Affinage

SETD1B

Histone-lysine N-methyltransferase SETD1B · UniProt Q9UPS6

Length
1966 aa
Mass
212.8 kDa
Annotated
2026-06-10
35 papers in source corpus 18 papers cited in narrative 19 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

SETD1B is the catalytic subunit of an ~450 kDa histone H3K4 methyltransferase complex that deposits H3K4me3 at active gene promoters to sustain target-gene expression (PMID:17355966). It assembles with the non-catalytic subunits CFP1, Rbbp5, Ash2, Wdr5, and Wdr82 through a 123-amino-acid region upstream of its catalytic SET domain, and complex incorporation reciprocally stabilizes the catalytic protein (PMID:17355966). SETD1B occupies a largely distinct set of euchromatic loci from its paralog SETD1A and performs non-redundant, developmentally and cell-type-specific functions: it is required after gastrulation in mouse development (PMID:24550110), cell-autonomously controls hematopoietic lineage genes such as Cebpa, Gata1, and Klf1 (PMID:29916805), and governs neuron-enriched genes marked by broad H3K4me3 peaks to support learning and memory (PMID:34806773). A recurring theme is that SETD1B catalytic activity maintains H3K4me3 breadth at specific promoters, with its SET domain required for MYC pathway gene expression in MLL-rearranged AML (PMID:40341256) and for expression of proapoptotic BCL2 family genes including BIM and BIK, such that SETD1B loss confers Venetoclax resistance in B-cell lymphoma that is reversible by KDM5 demethylase inhibition (PMID:39235528). Sequence-specific recruitment is achieved through interacting partners: the HIF transcription factor complex recruits SETD1B to hypoxia-responsive loci and SETD1B further engages RNA polymerase II to sustain HIF-driven transcription (PMID:34155378, PMID:41941749, PMID:41087863), while YTHDF2 directs SETD1B-dependent H3K4me3 at neuronal developmental genes in the cerebellum (PMID:41933071). SETD1B protein stability is controlled by USP15-mediated deubiquitination (PMID:40609959). Across oogenesis, SETD1B-linked, expression-coupled H3K4me3 is functionally distinct from and antagonistic to CpG-directed MLL2/KMT2B methylation (PMID:35137160).

Mechanistic history

Synthesis pass · year-by-year structured walk · 15 steps
  1. 2007 High

    Establishing that SETD1B is the catalytic core of a defined multi-subunit H3K4 methyltransferase resolved what biochemical activity and partners define the protein and showed it targets loci distinct from its paralog.

    Evidence Co-IP/mass spectrometry, in vitro HMT assay, deletion mutagenesis, and confocal imaging of nuclear speckles

    PMID:17355966

    Open questions at the time
    • Subunit stoichiometry and structural architecture of the complex not resolved
    • The basis for SETD1B vs SETD1A locus selectivity not identified
    • Direct genomic targets in vivo not mapped
  2. 2007 Medium

    Demonstrating that catalytic subunit levels depend on complex association revealed a feedback mechanism coupling SETD1B abundance to assembly with its non-catalytic partners.

    Evidence Inducible overexpression of SETD1A/B C-termini with Western blot readout of endogenous protein levels

    PMID:17355966

    Open questions at the time
    • Degradation pathway mediating destabilization not identified
    • Whether free catalytic subunit is targeted for proteolysis directly unaddressed
  3. 2012 Medium

    Identifying a direct Rbm15/Rbm15-Mkl1 interaction with SETD1B linked altered complex function to leukemogenesis, providing a first disease-associated binding partner.

    Evidence Co-IP with SPOC/LSD domain mapping and cytokine-independent proliferation assay

    PMID:22927943

    Open questions at the time
    • Effect of the fusion on SETD1B catalytic activity or genomic targeting not shown
    • In vivo relevance of the interaction not tested
  4. 2014 High

    Genetic comparison of Setd1a and Setd1b in mice and ESCs established that the two paralogs are non-redundant and act at distinct developmental stages.

    Evidence Conditional knockout embryo phenotyping plus negative Setd1b-overexpression rescue in ESCs

    PMID:24550110

    Open questions at the time
    • Molecular basis of non-redundancy not defined
    • Specific genes driving the post-gastrulation requirement not identified
  5. 2016 Medium

    Maternal Setd1b requirement for organizer gene activation placed SETD1B-dependent H3K4me3 downstream of Wnt/β-catenin in axis formation.

    Evidence Morpholino depletion in Xenopus embryos with in situ analysis of organizer genes

    PMID:27519569

    Open questions at the time
    • Direct genomic targets in organizer not mapped
    • Mechanism connecting Wnt signaling to SETD1B recruitment unknown
  6. 2018 High

    Conditional deletion in adult mice defined a cell-autonomous, non-redundant SETD1B role in hematopoiesis and identified downstream lineage-specification targets.

    Evidence Hematopoietic-specific conditional KO, bone marrow transplantation, and RNA expression profiling

    PMID:29916805

    Open questions at the time
    • Whether Cebpa/Gata1/Klf1 are direct H3K4me3 targets not shown by ChIP
    • Mechanism of lineage-specific recruitment unaddressed
  7. 2021 High

    Identifying HIF-complex recruitment of SETD1B to hypoxia-responsive loci provided a sequence-specific targeting mechanism linking the methyltransferase to inducible transcription.

    Evidence Genome-wide CRISPR screen, SET1B and H3K4me3 ChIP-seq, promoter acetylation analysis, and xenografts

    PMID:34155378

    Open questions at the time
    • Direct physical interface between SET1B and the HIF complex not mapped
    • How H3K4me3 feeds back to promoter acetylation not resolved
  8. 2021 High

    Neuron-specific deletion established that SETD1B preferentially controls broad-H3K4me3 neuronal genes underlying learning, distinguishing its role from Kmt2a/Kmt2b.

    Evidence Excitatory-neuron conditional KO with H3K4me3 ChIP-seq, RNA-seq, behavioral testing, and paralog comparison

    PMID:34806773

    Open questions at the time
    • What confers preference for broad-peak loci not defined
    • Recruitment machinery in neurons not identified
  9. 2022 High

    Oocyte deletion revealed two complementary H3K4me3 targeting logics—expression-coupled SETD1B versus CpG-directed MLL2—and showed SETD1B suppresses ectopic MLL2 methylation.

    Evidence Conditional KO oocytes with ultra-low-input H3K4me3 ChIP-seq, DNA methylation analysis, and RNA-seq

    PMID:35137160

    Open questions at the time
    • Mechanism by which SETD1B restrains MLL2 at CpG islands unknown
    • Direct competition vs indirect effect not distinguished
  10. 2024 Medium

    Linking SETD1B catalytic function to proapoptotic BCL2-family gene expression explained how its loss drives BCL2/MCL-1 inhibitor resistance and revealed a KDM5-inhibitor rescue strategy.

    Evidence Loss-of-function genetics, drug resistance assays, expression analysis, in vivo lymphoma model, and KDM5 inhibitor combination

    PMID:39235528

    Open questions at the time
    • Whether BIM/BIK are direct SETD1B targets shown only at the expression level
    • Mechanism of cooperation with KMT2D loss not detailed
  11. 2025 Medium

    CRISPR-tiling of the SET domain in MLL-rearranged AML established that catalytic activity per se maintains H3K4me3 breadth and MYC pathway gene expression required for leukemic growth.

    Evidence CRISPR-tiling screen, H3K4me3 ChIP-seq, and MYC overexpression / KDM5C disruption epistasis rescue

    PMID:40341256

    Open questions at the time
    • How breadth specifically controls MYC expression mechanistically unresolved
    • Whether SET-domain dependence generalizes beyond MLL-rearranged AML untested
  12. 2025 Medium

    Identifying USP15 as a deubiquitinase stabilizing SETD1B defined a post-translational control point governing its abundance and downstream H3K4me3 deposition.

    Evidence Co-IP, ubiquitination assay, siRNA knockdown, and ChIP at Nckap1l/Wasf2 promoters in ischemic stroke cells

    PMID:40609959

    Open questions at the time
    • E3 ligase that ubiquitinates SETD1B not identified
    • Ubiquitination site(s) not mapped
  13. 2025 Medium

    ChIP-based studies in disease models extended SETD1B's promoter-specific H3K4me3 control to Tfrc-driven ferroptosis and CXCR4-mediated suppression of pyroptosis, illustrating context-specific target genes.

    Evidence ChIP for H3K4me3 at Tfrc/CXCR4 promoters, SETD1B knockdown/overexpression, and ferroptosis/pyroptosis and behavioral assays

    PMID:38447691 PMID:40228655

    Open questions at the time
    • Recruitment mechanism to these loci not defined
    • Direct vs indirect promoter regulation not fully distinguished
  14. 2025 Medium

    A genome-wide SET1B DNA-binding map by DamID confirmed concordance of SET1B occupancy with HIF-1α sites, independently validating HIF-directed targeting.

    Evidence DamID-seq using SET1B-Dam fusion compared to HIF-1α ChIP-seq

    PMID:41087863

    Open questions at the time
    • Non-HIF SET1B binding sites not characterized
    • DamID resolution limits precise promoter assignment
  15. 2026 Medium

    Demonstrating SET1B–RNA polymerase II interaction and YTHDF2-directed recruitment refined the recruitment logic, showing SETD1B uses partner interactions and non-catalytic domains to sustain transcription in specific contexts.

    Evidence Co-IP (SET1B–RNAPII; YTHDF2–SETD1B), depletion/knockdown, HIF-2 inhibitor synergy, ATAC-seq, and epistasis rescue

    PMID:41933071 PMID:41941749

    Open questions at the time
    • Direct interaction interfaces not mapped
    • Relative contribution of catalytic vs non-catalytic functions not quantified

Open questions

Synthesis pass · forward-looking unresolved questions
  • How SETD1B achieves locus selectivity and broad-versus-narrow H3K4me3 deposition across cell types, and the structural basis of its partner interactions, remains unresolved.
  • No structural model of the SETD1B complex or its partner interfaces
  • The determinant of broad-peak target selection unidentified
  • Full E3/DUB regulatory circuit controlling SETD1B abundance incomplete

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0016740 transferase activity 3 GO:0042393 histone binding 1 GO:0140096 catalytic activity, acting on a protein 1
Localization
GO:0005694 chromosome 3 GO:0005634 nucleus 1 GO:0005654 nucleoplasm 1
Pathway
R-HSA-1266738 Developmental Biology 3 R-HSA-4839726 Chromatin organization 3 R-HSA-74160 Gene expression (Transcription) 2 R-HSA-8953897 Cellular responses to stimuli 1
Partners
ASH2LCFP1RBBP5RBM15USP15WDR5WDR82YTHDF2
Complex memberships
SETD1B/Set1B H3K4 methyltransferase complex (with CFP1, Rbbp5, Ash2, Wdr5, Wdr82)

Evidence

Reading pass · 19 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2007 SETD1B (Set1B/KIAA1076) forms an ~450 kDa histone methyltransferase complex containing five non-catalytic subunits: CFP1, Rbbp5, Ash2, Wdr5, and Wdr82. In vitro assays demonstrate the complex produces H3K4me3. A 123-amino acid fragment upstream of the SET domain is required for interaction with CFP1, Ash2, Rbbp5, and Wdr5. Confocal microscopy reveals SETD1B localizes to a largely non-overlapping set of euchromatic nuclear speckles compared to SETD1A, suggesting non-redundant target gene binding. Immunoprecipitation, mass spectrometry, in vitro histone methyltransferase assay, deletion mutagenesis, confocal microscopy The Journal of biological chemistry High 17355966
2007 SETD1B stability depends on its association with the methyltransferase complex: inducible expression of the carboxyl terminus of SETD1A or SETD1B decreases steady-state levels of both endogenous SETD1A and SETD1B protein without altering levels of the non-catalytic components, indicating feedback regulation through complex-dependent stability. Inducible overexpression, Western blot for steady-state protein levels The Journal of biological chemistry Medium 17355966
2012 Rbm15 and the leukemogenic Rbm15-Mkl1 fusion protein directly interact with SETD1B. This interaction requires the Rbm15 SPOC domain and the SETD1B LSD motif. Overexpression of Rbm15-Mkl1 leads to cytokine-independent cell growth that requires an intact SPOC domain mediating interaction with SETD1B, implicating altered SETD1B complex function in AMKL leukemogenesis. Co-immunoprecipitation, deletion/domain mutagenesis, cytokine-independent proliferation assay PloS one Medium 22927943
2014 In mice, Setd1b is dispensable until after gastrulation (embryos survive to E11.5 but are grossly retarded), whereas Setd1a is required at the epiblast stage. Overexpression of Setd1b cannot rescue the proliferation defects caused by loss of Setd1a in embryonic stem cells, demonstrating non-redundant and developmentally distinct roles for the two Set1 orthologs. Conditional knockout mouse genetics, embryo phenotyping, Setd1b overexpression rescue experiment in ESCs Development (Cambridge, England) High 24550110
2017 SETD1B activates iNOS (nos2) expression in tumor-induced myeloid-derived suppressor cells (MDSCs). ChIP revealed enrichment of H3K4me3 (the catalytic product of SETD1B) at the nos2 promoter in MDSCs; inhibition or silencing of SETD1B diminished iNOS expression, demonstrating that SETD1B-mediated H3K4me3 deposition at the nos2 promoter drives iNOS transcription in an IRF8-independent manner. Chromatin immunoprecipitation (ChIP), SETD1B silencing/inhibition, qRT-PCR/Western blot for iNOS Cancer research Medium 28381543
2018 Conditional deletion of Setd1b in adult mice using ubiquitous and hematopoietic-specific strategies results in peripheral thrombo- and lymphocytopenia, multilineage dysplasia, myeloid-biased extramedullary hematopoiesis, and lethality. Transplantation experiments and expression profiling show Setd1b is autonomously required in hematopoietic lineages and regulates key lineage specification genes including Cebpa, Gata1, and Klf1. Conditional knockout mouse genetics, bone marrow transplantation, RNA expression profiling, hematopoietic phenotyping eLife High 29916805
2021 SET1B (SETD1B) is recruited to HIF target gene loci by the HIF transcription factor complex in hypoxia. SET1B accumulates on chromatin under hypoxic conditions, and its loss selectively reduces H3K4me3 at HIF target loci, correlating with decreased promoter acetylation and gene expression. Genome-wide mutagenesis screen identified SET1B as required for HIF transcriptional activity. Genome-wide CRISPR mutagenesis screen, ChIP-seq for SET1B and H3K4me3, promoter acetylation analysis, xenograft tumor assays Nature genetics High 34155378
2021 Postnatal SETD1B in excitatory neurons controls expression of a set of genes with broad H3K4me3 peaks at their promoters, enriched for neuron-specific genes linked to learning and memory. Conditional deletion of Setd1b in excitatory forebrain neurons leads to severe learning impairment. Comparative ChIP-seq and RNA-seq with Kmt2a and Kmt2b conditional knockouts show SETD1B plays a more pronounced role in regulating neuron-enriched, broad-H3K4me3-marked genes. Neuron-specific conditional knockout, ChIP-seq (H3K4me3), RNA-seq, behavioral learning tests The EMBO journal High 34806773
2022 Loss of SETD1B in oocytes (conditional KO) causes redistribution of H3K4me3: losses at active gene promoters associated with downregulated gene expression, and gains at DNA-hypomethylated, transcriptionally inactive, CpG-rich regions (hallmarks of MLL2/KMT2B targets). This reveals two complementary mechanisms of H3K4me3 targeting in oogenesis—SETD1B linked to gene expression and MLL2 to CpG content—and shows SETD1B normally suppresses MLL2-mediated methylation at these sites. Conditional knockout oocytes, ultra-low input ChIP-seq for H3K4me3, DNA methylation analysis, RNA-seq Nucleic acids research High 35137160
2020 SETD1B is required for mycolactone-induced cell death. CRISPR/Cas9 inactivation of SETD1B renders cells resistant to lethal doses of mycolactone. Mechanistically, SETD1B is required for mycolactone-selective upregulation of CHAC1 (a GSH-degrading enzyme), and SETD1B loss prevents mycolactone-induced glutathione depletion and apoptotic gene induction. Haploid genetic screen, CRISPR/Cas9 knockout, transcriptome comparison (RNA-seq), glutathione level measurement PLoS neglected tropical diseases Medium 33006969
2024 SETD1B mutations/deletions in B cell lymphoma confer resistance to the BCL2 inhibitor Venetoclax and an MCL-1 inhibitor. Mechanistically, SETD1B is required for expression of several proapoptotic BCL2 family proteins (including BIM and BIK). KDM5 histone H3K4 demethylase inhibitors restore BIM and BIK expression and synergize with Venetoclax in SETD1B-deficient lymphomas. SETD1B cooperates with KMT2D loss in lymphoma development in vivo. Loss-of-function genetics (mutations/deletions), drug resistance assays, gene expression analysis, in vivo lymphoma model, KDM5 inhibitor combination treatment The Journal of experimental medicine Medium 39235528
2025 SETD1B SET domain disruption (via CRISPR tiling) in MLL-rearranged AML cells causes depletion of AML cells and downregulation of MYC pathway genes. SETD1B SET domain loss results in decreased H3K4me3 breadth at gene loci; exogenous MYC expression or disruption of H3K4 demethylase KDM5C rescues growth defects, establishing SETD1B's catalytic domain as required for broad H3K4me3 and MYC expression. CRISPR-tiling screen, H3K4me3 ChIP-seq, MYC overexpression rescue, KDM5C genetic disruption rescue Leukemia Medium 40341256
2026 SET1B interacts with RNA polymerase II to coordinate sustained HIF-mediated transcriptional activity through multiple functional domains beyond its histone methyltransferase activity. In clear cell renal cell carcinoma (ccRCC), SET1B is required for sustained HIF activity, and SET1B depletion enhances the efficacy of HIF-2 inhibitors. Co-immunoprecipitation (SET1B–RNAPII interaction), SET1B depletion, HIF-2 inhibitor combination experiments, patient sample correlation Cancer research Medium 41941749
2025 SETD1B promotes ferroptosis in ischemic stroke brain cells by increasing H3K4me3 enrichment at the Tfrc (transferrin receptor 1) promoter, upregulating TfR1 expression and driving iron accumulation and lipid peroxidation. SETD1B knockdown reduces H3K4me3 at the Tfrc promoter and reverses ferroptosis markers in OGD/R-treated HT22 cells and ischemic mouse brain. ChIP for H3K4me3 at Tfrc promoter, SETD1B siRNA knockdown, ferroptosis marker assays (iron, LPO, GPX4), OGD/R cell model and mouse stroke model Life sciences Medium 40228655
2025 USP15 deubiquitinates SETD1B, increasing its protein stability. In ischemic stroke cells, USP15 knockdown increases SETD1B ubiquitination and decreases SETD1B protein levels, thereby reducing H3K4me3 enrichment at the Nckap1l and Wasf2 promoters and attenuating disulfidptosis. Co-immunoprecipitation (USP15–SETD1B), ubiquitination assay, siRNA knockdown, ChIP for H3K4me3 at target promoters Biochimica et biophysica acta. Molecular cell research Medium 40609959
2024 SETD1B promotes CXCR4 expression by increasing H3K4me3 levels at the CXCR4 promoter, thereby suppressing NLRP1/Caspase1-mediated neuronal pyroptosis. SETD1B overexpression mitigates sevoflurane-induced cognitive impairment in neonatal mice by this mechanism. ChIP for SETD1B and H3K4me1/2/3 at CXCR4 promoter, SETD1B overexpression (adenovirus), behavioral tests, pyroptosis marker assays Neuroscience Medium 38447691
2016 In Xenopus, maternal Setd1b is required for organizer gene expression during dorsal axis development. Depletion of Setd1b impairs organizer gene activation, indicating that Setd1b-mediated H3K4 trimethylation is required downstream of the maternal Wnt/β-catenin pathway for proper organizer formation. Antisense morpholino depletion in Xenopus embryos, in situ hybridization, organizer gene expression analysis Mechanisms of development Medium 27519569
2026 YTHDF2 physically interacts with SETD1B (but not SETD1A or CXXC1) in the cerebellum. Loss of Ythdf2 suppresses Setd1b-mediated H3K4me3 deposition and reduces chromatin accessibility at neuronal developmental gene loci. Setd1b knockdown rescues the neural self-renewal and differentiation defects caused by Ythdf2 deletion, placing SETD1B downstream of YTHDF2 in cerebellar development. Co-immunoprecipitation (YTHDF2–SETD1B), H3K4me3 ChIP analysis, ATAC-seq (chromatin accessibility), Setd1b knockdown rescue of Ythdf2 KO phenotype Molecular psychiatry Medium 41933071
2025 DamID-seq using SET1B-Dam fusion protein provided the first genome-wide DNA binding map for SET1B, revealing strong concordance between SET1B chromatin occupancy and HIF-1α ChIP-seq data at HIF target loci. DamID-seq (Dam methyltransferase tagging of SET1B), bioinformatic comparison with HIF-1α ChIP-seq BMC genomics Medium 41087863

Source papers

Stage 0 corpus · 35 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2007 Identification and characterization of the human Set1B histone H3-Lys4 methyltransferase complex. The Journal of biological chemistry 208 17355966
2014 The H3K4 methyltransferase Setd1a is first required at the epiblast stage, whereas Setd1b becomes essential after gastrulation. Development (Cambridge, England) 153 24550110
2021 The HIF complex recruits the histone methyltransferase SET1B to activate specific hypoxia-inducible genes. Nature genetics 67 34155378
2017 SETD1B Activates iNOS Expression in Myeloid-Derived Suppressor Cells. Cancer research 60 28381543
2016 An atypical 12q24.31 microdeletion implicates six genes including a histone demethylase KDM2B and a histone methyltransferase SETD1B in syndromic intellectual disability. Human genetics 55 27106595
2019 A genome-wide DNA methylation signature for SETD1B-related syndrome. Clinical epigenetics 53 31685013
2012 Rbm15-Mkl1 interacts with the Setd1b histone H3-Lys4 methyltransferase via a SPOC domain that is required for cytokine-independent proliferation. PloS one 42 22927943
2014 Frameshift mutation of a histone methylation-related gene SETD1B and its regional heterogeneity in gastric and colorectal cancers with high microsatellite instability. Human pathology 40 24925220
2018 The H3K4 methyltransferase Setd1b is essential for hematopoietic stem and progenitor cell homeostasis in mice. eLife 37 29916805
2019 De novo variants in SETD1B cause intellectual disability, autism spectrum disorder, and epilepsy with myoclonic absences. Epilepsia open 34 31440728
2022 Loss of histone methyltransferase SETD1B in oogenesis results in the redistribution of genomic histone 3 lysine 4 trimethylation. Nucleic acids research 27 35137160
2021 Postnatal expression of the lysine methyltransferase SETD1B is essential for learning and the regulation of neuron-enriched genes. The EMBO journal 27 34806773
2022 Expression of the histone lysine methyltransferases SETD1B, SETDB1, SETD2, and CFP1 exhibits significant changes in the oocytes and granulosa cells of aged mouse ovaries. Histochemistry and cell biology 18 35445296
2019 A novel de novo frameshift variant in SETD1B causes epilepsy. Journal of human genetics 15 31110234
2009 Prevalence of the set-1B and astA genes encoding enterotoxins in uropathogenic Escherichia coli clinical isolates. Microbial pathogenesis 15 19755142
2020 Mycolactone induces cell death by SETD1B-dependent degradation of glutathione. PLoS neglected tropical diseases 14 33006969
2014 Complex karyotype in a polycythemia vera patient with a novel SETD1B/GTF2H3 fusion gene. American journal of hematology 10 24382738
2024 SETD1B mutations confer apoptosis resistance and BCL2 independence in B cell lymphoma. The Journal of experimental medicine 9 39235528
2022 The methyltransferase enzymes KMT2D, SETD1B, and ASH1L are key mediators of both metabolic and epigenetic changes during cellular senescence. Molecular biology of the cell 8 35196069
2024 Epigenetic Mechanism of SETD1B-mediated Histone Methylation in Cognitive Impairment Induced by Sevoflurane Anesthesia in Neonatal Mice. Neuroscience 7 38447691
2025 SETD1B promotes brain cell ferroptosis in ischemic stroke mice via increasing H3K4me3 enrichment on the Tfrc promoter. Life sciences 5 40228655
2016 The MLL/Setd1b methyltransferase is required for the Spemann's organizer gene activation in Xenopus. Mechanisms of development 4 27519569
2025 Regulation of H3K4me3 breadth and MYC expression by the SETD1B catalytic domain in MLL-rearranged leukemia. Leukemia 3 40341256
2025 USP15 promotes brain cell disulfidptosis in mouse subjected to ischemic stroke through a mechanism involving deubiquitination of SETD1B. Biochimica et biophysica acta. Molecular cell research 2 40609959
2025 Histone Methyltransferase SETD1B Maintains Cancer Stem Cell Niche by Regulating the Crosstalk between CD24 and Surface Adhesion Molecules in Hepatocellular Carcinoma. International journal of biological sciences 1 40860182
2024 Mental retardation, seizures and language delay caused by new SETD1B mutations: Three case reports. World journal of clinical cases 1 38313655
2024 Phenotypes of autism spectrum disorder and schizoaffective disorder associated with SETD1B gene but without intellectual disability and seizures. International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience 1 39169470
2026 Ketogenic Diet as an Epigenetic Therapy in SETD1B-Related Epilepsy. Annals of clinical and translational neurology 0 41714828
2026 Ythdf2/Setd1b regulatory axis is essential for cerebellar development through regulating epigenetic reprogramming. Molecular psychiatry 0 41933071
2026 SET1B Drives Sustained HIF activity and Disease Progression in Clear Cell Renal Cell Carcinoma. Cancer research 0 41941749
2026 CircSTK40 Modulates the SETD1B/H3K4me2/H3K4me3 Loop to Regulate Recurrent Pregnancy Loss. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 0 41964387
2025 [Clinical characteristics of epilepsy with intellectual disability associated with SETD1B gene in three pediatric cases and a literature review]. Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics 0 40462431
2025 [SETD1B gene related epilepsy and language delay: A case report and literature review]. Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics 0 40763969
2025 Mapping SET1B chromatin interactions with DamID using DamMapper, a comprehensive Snakemake workflow. BMC genomics 0 41087863
2024 SETD1B variants associated with absence seizures. European journal of paediatric neurology : EJPN : official journal of the European Paediatric Neurology Society 0 39765123

Missed literature

Know a paper Affinage missed for SETD1B? Flag it for the maintainers and the community.

No submissions yet.