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RNF144A

E3 ubiquitin-protein ligase RNF144A · UniProt P50876

Length
292 aa
Mass
32.9 kDa
Annotated
2026-06-10
29 papers in source corpus 17 papers cited in narrative 17 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

RNF144A is a membrane-anchored RBR (RING1-IBR-RING2) E3 ubiquitin ligase that controls diverse cellular programs by directing substrates to proteasomal degradation, including DNA repair signaling, growth-factor signaling, apoptosis, autophagy, and innate immunity (PMID:24979766, PMID:34400221, PMID:37955227, PMID:39608349). Its catalytic RING module coordinates two zinc atoms and presents the active site and E2-binding interface (PMID:32557973), while a C-terminal transmembrane (TM) domain performs two distinct functions: it targets RNF144A to cytoplasmic vesicles and the plasma membrane and, through self-association via a GXXXG (G252XXXG256) motif, activates ligase activity—mutation of these glycines preserves membrane localization but abolishes both self-association and catalysis (PMID:24979766, PMID:26216882). RNF144A is transcriptionally induced by p53 after DNA damage and can be epigenetically silenced by promoter CpG hypermethylation acting through MBD4 (PMID:24979766, PMID:29473320). Through K48-linked ubiquitination it degrades DNA-PKcs to sensitize cells to DNA damage-induced apoptosis (PMID:24979766, PMID:36969901) and degrades BECN1 at K117/K427 to suppress autophagy during bacterial infection (PMID:39608349); it likewise drives degradation of PARP1, HSPA2, PD-L1, BMI1, LIN28B, YY1, VRK3, VRK2, FTO, and TSHR, coupling its ligase output to PARP-inhibitor sensitivity, tumor-immune surveillance, ERK-dependent apoptosis, and stress granule assembly (PMID:29212245, PMID:31406303, PMID:33067254, PMID:34400221, PMID:33978933, PMID:35103856, PMID:40204710). In contrast to its degradative activity, RNF144A promotes non-degradative K6-linked ubiquitination of STING at K236 to enhance ER-to-Golgi translocation and DNA virus-triggered antiviral signaling (PMID:37955227). RNF144A also stabilizes EGFR and prolongs EGF/EGFR signaling during ligand stimulation, indicating that its ubiquitination outputs are substrate- and stimulus-dependent rather than uniformly destabilizing (PMID:30171075).

Mechanistic history

Synthesis pass · year-by-year structured walk · 17 steps
  1. 2014 High

    Established RNF144A as a functional RBR E3 ligase with a defined substrate and biological role, answering whether this protein has catalytic ubiquitination activity and what it does.

    Evidence In vitro ubiquitination, co-IP, subcellular fractionation, and p53-dependent expression analysis showing RNF144A degrades DNA-PKcs and sensitizes to DNA damage apoptosis

    PMID:24979766

    Open questions at the time
    • Ubiquitin linkage type on DNA-PKcs not fully resolved at this stage
    • Mechanism of vesicle/plasma membrane targeting not yet defined
  2. 2015 High

    Resolved how the TM domain governs activity, showing that membrane targeting and GXXXG-mediated self-association are separable and that self-association is required for full ligase activity.

    Evidence TM/GXXXG deletion and point mutagenesis (G252L/G256L, G252D) with in vitro ubiquitination, membrane fractionation, and co-IP for self-association

    PMID:26216882

    Open questions at the time
    • Structural basis of TM self-association not determined
    • How self-association allosterically activates the catalytic RBR module is unknown
  3. 2017 Medium

    Extended the substrate repertoire to PARP1 and linked RNF144A levels to chemotherapy response, addressing how RNF144A modulates PARP-inhibitor sensitivity.

    Evidence Reciprocal co-IP, K48-linked in-cell ubiquitination assays, and olaparib sensitivity assays in breast cancer cells

    PMID:29212245

    Open questions at the time
    • Single lab, no in vivo confirmation
    • Direct ubiquitination site on PARP1 not mapped
  4. 2018 Medium

    Showed RNF144A is not uniformly degradative, revealing a stimulus-dependent role in stabilizing EGFR and prolonging EGF/EGFR signaling.

    Evidence Knockdown/knockout with EGFR protein-level and signaling readouts, co-IP, proliferation and G1/S gene expression assays

    PMID:30171075

    Open questions at the time
    • Ubiquitin linkage type stabilizing EGFR not defined
    • How the same ligase stabilizes some substrates while degrading others mechanistically unresolved
  5. 2018 Medium

    Identified an epigenetic mechanism silencing RNF144A in cancer, answering how its expression is lost in tumors.

    Evidence Bisulfite methylation analysis, 5-Aza-2-deoxycytidine reactivation, and MBD4 knockdown/inhibition with RNF144A expression readouts

    PMID:29473320

    Open questions at the time
    • Direct MBD4 binding to the RNF144A promoter not demonstrated
    • Single lab
  6. 2019 High

    Used unbiased proteomics to identify HSPA2 as a substrate and tied catalytic activity to tumor suppression via rescue epistasis.

    Evidence Quantitative proteomics, ligase-dead mutagenesis, in-cell ubiquitination, and HSPA2 rescue with in vitro and in vivo tumor assays

    PMID:31406303

    Open questions at the time
    • HSPA2 ubiquitination sites not mapped
    • Linkage type not specified
  7. 2020 High

    Provided atomic-resolution detail of the catalytic RING domain, defining zinc coordination and the E2-binding interface.

    Evidence Solution NMR structure of the RING finger domain and metallochromic zinc stoichiometry assay

    PMID:32557973

    Open questions at the time
    • Full-length or IBR/RING2 structure not determined
    • No structure of substrate- or E2-bound complex
  8. 2020 Medium

    Connected RNF144A to ERK-dependent apoptosis through stress-regulated degradation of VRK3.

    Evidence Co-IP, in-cell ubiquitination, oxidative-stress fractionation, and RNF144A perturbation with VRK3/ERK and apoptosis readouts

    PMID:33067254

    Open questions at the time
    • Single lab
    • VRK3 ubiquitination sites and linkage not mapped
  9. 2021 High

    Established an in vivo immunoregulatory role, showing RNF144A degrades PD-L1 (and BMI1) and shapes tumor-infiltrating CD8+ T cells.

    Evidence Co-IP, ubiquitination assays, and Rnf144a knockout mice challenged with carcinogen (BBN) with IHC/flow cytometry for CD8+ T cells

    PMID:34400221

    Open questions at the time
    • BMI1 mechanism less developed than PD-L1
    • PD-L1 ubiquitination sites not mapped
  10. 2021 Medium

    Added LIN28B as a substrate linking RNF144A to stem-cell pluripotency programs in ovarian cancer.

    Evidence Co-IP, ubiquitination assays, LIN28B rescue of pluripotency markers, and xenograft model

    PMID:33978933

    Open questions at the time
    • Single lab
    • Direct versus indirect ubiquitination of LIN28B not fully distinguished
  11. 2022 Medium

    Showed RNF144A controls transcription indirectly by degrading the factor YY1 and blocking GMFG activation.

    Evidence Co-IP, ubiquitination, transcriptome profiling, and GMFG rescue in breast cancer cells

    PMID:35103856

    Open questions at the time
    • YY1 ubiquitination site not mapped
    • Single lab
  12. 2023 High

    Revealed a non-degradative ubiquitination output, with K6-linked ubiquitination of STING at K236 promoting ER-to-Golgi translocation and DNA-virus antiviral signaling.

    Evidence Linkage-specific ubiquitination assays, K236R mutant analysis, and Rnf144a-deficient mice with DNA virus challenge; negative result for RNA sensing

    PMID:37955227

    Open questions at the time
    • Structural basis for K6 versus K48 linkage selection unknown
    • How membrane-localized RNF144A engages STING at the ER not detailed
  13. 2023 Medium

    Extended DNA-PKcs targeting to hepatocellular carcinoma and linked RNF144A nuclear translocation/loss to radioresistance.

    Evidence Western blotting, IP, fractionation, confocal microscopy, and proteasome inhibitor treatment in HCC cells after radiation/topoisomerase inhibitor

    PMID:36969901

    Open questions at the time
    • Mechanism and signal driving nuclear translocation unresolved
    • Limited mechanistic follow-up, single lab
  14. 2024 High

    Defined RNF144A as a suppressor of autophagy through site-specific K48 ubiquitination of BECN1 at K117/K427, with an in vivo anti-bacterial consequence.

    Evidence Linkage-specific ubiquitination, BECN1 K117R/K427R mutagenesis, autophagosome flux, PLA, and rnf144a KO mice infected with L. monocytogenes

    PMID:39608349

    Open questions at the time
    • How autophagy suppression integrates with STING-driven antiviral role not reconciled
    • E2 partner for BECN1 ubiquitination not identified
  15. 2024 Medium

    Placed RNF144A within a FOXF2-driven transcriptional axis that degrades the m6A demethylase FTO to suppress M2 macrophage polarization.

    Evidence FOXF2/RNF144A perturbation with FTO readouts, ubiquitination assays, macrophage polarization, and promoter transcription analysis

    PMID:39447407

    Open questions at the time
    • FTO ubiquitination sites not mapped
    • Single lab
  16. 2025 Medium

    Identified an RNF144A-VRK2-G3BP1 axis regulating stress granule assembly and chemotherapy sensitivity.

    Evidence RNF144A-driven VRK2 degradation, G3BP1 phosphorylation readouts, stress granule imaging, and viability assays under chemotherapy

    PMID:40204710

    Open questions at the time
    • Direct ubiquitination of VRK2 by RNF144A versus indirect effect not fully resolved
    • Single lab
  17. 2025 Medium

    Added TSHR as a substrate in lung fibroblasts and connected MSC-exosome-induced RNF144A to protection from LPS pneumonia.

    Evidence GST pull-down, co-IP, knockdown with TSHR readouts, and LPS pneumonia mouse model with TSHR rescue

    PMID:41123861

    Open questions at the time
    • TSHR ubiquitination sites and linkage not mapped
    • Single lab

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unknown what determines RNF144A linkage-type selection (K48 degradative versus K6 non-degradative) and substrate choice across its many reported targets, and how its membrane localization is reconciled with action on nuclear, cytosolic, and ER-resident substrates.
  • No unifying mechanism for linkage choice
  • Cofactors/adaptors governing substrate selection unidentified
  • Relationship between subcellular targeting and substrate access unresolved

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0016740 transferase activity 5 GO:0140096 catalytic activity, acting on a protein 5 GO:0016874 ligase activity 2
Localization
GO:0005886 plasma membrane 3 GO:0031410 cytoplasmic vesicle 3 GO:0005634 nucleus 1
Pathway
R-HSA-392499 Metabolism of proteins 4 R-HSA-162582 Signal Transduction 3 R-HSA-168256 Immune System 3 R-HSA-5357801 Programmed Cell Death 2 R-HSA-73894 DNA Repair 2 R-HSA-9612973 Autophagy 1
Partners
BECN1DNA-PKCS (PRKDC)EGFRHSPA2PARP1PD-L1 (CD274)STING (TMEM173)VRK3

Evidence

Reading pass · 17 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2014 RNF144A is an RBR-domain E3 ubiquitin ligase that ubiquitinates DNA-PKcs in vitro and in vivo, promoting its proteasomal degradation and thereby sensitizing cells to DNA damage-induced apoptosis. RNF144A expression is induced by DNA damage in a p53-dependent manner. RNF144A localizes to cytoplasmic vesicles and the plasma membrane, where it interacts with cytoplasmic DNA-PKcs. In vitro ubiquitination assay, co-immunoprecipitation, subcellular fractionation, siRNA knockdown with cell viability/apoptosis readouts, p53-dependent expression analysis Proceedings of the National Academy of Sciences of the United States of America High 24979766
2015 The transmembrane (TM) domain of RNF144A has two independent functions: membrane localization and activation of E3 ligase activity. Self-association mediated through a GXXXG motif (G252XXXG256) in the TM domain is required for full ubiquitin ligase activity. Deletion of the TM domain abolishes membrane localization and significantly reduces E3 activity. A G252L/G256L mutant retains membrane localization but is defective in self-association and E3 activity. Loss of membrane localization alone does not abolish E3 activity if self-association is preserved, but additional G252L/G256L mutations block activity. A cancer-associated G252D mutant retains self-association and ligase activity but loses membrane localization and is rapidly turned over. Deletion and point mutagenesis of TM/GXXXG domains, in vitro ubiquitination assays, membrane fractionation, co-immunoprecipitation for self-association The Journal of biological chemistry High 26216882
2017 RNF144A interacts with PARP1 through its carboxy-terminal region containing the transmembrane domain, and targets PARP1 for K48-linked ubiquitination and subsequent proteasomal degradation. RNF144A-induced reduction of PARP1 renders breast cancer cells resistant to the PARP inhibitor olaparib; conversely, RNF144A knockdown increases PARP1 levels and sensitizes cells to olaparib. Co-immunoprecipitation, ubiquitination assays, RNF144A overexpression/knockdown with PARP1 protein-level readouts, olaparib sensitivity assays Oncotarget Medium 29212245
2018 RNF144A promotes EGFR ubiquitination, maintains EGFR protein stability, and prolongs EGF/EGFR signaling during EGF stimulation. EGFR ligands (but not DNA-damaging agents) induce a DNA-PKcs-independent interaction between RNF144A and EGFR. Depletion of RNF144A decreases EGFR expression and EGF/EGFR signaling, impairs G1/S progression gene activation, and reduces EGF-dependent cell proliferation. RNF144A also regulates EGFR transport in intracellular vesicles during EGF treatment. RNF144A knockdown/knockout with EGFR protein-level and signaling readouts, co-immunoprecipitation, cell proliferation assays, G1/S gene expression analysis The Journal of biological chemistry Medium 30171075
2018 RNF144A promoter contains a CpG island that is hypermethylated in breast cancer, leading to transcriptional silencing. The methyl-CpG-binding domain protein MBD4 contributes to this silencing, as genetic knockdown or pharmacological inhibition of MBD4 increases RNF144A expression. Treatment with the DNA methylation inhibitor 5-Aza-2-deoxycytidine reactivates RNF144A expression in hypermethylated cells. Bisulfite sequencing/methylation analysis, 5-Aza-2-deoxycytidine treatment, MBD4 siRNA knockdown and inhibitor treatment with RNF144A expression readouts Cancer medicine Medium 29473320
2019 RNF144A interacts with HSPA2 and targets it for ubiquitination and proteasomal degradation. Ligase activity-defective RNF144A mutants fail to induce HSPA2 ubiquitination/degradation and fail to suppress breast cancer cell proliferation, migration, and invasion. Ectopic HSPA2 expression rescues the anti-tumor effects of RNF144A overexpression. Quantitative proteomics, co-immunoprecipitation, ubiquitination assays, ligase-dead mutagenesis, HSPA2 rescue experiments, in vitro and in vivo tumor assays Cell death and differentiation High 31406303
2020 The solution NMR structure of the RNF144A RING finger domain was determined. The domain binds two zinc atoms (confirmed by spectrophotometric metallochromic indicator assay) and the structure delineates the active site and E2-binding interface at atomic resolution. Solution NMR structure determination, metallochromic indicator assay for zinc stoichiometry Protein science : a publication of the Protein Society High 32557973
2020 Under oxidative stress, VRK3 translocates from nucleus to cytoplasm, enabling its interaction with RNF144A, which promotes VRK3 polyubiquitylation and proteasomal degradation. Loss of VRK3 derepresses ERK activity, leading to ERK-dependent apoptosis. RNF144A overexpression increases ERK activity and promotes apoptosis via VRK3 downregulation; RNF144A depletion stabilizes VRK3 and protects cells from excessive ERK activation. Co-immunoprecipitation, ubiquitination assays, RNF144A overexpression/knockdown with VRK3 protein-level and ERK activity readouts, subcellular fractionation under oxidative stress Journal of cell science Medium 33067254
2021 RNF144A interacts with PD-L1 at the plasma membrane and intracellular vesicles and promotes its poly-ubiquitination and proteasomal degradation. RNF144A knockout in mice stabilizes PD-L1 and reduces tumor-infiltrating CD8+ T cell populations in carcinogen-induced bladder tumors. RNF144A also targets BMI1 for degradation. Co-immunoprecipitation, ubiquitination assays, Rnf144a knockout mouse model with carcinogen (BBN) challenge, immunohistochemistry and flow cytometry for CD8+ T cells Cancer letters High 34400221
2021 RNF144A interacts with LIN28B via co-immunoprecipitation and promotes its ubiquitination and proteasomal degradation in ovarian cancer cells. Ectopic LIN28B expression restores stem cell pluripotency-associated transcription factors in RNF144A-overexpressing cells, establishing an RNF144A–LIN28B epistatic relationship. Co-immunoprecipitation, ubiquitination assays, RNF144A overexpression/knockdown with LIN28B protein-level and stem-cell marker readouts, LIN28B rescue experiment, mouse xenograft model Cell biology and toxicology Medium 33978933
2022 RNF144A interacts with transcription factor YY1 and promotes its ubiquitination-dependent proteasomal degradation, thereby blocking YY1-driven transcriptional activation of GMFG. Ectopic GMFG expression partially rescues the anti-proliferative, anti-migratory, and anti-invasive effects of RNF144A overexpression in breast cancer cells. Co-immunoprecipitation, ubiquitination assays, transcriptome profiling (Affymetrix array), quantitative RT-PCR and western blot for GMFG, GMFG rescue experiment Medical oncology (Northwood, London, England) Medium 35103856
2023 RNF144A interacts with STING and promotes K6-linked ubiquitination of STING at lysine K236, enhancing STING translocation from the ER to the Golgi and downstream innate immune signaling. The K236R STING mutant shows reduced activity in innate immune signaling. RNF144A does not affect RNA virus- or cytosolic RNA-triggered innate immune responses (negative finding for RNA sensing). Rnf144a-deficient cells and mice show impaired DNA virus-triggered signaling. Co-immunoprecipitation, ubiquitination assays with linkage-specific antibodies, K236R STING mutant analysis, RNF144A knockdown/overexpression with interferon signaling readouts, Rnf144a-deficient mouse model with DNA virus challenge EMBO reports High 37955227
2023 In hepatocellular carcinoma cells, RNF144A mediates ubiquitination of DNA-PKcs following combined radiation and topoisomerase I inhibitor treatment, reducing DNA-PKcs prosurvival signaling. In PLC5 cells, RNF144A undergoes nuclear translocation and is decreased, correlating with DNA-PKcs accumulation and radioresistance. The ubiquitin/proteasome system is required for this effect (reversed by proteasome inhibition). Western blotting, immunoprecipitation, subcellular fractionation, confocal microscopy, proteasome inhibitor treatment Journal of clinical and translational hepatology Medium 36969901
2024 RNF144A interacts with BECN1 (Beclin-1) and promotes its K48-linked ubiquitination at K117 and K427, leading to proteasomal degradation of BECN1 and reduced autophagosome accumulation. This inhibits autophagy during L. monocytogenes infection. These two ubiquitination sites on BECN1 are required for the functional effect on autophagy and bacterial infection. rnf144a-deficient mice are protected from Lm infection and show enhanced innate immune responses. Co-immunoprecipitation, ubiquitination assays with K48-linkage-specific antibodies, site-directed mutagenesis of BECN1 ubiquitination sites (K117R, K427R), autophagosome flux assays, rnf144a KO mouse model with L. monocytogenes infection, proximity ligation assay Autophagy High 39608349
2024 FOXF2 transcriptionally activates RNF144A expression, and the resulting RNF144A protein promotes ubiquitination and proteasomal degradation of FTO (an m6A demethylase). This axis contributes to suppression of M2 macrophage (TAM) polarization in esophageal squamous cell carcinoma. Overexpression/knockdown of FOXF2 and RNF144A with FTO protein-level readouts, ubiquitination assays, macrophage polarization assays, promoter transcription analysis International immunopharmacology Medium 39447407
2025 RNF144A promotes proteasomal degradation of VRK2, which reduces VRK2-mediated phosphorylation of G3BP1, thereby promoting stress granule (SG) assembly. Overexpression of VRK2 inhibits SG formation and sensitizes cells to stress and chemotherapy. This establishes an RNF144A–VRK2–G3BP1 axis regulating SG formation. VRK2 overexpression/knockdown, RNF144A overexpression with VRK2 protein-level readouts, G3BP1 phosphorylation assays, stress granule imaging, cell viability under chemotherapy Cell death discovery Medium 40204710
2025 RNF144A interacts with thyroid-stimulating hormone receptor (TSHR) and promotes its ubiquitination and destabilization in lung fibroblasts. MSC-derived exosomes increase RNF144A expression, which suppresses TSHR protein levels and protects against LPS-induced pneumonia in vitro and in vivo. Re-expression of TSHR reverses the protective effects of MSC exosomes. GST pull-down, co-immunoprecipitation, immunoprecipitation, RNF144A knockdown with TSHR protein-level readouts, LPS pneumonia mouse model Applied biochemistry and biotechnology Medium 41123861

Source papers

Stage 0 corpus · 29 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1996 Prediction of the coding sequences of unidentified human genes. V. The coding sequences of 40 new genes (KIAA0161-KIAA0200) deduced by analysis of cDNA clones from human cell line KG-1. DNA research : an international journal for rapid publication of reports on genes and genomes 114 8724849
2014 RNF144A, an E3 ubiquitin ligase for DNA-PKcs, promotes apoptosis during DNA damage. Proceedings of the National Academy of Sciences of the United States of America 71 24979766
2019 RNF144A functions as a tumor suppressor in breast cancer through ubiquitin ligase activity-dependent regulation of stability and oncogenic functions of HSPA2. Cell death and differentiation 49 31406303
2023 RNF144A promotes antiviral responses by modulating STING ubiquitination. EMBO reports 30 37955227
2021 RNF144A deficiency promotes PD-L1 protein stabilization and carcinogen-induced bladder tumorigenesis. Cancer letters 27 34400221
2021 RNF144A-AS1, a TGF-β1- and hypoxia-inducible gene that promotes tumor metastasis and proliferation via targeting the miR-30c-2-3p/LOX axis in gastric cancer. Cell & bioscience 27 34583752
2015 Regulation of RNF144A E3 Ubiquitin Ligase Activity by Self-association through Its Transmembrane Domain. The Journal of biological chemistry 24 26216882
2017 RBR-type E3 ubiquitin ligase RNF144A targets PARP1 for ubiquitin-dependent degradation and regulates PARP inhibitor sensitivity in breast cancer cells. Oncotarget 23 29212245
2018 RNF144A sustains EGFR signaling to promote EGF-dependent cell proliferation. The Journal of biological chemistry 20 30171075
2018 Epigenetic silencing of RNF144A expression in breast cancer cells through promoter hypermethylation and MBD4. Cancer medicine 17 29473320
2021 RNF144A suppresses ovarian cancer stem cell properties and tumor progression through regulation of LIN28B degradation via the ubiquitin-proteasome pathway. Cell biology and toxicology 16 33978933
2020 LncRNA RNF144A-AS1 Promotes Bladder Cancer Progression via RNF144A-AS1/miR-455-5p/SOX11 Axis. OncoTargets and therapy 13 33177836
2022 RNF144A exerts tumor suppressor function in breast cancer through targeting YY1 for proteasomal degradation to downregulate GMFG expression. Medical oncology (Northwood, London, England) 8 35103856
2021 RNF144A-AS1 promotes the development of glioma cells by targeting miR-665/HMGA1 axis. Neuroscience letters 8 34560189
2020 RNF144a induces ERK-dependent cell death under oxidative stress via downregulation of vaccinia-related kinase 3. Journal of cell science 8 33067254
2024 The Role of Long Non-Coding RNF144A-AS1 in Cancer Progression. Cell biochemistry and biophysics 5 39014185
2023 Topoisomerase I Inhibition Radiosensitizing Hepatocellular Carcinoma by RNF144A-mediated DNA-PKcs Ubiquitination and Natural Killer Cell Cytotoxicity. Journal of clinical and translational hepatology 5 36969901
2025 RNF144A-VRK2-G3BP1 axis regulates stress granule assembly. Cell death discovery 3 40204710
2024 RNF144A-AS1 stabilizes TAF15 and promotes malignant biological behaviors of skin cutaneous melanoma. Molecular and cellular biochemistry 3 38878223
2024 FOXF2 suppressed esophageal squamous cell carcinoma by reducing M2 TAMs via modulating RNF144A-FTO axis. International immunopharmacology 3 39447407
2024 RNF144A inhibits autophagy by targeting BECN1 for degradation during L. monocytogenes infection. Autophagy 3 39608349
2023 An advanced NSCLC patient with ALK-RNF144A and HIP1-ALK fusions treated with ALK-TKI combination therapy: a case report. Translational lung cancer research 3 38205210
2020 Solution structure of the zinc finger domain of human RNF144A ubiquitin ligase. Protein science : a publication of the Protein Society 3 32557973
2025 RNF144A and RNF144B: Important molecules for health. Open life sciences 2 40756570
2024 LncRNA RNF144A-AS1 gene polymorphisms and their influence on lung cancer patients in the Chinese Han population. Non-coding RNA research 1 39611047
2026 LncRNA RNF144A-AS1 increases P300-mediated H4K5 acetylation of PDE4 to promote keloid fibrosis. Biomedical engineering online 0 41691288
2025 m6A methylation-mediated lncRNA RNF144A-AS1 promotes hepatocellular carcinoma progression through the miR-1301-3p/RNF38 pathway. Biology direct 0 40734179
2025 Exosomal RNF144A Derived From Mesenchymal Stem Cells Ameliorates LPS-induced Pneumonia in Experimental Models By Inducing TSHR Ubiquitination. Applied biochemistry and biotechnology 0 41123861
2024 RNF144A as a potential risk gene for endometrial carcinoma: Insights from Mendelian randomization, bulk RNA sequencing, single-cell RNA, and experimental analysis. Medicine 0 39465767

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