-recognition C1A-domain interaction with all classes of protein kinase C, which it ubiquitinates to drive PKC degradation independently of phorbol-ester downregulation (PMID:17893151). In antiviral restriction, TRIM41 binds viral nucleoproteins—influenza A virus NP via its SPRY domain and VSV N protein—and targets them for polyubiquitination and proteasomal degradation, with RING-dead mutants abolishing restriction (PMID:29899090, PMID:31979016). TRIM41 also positively shapes innate immune signaling: it monoubiquitinates cGAS to enhance cGAMP synthesis and type I interferon output (PMID:29760876), and catalyzes K63-linked ubiquitination of BCL10 within the CBM complex to recruit NEMO and activate NF-κB and the TBK1–IRF3 axis (PMID:33640899). Through K48-linked degradative ubiquitination it controls additional substrates, including NRF2 to restrain antioxidant gene expression in intestinal epithelium (PMID:37844381), the transcription factor ZSCAN21 to limit α-synuclein (SNCA) transcription (PMID:30485814), LINE-1 ORF2p to suppress retrotransposition in a nuclear-cGAS-assisted manner (PMID:38086852), and PKD1, p53, and c-Maf in various cellular contexts (PMID:34324862, PMID:36705889, PMID:38883815). In vivo, TRIM41 is required for male meiotic progression, where its RING activity regulates SYCP3 loading dynamics on chromosome axes (PMID:35648791).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 2005 Medium

    Established where TRIM41 protein resides and that an N-terminal segment governs its trafficking, framing it as a dual cytoplasmic/nuclear factor before any catalytic role was known.

    Evidence GFP-fusion live imaging of truncation mutants and subcellular fractionation

    PMID:16022281

    Open questions at the time
    • Functional consequence of speckle localization unknown
    • NLS-independent nuclear transport mechanism not resolved
    • Single lab, descriptive
  2. 2007 High

    Defined TRIM41 as a bona fide E3 ubiquitin ligase and identified its first substrate, showing it targets PKC isozymes via their C1A domain for degradation independently of phorbol-ester-induced turnover.

    Evidence Yeast two-hybrid, co-IP, in vitro and cellular ubiquitination assays, siRNA/overexpression

    PMID:17893151

    Open questions at the time
    • Ubiquitin linkage type on PKC not defined
    • Physiological context of PKC regulation unclear
    • RING-dependence not formally tested here
  3. 2018 High

    Revealed an antiviral function: TRIM41 recognizes influenza A NP through its SPRY domain and degrades it, with RING activity required for restriction, establishing a substrate-recognition-domain architecture.

    Evidence Co-IP, in vitro ubiquitination, RNAi/CRISPR KO, E3-dead mutant, IAV infection assays

    PMID:29899090

    Open questions at the time
    • Generality across viral nucleoproteins not yet shown
    • In vivo relevance untested
  4. 2018 High

    Showed TRIM41 can act as a positive immune regulator via non-degradative ubiquitination, monoubiquitinating cGAS to enhance cGAMP synthesis and interferon induction.

    Evidence CRISPR KO, co-IP, ubiquitination assay, cGAMP measurement, TBK1/IRF3 phospho-readouts, HSV-1 infection

    PMID:29760876

    Open questions at the time
    • Monoubiquitination site on cGAS not mapped
    • Relationship to TRIM41's degradative activity unclear
  5. 2018 High

    Connected TRIM41 to transcriptional control of α-synuclein by degrading ZSCAN21, and placed it in an antagonistic relationship with TRIM17.

    Evidence siRNA, reciprocal co-IP, ubiquitination assay, SNCA mRNA readout, patient variant assay

    PMID:30485814

    Open questions at the time
    • Neuronal phenotype in vivo not established
    • Disease causation not demonstrated
  6. 2020 High

    Extended the antiviral nucleoprotein-degradation paradigm to VSV N protein, reinforcing RING-dependent restriction of negative-strand RNA viruses.

    Evidence Co-IP, in vitro/cellular ubiquitination, KD/OE, E3-dead mutant, infection with proteasome inhibitor

    PMID:31979016

    Open questions at the time
    • Ubiquitin linkage on VSV N not defined
    • Breadth of viral nucleoprotein targeting unknown
  7. 2021 High

    Identified BCL10 as a K63-ubiquitination substrate, showing TRIM41 drives NEMO recruitment and NF-κB/TBK1–IRF3 activation downstream of nucleic-acid sensing, validated in knockout mice.

    Evidence Reciprocal co-IP, K63-linkage-specific ubiquitination assay, Trim41 KO mice, macrophage stimulation/infection, cytokine readouts

    PMID:33640899

    Open questions at the time
    • K63 chain assembly mechanism on BCL10 not structurally resolved
    • Interplay with cGAS-monoubiquitination role unclear
  8. 2021 Medium

    Placed TRIM41 in a cancer-relevant degradation axis by targeting PKD1, antagonized by ANXA10, linking it to TGF-β/SMAD signaling and melanoma metastasis.

    Evidence Co-IP, protein stability assay, ANXA10 KO, migration and in vivo metastasis assays

    PMID:34324862

    Open questions at the time
    • Direct in vitro ubiquitination of PKD1 not reconstituted
    • Ubiquitin linkage type undefined
    • Single lab
  9. 2022 High

    Demonstrated a physiological in vivo role in male meiosis, where RING activity controls SYCP3 loading on chromosome axes, with a RING-deletion knock-in phenocopying full knockout.

    Evidence Trim41 KO and RING-deletion knock-in mice, meiotic chromosome-spread immunofluorescence, fertility assays

    PMID:35648791

    Open questions at the time
    • Whether SYCP3 is a direct ubiquitination substrate not shown
    • Mechanism of axis recruitment unresolved
  10. 2023 High

    Showed TRIM41 suppresses LINE-1 retrotransposition by degrading ORF2p, with nuclear cGAS and CHK2-driven cGAS phosphorylation enhancing the TRIM41–ORF2p association upon DNA damage.

    Evidence Co-IP, ubiquitination assay, KD, L1 retrotransposition reporter, phospho-mutant and cancer-variant analysis

    PMID:38086852

    Open questions at the time
    • Structural basis of cGAS-enhanced recruitment unknown
    • ORF2p ubiquitination sites not mapped
  11. 2023 High

    Established TRIM41 as a negative regulator of NRF2 via K48-linked degradation in intestinal epithelium, with loss protecting against colitis and early colorectal cancer in vivo.

    Evidence Reciprocal co-IP, K48-linkage ubiquitination assay, IEC-specific KO/OE mice, AAV/lentiviral KD, colitis/tumor models

    PMID:37844381

    Open questions at the time
    • NRF2 ubiquitination sites not defined
    • Tissue specificity of this regulation not explained
  12. 2023 Medium

    Showed circRNA_0067717 scaffolds TRIM41 to p53, enabling p53 degradation and paclitaxel resistance, illustrating RNA-directed substrate selection.

    Evidence RNA pulldown, RIP, FISH, siRNA, ubiquitination assay, circRNA deletion mapping

    PMID:36705889

    Open questions at the time
    • TRIM41 activity on p53 not shown independent of the circRNA scaffold
    • Direct p53 ubiquitination linkage undefined
    • Single lab
  13. 2024 Medium

    Linked TRIM41 to immune tolerance by degrading c-Maf in airway dendritic cells, reducing IL-10 and promoting allergy.

    Evidence Trim41 OE/inhibition in DCs, c-Maf and IL-10 readouts, murine airway allergy model

    PMID:38883815

    Open questions at the time
    • Direct ubiquitination assay for c-Maf not described
    • Single lab, cellular manipulation only

Open questions

Synthesis pass · forward-looking unresolved questions
  • How TRIM41 selects among its diverse substrates and switches between K48-degradative, K63-signaling, and monoubiquitination outputs remains unresolved.
  • No structural model of substrate or chain-type selection
  • Determinants directing degradative vs signaling ubiquitination unknown
  • Regulation of TRIM41 abundance/activity uncharacterized

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0016874 ligase activity 6 GO:0140096 catalytic activity, acting on a protein 6
Localization
GO:0005634 nucleus 1 GO:0005829 cytosol 1
Pathway
R-HSA-168256 Immune System 5 R-HSA-392499 Metabolism of proteins 5 R-HSA-1474165 Reproduction 1

Evidence

Reading pass · 13 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2007 TRIM41/RINCK was identified as an E3 ubiquitin ligase that interacts with protein kinase C (PKC) via the C1A domain of PKC (identified by yeast two-hybrid with PKCβ N-terminus as bait). TRIM41 ubiquitinates PKC both in vitro and in cells, leading to PKC degradation and reduced PKC levels; this mechanism is independent of phorbol ester-mediated PKC downregulation and applies to conventional, novel, and atypical PKC isozymes. Yeast two-hybrid screen, co-immunoprecipitation, in vitro and cellular ubiquitination assay, overexpression and siRNA knockdown with PKC level readout The Journal of biological chemistry High 17893151
2005 TRIM41 protein (isoforms alpha and beta) localizes as speckles in both cytoplasm and nucleus of cells. Nuclear transport is mediated by an N-terminal segment common to both isoforms but is independent of a classical nuclear localization signal sequence, as determined by GFP fusion constructs and subcellular fractionation. GFP fusion live-cell imaging of truncation mutants, Western blot of cellular fractions Molecular biology reports Medium 16022281
2018 TRIM41 interacts with influenza A virus nucleoprotein (NP) through its SPRY domain, ubiquitinates NP in vitro and in cells, and promotes NP polyubiquitination and proteasomal degradation, thereby restricting IAV infection. A TRIM41 RING-domain mutant lacking E3 ligase activity failed to inhibit IAV infection, demonstrating that E3 ligase activity is essential for antiviral function. Co-immunoprecipitation, in vitro ubiquitination assay, RNAi knockdown and CRISPR knockout of TRIM41, TRIM41 overexpression, E3 ligase-dead mutant analysis, viral infection assays Journal of virology High 29899090
2018 TRIM41/RINCK binds to cGAS and promotes monoubiquitination of cGAS, positively regulating cGAS-mediated cGAMP synthesis and downstream type I interferon production. CRISPR/Cas9 deletion of RINCK dampened interferon production in response to cytosolic DNA and HSV-1 infection, and reduced TBK1 and IRF3 phosphorylation. CRISPR/Cas9 deletion, co-immunoprecipitation, ubiquitination assay, cGAMP measurement, TBK1/IRF3 phosphorylation assay, viral infection with IFN readout Cell & bioscience High 29760876
2018 TRIM41 acts as an E3 ubiquitin ligase for the transcription factor ZSCAN21, promoting its degradation and thereby reducing SNCA (α-synuclein) transcription in neuronal cells. TRIM17 antagonizes this pathway by decreasing TRIM41-mediated degradation of ZSCAN21. TRIM41 knockdown increased SNCA expression, while ZSCAN21 silencing and TRIM17 silencing both reduced it. siRNA knockdown, co-immunoprecipitation, ubiquitination assay, gene expression analysis, patient variant functional assay Cell reports High 30485814
2020 TRIM41 interacts with and ubiquitinates the nucleoprotein (N) of vesicular stomatitis virus (VSV), leading to proteasomal degradation of VSV-N and restriction of VSV infection. An E3 ligase-defective TRIM41 mutant failed to limit VSV infection, confirming that ubiquitin ligase activity is required. Co-immunoprecipitation, in vitro and cellular ubiquitination assay, TRIM41 overexpression and knockdown, E3 ligase-dead mutant, viral infection assay with proteasome inhibitor Viruses High 31979016
2021 TRIM41 directly interacts with BCL10, a core component of the CBM (CARD-BCL10-MALT1) complex, and catalyzes K63-linked polyubiquitination of BCL10. This K63-ubiquitination of BCL10 recruits NEMO, leading to activation of NF-κB and the TBK1-IRF3 pathway downstream of nucleic acid sensing, and is required for innate antiviral cytokine and interferon production. Co-immunoprecipitation, ubiquitination assay (K63 linkage-specific), TRIM41 knockout mice (in vivo), macrophage nucleic acid transfection and viral infection assays, cytokine/IFN measurement, NF-κB/TBK1/IRF3 activation readouts Signal transduction and targeted therapy High 33640899
2021 TRIM41 targets PKD1 for ubiquitin-mediated degradation; ANXA10 interacts with PKD1 and protects it from TRIM41-directed degradation. In melanoma cells, ANXA10-mediated stabilization of PKD1 suppresses SMAD6 expression (via TGF-β/SMAD pathway) to promote cell migration and metastasis. Co-immunoprecipitation, protein stability assay, ANXA10 knockout, ubiquitination assay (inferred), cell migration and in vivo metastasis assays Cancer letters Medium 34324862
2022 TRIM41 is required for proper meiotic progression in male mice. Trim41 knockout spermatocytes exhibit overloading of SYCP3 on chromosome axes, particularly the X chromosome. A RING-domain deletion mutant of TRIM41 (which abolishes E3 ubiquitin ligase activity) phenocopies the full knockout, and mutant ΔRING-TRIM41 accumulates on chromosome axes with overloaded SYCP3, indicating TRIM41 regulates chromosome axis protein dynamics via its E3 ligase activity. Trim41 knockout mice, RING-domain deletion knock-in mutant mice, immunofluorescence of meiotic chromosome spreads for SYCP3, fertility assays PLoS genetics High 35648791
2023 TRIM41 interacts with LINE-1 ORF2p and ubiquitinates it, promoting its proteasomal degradation and suppressing L1 retrotransposition. Nuclear cGAS enhances the association between ORF2p and TRIM41, thereby promoting TRIM41-mediated ORF2p degradation. Upon DNA damage, CHK2 phosphorylates cGAS at S120 and S305, which strengthens cGAS-TRIM41 association and further promotes ORF2p degradation. Co-immunoprecipitation, ubiquitination assay, TRIM41 knockdown, L1 retrotransposition reporter assay, phospho-mutant analysis, cancer-associated cGAS variant functional analysis Nature communications High 38086852
2023 TRIM41/RINCK directly interacts with NRF2 and promotes its K48-linked polyubiquitination and proteasomal degradation in intestinal epithelial cells, suppressing NRF2 nuclear translocation and downstream antioxidant gene expression. IEC-specific Rinck knockout mitigated OTA/DSS-induced colitis and associated early colorectal cancer in mice. Co-immunoprecipitation, K48-linkage ubiquitination assay, IEC-specific Rinck knockout and overexpression transgenic mice, AAV-mediated knockdown, lentiviral knockdown, NRF2 nuclear localization assay, in vivo colitis and tumor models Phytomedicine High 37844381
2023 circRNA_0067717 acts as a molecular scaffold that bridges TRIM41 and p53, promoting TRIM41-mediated ubiquitination and degradation of p53 in NPC paclitaxel-resistant cells. The 301–425 nt region of circRNA_0067717 binds TRIM41 and the 1–176 nt region binds p53. Blocking these regions reduced paclitaxel resistance. RNA pulldown, RNA immunoprecipitation, RNA FISH, siRNA knockdown, ubiquitination assay, deletion mapping of circRNA binding sites Cellular oncology Medium 36705889
2024 TRIM41 promotes the ubiquitination and degradation of c-Maf in airway dendritic cells, reducing IL-10 expression and compromising tolerogenic DC properties, thereby contributing to airway allergy pathogenesis. Trim41 overexpression and inhibition in DCs, c-Maf protein level assay, IL-10 expression assay, murine airway allergy model iScience Medium 38883815

Source papers

Stage 0 corpus · 13 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2018 TRIM41-Mediated Ubiquitination of Nucleoprotein Limits Influenza A Virus Infection. Journal of virology 77 29899090
2018 RINCK-mediated monoubiquitination of cGAS promotes antiviral innate immune responses. Cell & bioscience 56 29760876
2007 Amplitude control of protein kinase C by RINCK, a novel E3 ubiquitin ligase. The Journal of biological chemistry 53 17893151
2023 Nuclear cGAS restricts L1 retrotransposition by promoting TRIM41-mediated ORF2p ubiquitination and degradation. Nature communications 38 38086852
2018 The E3 Ubiquitin Ligases TRIM17 and TRIM41 Modulate α-Synuclein Expression by Regulating ZSCAN21. Cell reports 35 30485814
2020 TRIM41-Mediated Ubiquitination of Nucleoprotein Limits Vesicular Stomatitis Virus Infection. Viruses 24 31979016
2021 TRIM41 is required to innate antiviral response by polyubiquitinating BCL10 and recruiting NEMO. Signal transduction and targeted therapy 22 33640899
2023 circRNA_0067717 promotes paclitaxel resistance in nasopharyngeal carcinoma by acting as a scaffold for TRIM41 and p53. Cellular oncology (Dordrecht, Netherlands) 20 36705889
2021 ANXA10 promotes melanoma metastasis by suppressing E3 ligase TRIM41-directed PKD1 degradation. Cancer letters 19 34324862
2023 Ochratoxin A promotes chronic enteritis and early colorectal cancer progression by targeting Rinck signaling. Phytomedicine : international journal of phytotherapy and phytopharmacology 13 37844381
2005 Intracellular localization and domain organization of human TRIM41 proteins. Molecular biology reports 7 16022281
2024 TRIM41 contributes to the pathogenesis of airway allergy by compromising dendritic cells' tolerogenic properties. iScience 1 38883815
2022 Trim41 is required to regulate chromosome axis protein dynamics and meiosis in male mice. PLoS genetics 1 35648791

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