Affinage

DCAF13

DDB1- and CUL4-associated factor 13 · UniProt Q9NV06

Length
445 aa
Mass
51.4 kDa
Annotated
2026-06-09
30 papers in source corpus 19 papers cited in narrative 19 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 5/5 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

DCAF13 is a nucleolar WD40-repeat protein that serves as a substrate receptor for the CRL4 (CUL4–DDB1–RBX1) E3 ubiquitin ligase and, independently, as a ribosome biogenesis factor, making it an essential regulator of epigenetic reprogramming, translational capacity, and proliferation in development and cancer (PMID:30111536, PMID:30283081, PMID:37353483). As a CRL4 adaptor it directs polyubiquitination and proteasomal degradation of a context-dependent set of substrates: SUV39H1 to lower H3K9me3 and license zygotic gene expression (PMID:30111536), PTEN to sustain PI3K/AKT signaling required for meiotic resumption and neural crest development (PMID:31492966, PMID:41492083), MeCP2 to restrain DNA methylation in growing oocytes (PMID:38578457), the TOP1–DNA-protein crosslink for replication-coupled repair (PMID:37353483), PERP, FRAS1, and p53 in various cancers (PMID:35178836, PMID:39367995, PMID:38163876). Beyond degradative ubiquitination, DCAF13 catalyzes non-degradative chain types that promote ribosome production—K63-linked ubiquitination of the Pol I subunit RPA194 to stimulate rDNA transcription, and K27-linked ubiquitination of RRS1 to stabilize it during hematopoietic ribosome assembly (PMID:39788980, PMID:41787937). It also supports 18S rRNA processing through interactions with fibrillarin, NPM1/UTP23, and the Pol I preinitiation factor TAF1A, the latter two coupling DCAF13 to nucleolar condensate formation and preinitiation complex assembly (PMID:30283081, PMID:37615668, PMID:40902972). Loss of DCAF13 produces ribosome biogenesis failure, p53 pathway activation, and developmental arrest across oocytes, embryos, hematopoietic stem cells, and uterine tissue (PMID:30283081, PMID:41787937, PMID:40750792).

Mechanistic history

Synthesis pass · year-by-year structured walk · 16 steps
  1. 2017 High

    Established that DCAF13 functions catalytically as a CRL4 substrate receptor, defining its first degradation target and demonstrating it assembles into a CUL4B–DDB1 ligase.

    Evidence Co-IP, in vitro/in vivo ubiquitination, knockdown and overexpression in osteosarcoma cells targeting PTEN

    PMID:29499938

    Open questions at the time
    • Degron/substrate recognition motif on PTEN not defined
    • Specificity vs other DCAFs not addressed
  2. 2018 High

    Connected DCAF13 to epigenetic reprogramming by showing CRL4-DCAF13 degrades the H3K9 methyltransferase SUV39H1 to erase repressive marks and enable zygotic gene activation in vivo.

    Evidence Dcaf13 knockout mice, reciprocal Co-IP, ubiquitination assays, H3K9me3 immunofluorescence

    PMID:30111536

    Open questions at the time
    • Whether SUV39H2 is also a substrate not resolved here
    • Direct enzymatic specificity vs indirect effects on H3K9me3
  3. 2018 High

    Revealed a degradation-independent role in ribosome biogenesis, placing DCAF13 in the nucleolar rRNA-processing machinery via fibrillarin interaction.

    Evidence Oocyte conditional KO, Co-IP with fibrillarin, northern blot for pre-rRNA, ribosome assembly and protein synthesis assays

    PMID:30283081

    Open questions at the time
    • Direct rRNA cleavage role vs scaffolding not separated
    • Molecular basis of fibrillarin binding unknown
  4. 2019 High

    Linked DCAF13-mediated PTEN degradation to a physiological signaling outcome—maintaining PI3K activity and CDK1 for oocyte meiotic resumption.

    Evidence Oocyte-specific KO, ubiquitination assays, PI3K and CDK1 activity measurement, spindle/chromosome imaging

    PMID:31492966

    Open questions at the time
    • How DCAF13 substrate choice is restricted to PTEN in this context unclear
  5. 2019 Medium

    Showed maternal DCAF13 is required for higher-order chromatin organization and nucleolar reorganization in oocytes, broadening its role beyond single-substrate effects.

    Evidence Oocyte conditional KO, RNA-seq of MII oocytes and 2-cell embryos, mRNA rescue attempt, immunofluorescence

    PMID:31000741

    Open questions at the time
    • mRNA rescue failed, leaving causal mechanism for chromatin tightness incomplete
    • Molecular link between nucleolar function and chromatin not defined
  6. 2020 Medium

    Proposed an RNA-binding activity distinct from ubiquitin ligation, with DCAF13 destabilizing DTX3 mRNA via ARE binding to drive NOTCH4 signaling in cancer.

    Evidence RIP, mRNA stability assays, migration/invasion assays, NOTCH4 ubiquitination in TNBC cells

    PMID:33300431

    Open questions at the time
    • Direct vs indirect ARE binding not structurally confirmed
    • Relationship of RBP activity to WD40 scaffold unknown
  7. 2022 Medium

    Extended the CRL4-DCAF13 substrate repertoire to PERP in breast cancer, coupling its degradation to apoptosis and senescence suppression.

    Evidence CRISPR KO, Co-IP of DCAF13–DDB1–PERP ternary complex, DDB1-dependent ubiquitination, RNA-seq

    PMID:35178836

    Open questions at the time
    • mRNA accumulation of PERP upon KO implies an additional transcriptional layer not explained
    • Degron not mapped
  8. 2023 High

    Defined DCAF13 as the CRL4 receptor recognizing TOP1-DPCs for replication-coupled repair, with the complex undergoing auto-NEDDylation and exploitable by NEDD8 inhibition.

    Evidence Chemical genetic screens, Co-IP, ubiquitination assays, DPC repair in CRC cells, organoids, xenografts, pevonedistat combination

    PMID:37353483

    Open questions at the time
    • How DCAF13 discriminates crosslinked TOP1 from native TOP1 unresolved
  9. 2023 Medium

    Showed DCAF13 drives nucleolar phase separation through NPM1 to recruit UTP23 and accelerate 18S rRNA maturation, linking ribosome biogenesis to rapid proliferation.

    Evidence T cell-specific KO, phase separation assays, rRNA processing, ribosome assembly and nascent protein synthesis assays

    PMID:37615668

    Open questions at the time
    • Whether DCAF13 itself undergoes phase separation or only promotes NPM1 condensation unclear
    • Direct UTP23 contact not shown
  10. 2024 High

    Identified MeCP2 as an oocyte CRL4-DCAF13 substrate, connecting its degradation to control of DNA methylation, validated by genetic rescue.

    Evidence Dcaf13-null oocytes, ubiquitination assays, MeCP2 knockdown rescue, RNA-seq, DNA methylation analysis

    PMID:38578457

    Open questions at the time
    • Only partial rescue indicates additional substrates contribute to phenotype
  11. 2024 Medium

    Established DCAF13 as a negative regulator of p53 across cancers, promoting K48-linked p53 degradation and, downstream, ferroptosis suppression via xCT.

    Evidence Co-IP, K48-linked ubiquitination assays, RNA-seq, ChIP-qPCR in lung adenocarcinoma; STAT5B reporter, ubiquitination and xenografts in mantle cell lymphoma

    PMID:38163876 PMID:38979130

    Open questions at the time
    • Whether p53 ubiquitination is CRL4-dependent not formally shown in both contexts
    • Direct vs scaffolded p53 recognition unresolved
  12. 2024 Medium

    Added FRAS1 as a CRL4-DCAF13 substrate whose degradation sustains FAK signaling and tumor cell proliferation/migration in ovarian cancer.

    Evidence CRISPR KO, ubiquitination assays, FAK pathway western blots, Co-IP, xenografts

    PMID:39367995

    Open questions at the time
    • Mechanism linking FRAS1 level to FAK activity not detailed
  13. 2025 High

    Demonstrated non-degradative ubiquitination as a DCAF13 mechanism, with K63-linked modification of RPA194 stimulating Pol I transcription, and direct TAF1A binding required for preinitiation complex assembly.

    Evidence K63-specific ubiquitination and Pol I transcription assays in breast cancer (RPA194); Co-IP and rDNA transcription assays in NSCLC (TAF1A)

    PMID:39788980 PMID:40902972

    Open questions at the time
    • Whether RPA194 K63 ubiquitination uses the CRL4 scaffold or a different E3 unclear
    • Coordination between RPA194 and TAF1A roles not integrated
  14. 2025 High

    Identified a third ubiquitin chain type—K27-linked stabilization of RRS1—and showed DCAF13 sustains hematopoietic stem cell ribosome assembly upstream of the p53 pathway.

    Evidence Hematopoietic conditional KO, Co-IP, K27-specific ubiquitination assays, ribosome assembly assays, Trp53 epistasis

    PMID:41787937

    Open questions at the time
    • Only partial p53-independent rescue; full downstream effector set undefined
    • How chain-type selectivity (K27 vs K48 vs K63) is achieved unknown
  15. 2025 Medium

    Extended DCAF13's developmental requirement to uterine receptivity, where its loss raises H3K9me3 and dysregulates hormone receptors to cause implantation failure.

    Evidence Uterine conditional KO, RNA-seq, H3K9me3 immunofluorescence, hormone receptor western blot, implantation assay

    PMID:40750792

    Open questions at the time
    • Direct substrate driving SUV39H2/H3K9me3 change not pinpointed in uterus
  16. 2025 Low

    Proposed a metabolic role via G6PD interaction enhancing glycolysis, with DCAF13 mRNA itself under m6A/YTHDF1 control in hepatocellular carcinoma.

    Evidence Co-IP, molecular dynamics, MeRIP-qPCR and RIP, CRISPR KO, glycolysis flux assays

    PMID:40708455

    Open questions at the time
    • Single Co-IP plus simulation; functional dependence of glycolysis on direct DCAF13–G6PD binding not established
    • m6A regulation inferred indirectly

Open questions

Synthesis pass · forward-looking unresolved questions
  • How DCAF13 selects among degradative (K48), and non-degradative (K63, K27) ubiquitin chain types and switches between its E3 adaptor and ribosome biogenesis functions remains unresolved.
  • No structural model of substrate or chain-type determinants
  • Mechanism partitioning DCAF13 between CRL4 and nucleolar machinery unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140096 catalytic activity, acting on a protein 10 GO:0003723 RNA binding 2 GO:0060090 molecular adaptor activity 2 GO:0098772 molecular function regulator activity 2
Localization
GO:0005730 nucleolus 3 GO:0005634 nucleus 2
Pathway
R-HSA-392499 Metabolism of proteins 5 R-HSA-8953854 Metabolism of RNA 5 R-HSA-4839726 Chromatin organization 2 R-HSA-1640170 Cell Cycle 1 R-HSA-73894 DNA Repair 1
Partners
CUL4BDDB1FBLNPM1RPA194RRS1TAF1AUTP23
Complex memberships
CRL4 (CUL4-DDB1-RBX1) E3 ubiquitin ligasePol I preinitiation complex

Evidence

Reading pass · 19 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2018 CRL4-DCAF13 acts as an E3 ubiquitin ligase complex that targets SUV39H1 for polyubiquitination and proteasomal degradation, thereby facilitating H3K9me3 removal and enabling zygotic gene expression during preimplantation embryonic development. Dcaf13 knockout mice arrest at the 8-16 cell stage with elevated H3K9me3. Dcaf13 knockout mice, ubiquitination assays, co-immunoprecipitation, western blotting, immunofluorescence for H3K9me3 The EMBO journal High 30111536
2018 DCAF13 is a nucleolar protein that functions as a component of the rRNA-processing complex essential for 18S rRNA processing in growing oocytes. DCAF13 interacts with the box C/D ribonucleoprotein component fibrillarin. Conditional knockout of Dcaf13 causes pre-rRNA accumulation, ribosome assembly disorder, reduced global protein synthesis, and arrest of oocyte NSN-to-SN chromatin configuration transition. Conditional knockout mice, co-immunoprecipitation (DCAF13-fibrillarin interaction), northern blotting for pre-rRNA, ribosome assembly analysis, protein synthesis assays Cell death and differentiation High 30283081
2017 CRL4B-DCAF13 E3 ligase complex (comprising CUL4B, DDB1, and DCAF13) targets PTEN for ubiquitination and proteasomal degradation in osteosarcoma cells. Disruption of this complex causes PTEN accumulation. Co-immunoprecipitation, in vitro and in vivo ubiquitination assays, siRNA knockdown, DCAF13 overexpression Molecular therapy. Nucleic acids High 29499938
2019 CRL4-DCAF13 targets PTEN for polyubiquitination and proteasomal degradation in oocytes, thereby maintaining PI3K signaling pathway activity required for meiotic resumption. Dcaf13 knockout oocytes show decreased CDK1 activity, chromosome condensation defects, spindle assembly checkpoint activation, and arrest at prometaphase I. Oocyte-specific Dcaf13 knockout, ubiquitination assays, PI3K pathway activity measurement, CDK1 kinase assay, immunofluorescence for spindle/chromosome alignment Cellular and molecular life sciences : CMLS High 31492966
2019 Maternal DCAF13, highly expressed in the growing oocyte nucleolus, is required for chromatin tightness in fully grown germinal vesicle oocytes and for proper chromosome condensation at MII. Loss of maternal DCAF13 leads to loose chromatin structure in GV oocytes, improperly condensed MII chromosomes, abnormal nuclear/nucleolar reorganization, and inactive transcription in zygotes, causing two-cell stage arrest. Oocyte-specific conditional knockout, RNA-seq of MII oocytes and 2-cell embryos, mRNA injection rescue attempt, immunofluorescence Scientific reports Medium 31000741
2020 DCAF13 functions as an RNA-binding protein (RBP) that binds to the AU-rich element (ARE) in the 3'UTR of DTX3 mRNA to accelerate its degradation, thereby activating NOTCH4 signaling (since DTX3 normally promotes ubiquitination and degradation of NOTCH4) and promoting triple-negative breast cancer metastasis. RNA immunoprecipitation (RIP), mRNA stability assays, overexpression and knockdown, migration/invasion assays, NOTCH4 ubiquitination assay Cell cycle (Georgetown, Tex.) Medium 33300431
2022 CRL4-DCAF13 E3 ligase targets PERP for ubiquitination and proteasomal degradation in breast cancer cells. Co-immunoprecipitation showed DCAF13 and DDB1 directly interact with PERP, and DDB1 overexpression significantly increased PERP polyubiquitination. DCAF13 deletion causes both mRNA and protein accumulation of PERP, leading to apoptosis and senescence. CRISPR/Cas9 knockout, co-immunoprecipitation (DCAF13-DDB1-PERP), ubiquitination assay with DDB1 overexpression, genome-wide RNAseq, western blotting Cancer science Medium 35178836
2023 DCAF13 is identified as the substrate receptor (DDB1- and Cullin-associated factor) of the CRL4 ubiquitin ligase that recognizes TOP1-DNA-protein crosslinks (TOP1-DPCs) for ubiquitination and proteasomal degradation during replication-coupled repair. The CUL4-RBX1 complex undergoes auto-NEDD8 modification and acts on TOP1-DPCs. Chemical genetic screens, co-immunoprecipitation, ubiquitination assays, TOP1-DPC repair assays in CRC cells and patient-derived organoids, xenograft models, pevonedistat (NEDD8 inhibitor) combination studies Nature communications High 37353483
2023 DCAF13 promotes NPM1 phase separation in nucleolar condensates to accelerate pre-rRNA enrichment and recruitment of the endonuclease UTP23, thereby facilitating 18S rRNA maturation and rapid T cell proliferation. DCAF13 depletion in T cells causes 18S rRNA maturation failure, abnormal ribosome assembly in nucleoli, and insufficient nascent protein production. Conditional knockout (T cell-specific), phase separation assays, rRNA processing analysis, ribosome assembly assays, nascent protein synthesis assay, immunofluorescence The Journal of cell biology Medium 37615668
2024 CRL4-DCAF13 E3 ubiquitin ligase targets MeCP2 (methyl-CpG-binding protein 2) for polyubiquitination and proteasomal degradation in growing oocytes. Dcaf13-null oocytes accumulate MeCP2 protein, leading to transcription dysregulation and DNA hypermethylation; partial rescue of follicle growth arrest was achieved by MeCP2 knockdown. Dcaf13-null oocytes (conditional KO), ubiquitination assay in cells and oocytes, MeCP2 knockdown rescue, RNA-seq, DNA methylation analysis Cellular and molecular life sciences : CMLS High 38578457
2024 DCAF13 promotes p53 K48-linked ubiquitination and proteasomal degradation in lung adenocarcinoma cells, acting as a negative regulator of the p53 signaling pathway and suppressing p53 downstream targets including p21, BAX, FAS, and PIDD1. Co-immunoprecipitation (DCAF13-p53 binding), ubiquitination assay (K48-linked), RNA-sequencing, chromatin immunoprecipitation-qPCR, immunofluorescence, knockdown/overexpression assays Journal of experimental & clinical cancer research : CR Medium 38163876
2024 DCAF13 promotes p53 ubiquitination and degradation in mantle cell lymphoma, and STAT5B transcriptionally activates DCAF13 expression. DCAF13-mediated p53 degradation leads to upregulation of xCT and suppression of ferroptosis in MCL cells. STAT5B silencing, DCAF13 overexpression/silencing, ubiquitination assay with MG132, luciferase reporter for STAT5B-DCAF13 transcription, tumor-bearing nude mouse model Biologics : targets & therapy Medium 38979130
2024 CRL4-DCAF13 targets Fraser extracellular matrix complex subunit 1 (FRAS1) for polyubiquitination and proteasomal degradation in ovarian cancer cells. FRAS1 accumulation (upon DCAF13 knockout) inhibits the focal adhesion kinase (FAK) signaling pathway, suppressing proliferation and migration. CRISPR/Cas9 knockout of DCAF13, ubiquitination assays, FAK signaling pathway analysis (western blot), co-immunoprecipitation, xenograft mouse model Cellular and molecular life sciences : CMLS Medium 39367995
2025 DCAF13 promotes RNA polymerase I (Pol I) transcription by facilitating K63-linked ubiquitination of RPA194 (the largest Pol I subunit), a non-degradative modification that stimulates Pol I transcriptional activity, thereby enhancing ribosome biogenesis and global protein synthesis in breast cancer cells. Multi-omics analysis, ubiquitination assays (K63-specific), Pol I transcription assays, co-immunoprecipitation, in vitro and in vivo proliferation assays Nature communications High 39788980
2025 DCAF13 directly interacts with TAF1A, a component of the RNA polymerase I preinitiation complex, and this interaction is necessary for preinitiation complex assembly and rDNA transcription. DCAF13 knockdown impairs rDNA transcription, ribosome biogenesis, and protein synthesis in non-small cell lung cancer cells. Co-immunoprecipitation (DCAF13-TAF1A), rDNA transcription assays, ribosome biogenesis analysis, protein synthesis assay, DCAF13 knockdown The Journal of biological chemistry Medium 40902972
2025 DCAF13 directly binds RRS1 (a ribosome biogenesis factor) and catalyzes K27-linked polyubiquitination of RRS1, a non-degradative modification that enhances RRS1 protein stability, thereby supporting ribosome assembly and protein synthesis in hematopoietic stem cells. Conditional deletion of Dcaf13 causes severe pancytopenia, HSC depletion, and activates the p53 pathway; Trp53 ablation only partially rescues this phenotype. Conditional knockout in hematopoietic cells, co-immunoprecipitation (DCAF13-RRS1), K27-specific ubiquitination assay, ribosome assembly analysis, protein synthesis assay, Trp53 double knockout epistasis Advanced science (Weinheim, Baden-Wurttemberg, Germany) High 41787937
2025 In the uterus, DCAF13 deficiency leads to elevated H3K9me3 levels (associated with increased SUV39H2 transcription), dysregulated estrogen and progesterone receptor expression, and insufficient endometrial cell proliferation, causing embryo implantation failure and infertility. Uterine conditional knockout of Dcaf13, RNA-seq, immunofluorescence for H3K9me3, hormone receptor western blot, in vivo implantation assay Cell death discovery Medium 40750792
2026 In cranial neural crest cells, DCAF13 deficiency causes PTEN accumulation (a substrate it normally degrades), which suppresses PI3K/AKT signaling, thereby impairing proliferation and differentiation of CNC-derived cells and causing craniofacial malformations. Neural crest-specific conditional knockout of Dcaf13, western blot for PTEN and AKT phosphorylation, immunofluorescence, skeletal staining Genesis (New York, N.Y. : 2000) Medium 41492083
2025 DCAF13 interacts with glucose-6-phosphate dehydrogenase (G6PD) to enhance glycolytic flux in hepatocellular carcinoma cells. The stability of DCAF13 mRNA is maintained by METTL3-mediated m6A modification and YTHDF1 binding. Co-immunoprecipitation (DCAF13-G6PD), molecular dynamics simulation, MeRIP-qPCR and RIP assays for m6A/YTHDF1, CRISPR/Cas9 knockout, glycolysis flux assays Journal of gastroenterology and hepatology Low 40708455

Source papers

Stage 0 corpus · 30 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2018 DCAF13 promotes pluripotency by negatively regulating SUV39H1 stability during early embryonic development. The EMBO journal 67 30111536
2018 Mammalian nucleolar protein DCAF13 is essential for ovarian follicle maintenance and oocyte growth by mediating rRNA processing. Cell death and differentiation 62 30283081
2017 MicroRNA-300 Regulates the Ubiquitination of PTEN through the CRL4BDCAF13 E3 Ligase in Osteosarcoma Cells. Molecular therapy. Nucleic acids 60 29499938
2019 The CRL4-DCAF13 ubiquitin E3 ligase supports oocyte meiotic resumption by targeting PTEN degradation. Cellular and molecular life sciences : CMLS 44 31492966
2022 DCAF13 promotes breast cancer cell proliferation by ubiquitin inhibiting PERP expression. Cancer science 36 35178836
2021 Doxorubicin promotes breast cancer cell migration and invasion via DCAF13. FEBS open bio 35 34775691
2023 Targeting neddylation sensitizes colorectal cancer to topoisomerase I inhibitors by inactivating the DCAF13-CRL4 ubiquitin ligase complex. Nature communications 29 37353483
2020 DCAF13 promotes triple-negative breast cancer metastasis by mediating DTX3 mRNA degradation. Cell cycle (Georgetown, Tex.) 28 33300431
2024 DCAF13 inhibits the p53 signaling pathway by promoting p53 ubiquitination modification in lung adenocarcinoma. Journal of experimental & clinical cancer research : CR 27 38163876
2023 T cell proliferation requires ribosomal maturation in nucleolar condensates dependent on DCAF13. The Journal of cell biology 16 37615668
2019 Maternal DCAF13 Regulates Chromatin Tightness to Contribute to Embryonic Development. Scientific reports 16 31000741
2023 A multidimensional pan-cancer analysis of DCAF13 and its protumorigenic effect in lung adenocarcinoma. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 13 36884358
2022 DCAF13 is essential for the pathogenesis of preeclampsia through its involvement in endometrial decidualization. Molecular and cellular endocrinology 11 35932979
2010 Identification of non-synonymous polymorphisms in the WDSOF1 gene as novel susceptibility markers for low bone mineral density in Japanese postmenopausal women. Bone 10 20601284
2024 CRL4DCAF13 E3 ubiquitin ligase targets MeCP2 for degradation to prevent DNA hypermethylation and ensure normal transcription in growing oocytes. Cellular and molecular life sciences : CMLS 9 38578457
2024 STAT5B Suppresses Ferroptosis by Promoting DCAF13 Transcription to Regulate p53/xCT Pathway to Promote Mantle Cell Lymphoma Progression. Biologics : targets & therapy 6 38979130
2024 DCAF13 promotes ovarian cancer progression by activating FRAS1-mediated FAK signaling pathway. Cellular and molecular life sciences : CMLS 5 39367995
2023 A biallelic variant of DCAF13 implicated in a neuromuscular disorder in humans. European journal of human genetics : EJHG 5 36797467
2023 DCAF13 and RNF114 participate in the regulation of early porcine embryo development. Reproduction (Cambridge, England) 5 37855431
2025 DCAF13-mediated K63-linked ubiquitination of RNA polymerase I promotes uncontrolled proliferation in Breast Cancer. Nature communications 4 39788980
2025 DCAF13 Regulates Cell Proliferation and Immune Escape of Hepatocellular Carcinoma Through Activating the NF-κB Pathway. Cell biochemistry and biophysics 3 40603761
2025 DCAF13 influences breast cancer chemotherapy resistance through metabolic reprogramming by regulating c-Myc expression. Medical oncology (Northwood, London, England) 2 40268788
2025 m6A Modification-Mediated Regulation of DCAF13 Promotes Glycolytic Metabolism and Drives Hepatocellular Carcinoma Progression via Interaction With G6PD. Journal of gastroenterology and hepatology 2 40708455
2022 DCAF-13 is required for C. elegans growth, development, and fertility. microPublication biology 2 36217444
2018 Whole exome sequencing reveals novel NOV and DCAF13 variants in a Chinese pedigree with familial cortical myoclonic tremor with epilepsy. Neuroscience letters 2 30003937
2025 DCAF13 is essential for mouse uterine function and fertility. Cell death discovery 1 40750792
2025 Nucleolar protein DCAF13 promotes non-small cell lung cancer cell proliferation via facilitating rDNA transcription and ribosome biogenesis. The Journal of biological chemistry 1 40902972
2026 The E3 Ubiquitin Ligase DCAF13 Is Essential for Craniofacial Development. Genesis (New York, N.Y. : 2000) 0 41492083
2026 DCAF13 Safeguards Hematopoietic Stem Cells via RRS1-Regulated Ribosome Biogenesis. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 0 41787937
2026 Pro-tumourigenic effects of DCAF13 on the progression of colorectal cancer. Oncology letters 0 41797888

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