Affinage

SIN3B

Paired amphipathic helix protein Sin3b · UniProt O75182

Length
1162 aa
Mass
133.1 kDa
Annotated
2026-06-10
31 papers in source corpus 21 papers cited in narrative 21 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

SIN3B is the scaffold subunit of a Sin3/HDAC histone deacetylase co-repressor complex that enforces chromatin-based transcriptional repression and controls cell-cycle exit, senescence, and the DNA damage response (PMID:37137925, PMID:19654306). Structurally, SIN3B encircles HDAC1/2 and contacts an allosteric basic patch to stimulate catalysis, inserting a loop into the catalytic tunnel that rearranges to accommodate and stabilize the acetyl-lysine substrate for deacetylation (PMID:37137925); it engages HDAC1/2 through a surface distinct from that used by other co-repressor complexes such as NuRD and CoREST [PMID:bio_10.1101_2025.02.24.639909]. SIN3B couples this enzymatic core to sequence-specific factors through its PAH domains, whose PAH2 module forms a wedged helical bundle that clamps an amphipathic Mad1 helix (PMID:11101889), and it is recruited by MNF-beta, p53, MYC, RFX5, and the DREAM complex to deacetylate and silence target promoters (PMID:10620510, PMID:22028823, PMID:24951594, PMID:30517867, PMID:24709079). Within transcribed genes, SIN3B operates in a complex with HDAC1, Mrg15, and Pf1 that restrains RNA polymerase II progression downstream of transcription start sites (PMID:21041482). SIN3B is required for replicative and oncogene-induced senescence, linking KRAS-driven senescence to inflammatory SASP signaling, and its expression is held in check by Bmi-1 repression that is relieved under oncogenic stress (PMID:19654306, PMID:24691445, PMID:25263442); it maintains quiescence by repressing DREAM/E2F targets in cooperation with APC/C-CDH1 (PMID:30517867). SIN3B protein levels are controlled by RNF220-mediated ubiquitination and proteasomal degradation (PMID:20170641). In the DNA damage response SIN3B is recruited to double-strand breaks, directs MDC1 accumulation, and biases repair pathway choice toward canonical NHEJ (PMID:37314748). SIN3B haploinsufficiency in humans causes enhancer/promoter hyperacetylation and a neurodevelopmental disorder, with zebrafish sin3b loss producing craniofacial and axonal patterning defects (PMID:33811806).

Mechanistic history

Synthesis pass · year-by-year structured walk · 17 steps
  1. 2000 High

    Establishing how SIN3B engages sequence-specific repressors defined the structural logic of co-repressor recruitment via its PAH domains.

    Evidence NMR solution structure of the SIN3B PAH2 domain bound to a Mad1 peptide

    PMID:11101889

    Open questions at the time
    • Does not address PAH1/PAH3/PAH4 partner specificity
    • Does not connect the interaction to HDAC catalytic activation
  2. 2000 Medium

    Identification of MNF-beta as a SIN3B partner showed that SIN3B-anchored repression mediates negative growth regulation by forkhead factors.

    Evidence Co-IP and repression/transformation assays with mSin3-binding-defective MNF-beta mutants

    PMID:10620510

    Open questions at the time
    • No structural definition of the MNF-beta/SIN3B interface
    • Did not establish direct target genes
  3. 2008 Medium

    Linking SIN3B to ETO/MTG16 leukemia fusion partners extended its repressor reach to hematopoietic oncoproteins and a nucleolar pool.

    Evidence Co-IP with domain mapping and nucleolar colocalization in leukemia cells

    PMID:18205948

    Open questions at the time
    • No functional transcriptional readout
    • Significance of nucleolar localization unresolved
  4. 2009 High

    Genetic loss- and gain-of-function established SIN3B as a required driver of replicative and oncogene-induced senescence, beyond a passive co-repressor role.

    Evidence Sin3B-/- fibroblasts, overexpression, senescence and heterochromatic foci assays

    PMID:19654306

    Open questions at the time
    • Target genes mediating the senescence program not fully defined
    • Relationship to the deacetylase activity not dissected
  5. 2010 High

    Defining the SIN3B-HDAC1-Mrg15-Pf1 complex placed SIN3B within gene bodies as a brake on RNA polymerase II elongation.

    Evidence Reciprocal Co-IP, ChIP localization, and knockdown with RNAP II progression assays

    PMID:21041482

    Open questions at the time
    • Mechanism by which deacetylation restrains elongation not resolved
    • Recruitment signal within transcribed regions unknown
  6. 2010 Medium

    Identifying RNF220 as a SIN3B E3 ligase revealed post-translational control of Sin3/HDAC complex abundance.

    Evidence Yeast two-hybrid, Co-IP, ubiquitination assay, proteasome inhibitor rescue

    PMID:20170641

    Open questions at the time
    • Ubiquitination sites on SIN3B not mapped
    • Physiological signals triggering degradation unknown
  7. 2011 Medium

    Demonstrating p53-directed recruitment of SIN3B/HDAC1 under genotoxic stress connected SIN3B to a stress-responsive repression arm of the p53 program.

    Evidence Co-IP with deletion mapping, ChIP, shRNA, p53+/+ vs p53-/- comparison after Adriamycin

    PMID:22028823

    Open questions at the time
    • Single lab; reciprocal validation limited
    • How SIN3B selects p53-repressed vs activated targets unclear
  8. 2013 Medium

    Discovery of SIN3B binding to Nav channel C-termini raised a cytoplasmic, non-transcriptional function in ion channel regulation.

    Evidence Yeast two-hybrid, pulldown, Co-IP, colocalization, electrophysiology

    PMID:24077057

    Open questions at the time
    • Whether effect reflects trafficking vs membrane stability not resolved
    • Isoform/tissue context of this function undefined
  9. 2014 Medium

    Multiple 2014 studies integrated SIN3B into senescence signaling: it is de-repressed from Bmi-1, drives KRAS-induced senescence and IL-1alpha/SASP, and deacetylates/degrades MYC.

    Evidence ChIP and epistasis of Bmi-1/Sin3B; PDAC genetic KO with IL-1alpha readout; Y2H/Co-IP/PLA with MYC and HDAC inhibitor/KD/OE

    PMID:24691445 PMID:24951594 PMID:25263442

    Open questions at the time
    • Direct vs indirect contribution to SASP gene expression not fully separated
    • MYC interaction lacks structural definition
  10. 2014 Medium

    RFX5-directed recruitment cooperating with G9a showed SIN3B integrates deacetylation with histone methylation to silence collagen during IFN-gamma signaling.

    Evidence ChIP, shRNA, Co-IP, histone modification assays at COL1A2

    PMID:24709079

    Open questions at the time
    • Order of HDAC2/G9a recruitment not fully resolved
    • Generalizability beyond COL1A2 untested
  11. 2016 Medium

    Isoform and paralog studies revealed that only the long, HDAC-recruiting SIN3B isoform represses BMP4 targets and that SIN3B versus SIN3A have opposing roles in breast cancer invasion.

    Evidence Isoform-specific siRNA with reporter/RNA-seq; three-shRNA KD with invasion, 3D, and in vivo metastasis assays

    PMID:27324164 PMID:27780928

    Open questions at the time
    • Splicing control of SIN3B isoforms incompletely defined
    • Mechanistic basis of SIN3A/SIN3B target divergence unknown
  12. 2018 High

    Placing SIN3B in the DREAM complex defined its role in quiescence maintenance through E2F target repression cooperating with APC/C-CDH1.

    Evidence Proteomics, Sin3B-/- RNA-seq, genetic epistasis with APC/C-CDH1 inactivation

    PMID:30517867

    Open questions at the time
    • Direct DREAM contact subunit not mapped
    • How SIN3B loss alone is buffered for cell-cycle re-entry only partially explained
  13. 2021 High

    Human haploinsufficiency and zebrafish models established SIN3B as essential for enhancer/promoter deacetylation in development and defined a neurodevelopmental disorder.

    Evidence H3K27ac ChIP-seq in patient PBMCs, zebrafish CRISPR KO and morpholino phenotypes

    PMID:33811806

    Open questions at the time
    • Specific dysregulated loci driving the phenotype not pinpointed
    • Genotype-phenotype spectrum not fully delineated
  14. 2023 High

    The cryo-EM holo-complex structure resolved how SIN3B mechanically activates HDAC1/2 and presents substrate, defining the enzymatic core at atomic resolution.

    Evidence Cryo-EM with and without substrate mimic plus in vitro deacetylase assays

    PMID:37137925

    Open questions at the time
    • Does not capture transcription-factor-bound states
    • Dynamics of substrate selection in vivo not addressed
  15. 2023 Medium

    Recruitment of SIN3B to double-strand breaks and control of MDC1 accumulation revealed a direct role in DNA repair pathway choice and chemosensitivity.

    Evidence SIN3B-/- cells, damage foci analysis, MDC1 localization, NHEJ reporters, drug sensitivity

    PMID:37314748

    Open questions at the time
    • How SIN3B is recruited to break sites unknown
    • Whether deacetylase activity is required at breaks not established
  16. 2024 Medium

    SIN3B loss was shown to remodel the PDAC immune microenvironment via a CXCL9/10-CXCR3 feedback loop, linking its chromatin function to anti-tumor immunity and checkpoint sensitivity.

    Evidence Murine PDAC genetic inactivation, cytokine measurement, H3K27Ac ChIP-seq, immune infiltration, anti-PD1 treatment

    PMID:39316363

    Open questions at the time
    • Direct SIN3B-repressed immune loci not fully defined
    • Single model system
  17. 2025 Medium

    Comparative structural and mutational analysis demonstrated that SIN3B uses a distinct HDAC1/2 surface from ELM2/SANT-based complexes, explaining co-repressor-specific recruitment.

    Evidence HDAC1 Y48E/E63R mutation, Co-IP/MS, structural comparison, rescue in HDAC1/2 double-KO cells (preprint)

    PMID:bio_10.1101_2025.02.24.639909

    Open questions at the time
    • Preprint, not peer reviewed
    • Functional consequence of selective disruption for SIN3-specific gene programs untested

Open questions

Synthesis pass · forward-looking unresolved questions
  • How SIN3B is targeted to specific genomic and damage sites in vivo, and how its enzymatic, structural, and signaling functions are integrated across senescence, repair, and development, remains unresolved.
  • Genome-wide recruitment determinants undefined
  • Causal targets linking SIN3B to each phenotype incompletely mapped

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140110 transcription regulator activity 4 GO:0060090 molecular adaptor activity 3 GO:0098772 molecular function regulator activity 2 GO:0140096 catalytic activity, acting on a protein 2
Localization
GO:0005634 nucleus 3 GO:0000228 nuclear chromosome 2 GO:0005730 nucleolus 1
Pathway
R-HSA-4839726 Chromatin organization 4 R-HSA-74160 Gene expression (Transcription) 3 R-HSA-8953897 Cellular responses to stimuli 3 R-HSA-1640170 Cell Cycle 2 R-HSA-73894 DNA Repair 1
Partners
HDAC1HDAC2MAD1MDC1MYCP53RFX5RNF220
Complex memberships
DREAM complexSIN3B-HDAC1-Mrg15-Pf1 complexSin3/HDAC co-repressor complex

Evidence

Reading pass · 21 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2023 Cryo-EM structure of the complete human SIN3B histone deacetylase holo-complex (with and without substrate mimic) reveals that SIN3B encircles HDAC1/2 and contacts its allosteric basic patch to stimulate catalysis; a SIN3B loop inserts into the catalytic tunnel, rearranges to accommodate the acetyl-lysine moiety, and stabilizes the substrate for deacetylation guided by a substrate receptor subunit. Cryo-EM structure determination, in vitro deacetylase assays, substrate mimic binding Nature communications High 37137925
2000 NMR solution structure of SIN3B PAH2 domain in complex with a Mad1 N-terminal peptide defines a 'wedged helical bundle' interaction fold: four PAH2 alpha-helices form a hydrophobic cleft that accommodates an amphipathic Mad1 alpha-helix, and Mad1 binding stabilizes secondary structure elements of PAH2. NMR solution structure determination Nature structural biology High 11101889
2010 SIN3B forms a mammalian complex with HDAC1, Mrg15, and PHD-finger protein Pf1; this complex localizes ~1 kb downstream of transcription start sites of transcribed genes, requires Pf1 and Mrg15 for chromatin association, and its inactivation promotes increased RNA polymerase II progression and transcription within transcribed regions. Co-immunoprecipitation, ChIP, siRNA knockdown, RNAP II progression assays Molecular and cellular biology High 21041482
2010 RNF220, a RING finger E3 ubiquitin ligase, directly binds SIN3B (identified by yeast two-hybrid and confirmed by co-immunoprecipitation) and promotes its ubiquitination and proteasomal degradation, thereby regulating Sin3/HDAC complex levels. Yeast two-hybrid, co-immunoprecipitation, ubiquitination assay, proteasome inhibitor rescue Biochemical and biophysical research communications Medium 20170641
2000 MNF-beta (myocyte nuclear factor beta), a winged-helix/forkhead protein, forms a co-repressor complex with mammalian SIN3B; MNF-beta mutants unable to bind mSin3 are defective in transcriptional repression and negative growth regulation. Co-immunoprecipitation, transcriptional repression assay, oncogenic transformation assay with binding-defective mutants The Biochemical journal Medium 10620510
2011 Human SIN3B directly interacts with p53 (amino acids 1-399 of SIN3B bind the N-terminal region, aa 1-108, of p53); genotoxic stress (Adriamycin) increases SIN3B levels and recruits the SIN3B/HDAC1 complex to promoters of p53 target genes (HSPA8, MAD1, CRYZ) in a p53-dependent manner, resulting in their repression and increased H3K9 tri-methylation. Co-immunoprecipitation with deletion mapping, ChIP, shRNA knockdown, p53+/+ vs p53-/- cell comparison PloS one Medium 22028823
2018 SIN3B associates with the DREAM complex (identified by unbiased proteomics); genetic inactivation of Sin3B de-represses DREAM target genes during quiescence but is insufficient alone to allow quiescent cells to re-enter the cell cycle; however, inactivation of APC/C-CDH1 was sufficient to drive Sin3B-/- cells back into the cell cycle, revealing functional cooperation between SIN3B-mediated E2F target repression and APC/C-CDH1 in negative regulation of cell cycle progression. Proteomics/mass spectrometry, genetic inactivation (Sin3B-/-), RNA-seq, genetic epistasis (APC/C-CDH1 inactivation in Sin3B-/- background) Cell reports High 30517867
2009 SIN3B is required for replicative and oncogene-induced senescence in fibroblasts; Sin3B-inactivated fibroblasts fail to undergo senescence and overexpression of Sin3B triggers senescence and formation of senescence-associated heterochromatic foci. Genetic inactivation (Sin3B-/- mouse-derived fibroblasts), overexpression, senescence assays, heterochromatic foci imaging Cancer research High 19654306
2014 SIN3B is required for KRAS-induced senescence in vivo in pancreatic cells; Sin3B inactivation impairs IL-1α production associated with oncogene-induced senescence, indicating SIN3B links senescence to inflammatory signaling (SASP) that promotes pancreatic cancer progression. Genetic inactivation in mouse PDAC model, IL-1α measurement, correlation with human tissue samples The Journal of clinical investigation High 24691445
2014 SIN3B directly interacts with MYC protein in a Max-independent manner; HDAC1 is recruited to Myc-Sin3B complexes; Sin3B overexpression induces Myc deacetylation and degradation, while Sin3B silencing leads to Myc upregulation. Yeast two-hybrid, co-immunoprecipitation, immunofluorescence, proximity ligation assay, HDAC inhibitor treatment, Sin3B knockdown/overexpression The Journal of biological chemistry Medium 24951594
2014 Bmi-1 directly represses the Sin3B locus to prevent senescence; oncogenic stress causes dissociation of Bmi-1 from the Sin3B locus, de-repressing Sin3B expression; Sin3B is required for the senescent phenotype and elevated reactive oxygen species upon Bmi-1 depletion. ChIP (Bmi-1 occupancy at Sin3B locus), Bmi-1 depletion, genetic epistasis (Sin3B requirement downstream of Bmi-1 loss) Oncogene Medium 25263442
2014 SIN3B is recruited by RFX5 to the COL1A2 transcription start site in response to IFN-γ; SIN3B cooperates with G9a histone methyltransferase to establish a repressive chromatin structure; recruitment involves HDAC2-mediated deacetylation of RFX5; SIN3B knockdown abrogates IFN-γ-induced collagen repression. ChIP, shRNA knockdown, co-immunoprecipitation, histone modification assays Biochemical and biophysical research communications Medium 24709079
2008 hSIN3B interacts with ETO and MTG16 (but not MTGR1) ETO homologues; the interaction requires an intact ETO amino-terminus and NHR2 domain; hSIN3B and ETO homologues co-localize in the nucleolus of leukemia cells. Co-immunoprecipitation (ectopic and endogenous), immunolocalization, protein domain deletion analysis BMC molecular biology Medium 18205948
2013 SIN3B directly binds voltage-gated sodium (Nav) channels; the N-terminal region of SIN3B (containing PAH1/PAH2 domains) mediates binding to a 132-residue portion of the Nav channel cytoplasmic C-terminus; expression of the short Sin3B variant reduces native sodium current and Nav channel gating charge without affecting voltage-dependence of activation, suggesting Sin3B influences Nav channel trafficking or membrane stability. Yeast two-hybrid, pulldown, co-immunoprecipitation, immunofluorescence colocalization, electrophysiology Scientific reports Medium 24077057
2016 BMP4 induces a shift in SIN3B splicing toward the long isoform (which recruits HDACs); RBM39 knockdown prevents this isoform shift and enhances BMP4-dependent transcription; knockdown of long-isoform SIN3B enhances BMP4-dependent transcription whereas knockdown of the short isoform (lacking HDAC recruitment capacity) does not. siRNA knockdown, luciferase reporter assay, RNA-seq isoform analysis, isoform-specific knockdown Scientific reports Medium 27324164
2021 SIN3B haploinsufficiency in humans causes hyperacetylation of a subset of enhancers and promoters (shown by H3K27ac ChIP-seq in patient PBMCs); zebrafish sin3b disruption causes craniofacial patterning defects, commissural axon defects, and reduced body length, establishing an essential role for Sin3B in chromatin-based transcriptional repression in neurodevelopment. H3K27ac ChIP-seq in patient cells, CRISPR-Cas9 zebrafish knockout, morpholino knockdown American journal of human genetics High 33811806
2023 SIN3B is rapidly recruited to DNA double-strand break sites and directs the accumulation of MDC1; SIN3B inactivation delays DSB resolution, sensitizes cancer cells to cisplatin and doxorubicin, and shifts DNA repair pathway choice from canonical NHEJ toward alternative NHEJ. Genetic inactivation (SIN3B-/-), DNA damage foci analysis, co-immunoprecipitation/localization of MDC1, NHEJ pathway reporter assays, drug sensitivity assays Molecular cancer research : MCR Medium 37314748
2016 SIN3B knockdown in breast cancer cells significantly decreases Matrigel invasion and invasive colony formation in 3D matrix, and reduces experimental lung metastases in vivo, while SIN3A knockdown has the opposite effect; RNA-seq identified unique target gene sets for each paralog. Stable shRNA knockdown (three non-overlapping shRNA), transwell invasion assay, 3D colony assay, in vivo experimental metastasis, RNA-seq Oncotarget Medium 27780928
2024 Sin3B loss in PDAC tumor cells amplifies CXCL9/10 secretion in response to IFN-γ, creates a CXCL9/10-CXCR3 positive feedback loop increasing CD8+ T cell infiltration and cytotoxicity, and correlates with enhanced H3K27Ac distribution on immune response genes; Sin3B loss also enhances sensitivity to anti-PD1 treatment in murine PDAC models. Murine PDAC genetic inactivation, cytokine measurements, H3K27Ac ChIP-seq, immune cell infiltration analysis, anti-PD1 treatment in vivo Advanced science Medium 39316363
2019 SIN3B promotes integrin αV gene transcription in hepatocellular carcinoma in the presence of sulfatide: sulfatide binds SIN3B (confirmed by mass spectrometry and fat blot), induces a conformational change in the PAH2 domain (from α-helices to β-sheet), causing SIN3B to lose binding affinity for MAD1 and HDAC2, reducing HDAC2 recruitment to the integrin αV promoter and preventing histone H3 deacetylation. Mass spectrometry, fat blot, molecular modeling, co-immunoprecipitation, ChIP, promoter reporter assay, migration assay Journal of molecular cell biology Low 30215728
2025 Comparison of SIN3B/HDAC2 and MTA1/HDAC1 structures confirms differential modes of HDAC recruitment: HDAC1 Y48 interacts with ELM2/SANT domain-containing proteins (NuRD, CoREST, MIDAC) but not SIN3; a Y48E mutation in HDAC1 disrupts all complexes except SIN3, demonstrating that SIN3B recruits HDAC1/2 through a distinct surface from other co-repressor complexes. HDAC1 surface mutation (Y48E, E63R), co-immunoprecipitation/mass spectrometry, structural comparison, rescue experiments in HDAC1/2 double-KO cells bioRxivpreprint Medium bio_10.1101_2025.02.24.639909

Source papers

Stage 0 corpus · 31 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2014 Senescence-associated SIN3B promotes inflammation and pancreatic cancer progression. The Journal of clinical investigation 67 24691445
2010 A novel mammalian complex containing Sin3B mitigates histone acetylation and RNA polymerase II progression within transcribed loci. Molecular and cellular biology 67 21041482
2000 The winged-helix/forkhead protein myocyte nuclear factor beta (MNF-beta) forms a co-repressor complex with mammalian sin3B. The Biochemical journal 62 10620510
2000 The Mad1-Sin3B interaction involves a novel helical fold. Nature structural biology 52 11101889
2009 Sin3B expression is required for cellular senescence and is up-regulated upon oncogenic stress. Cancer research 49 19654306
2010 RNF220, an E3 ubiquitin ligase that targets Sin3B for ubiquitination. Biochemical and biophysical research communications 39 20170641
2016 SIN3A and SIN3B differentially regulate breast cancer metastasis. Oncotarget 35 27780928
2011 Tumor suppressor protein p53 recruits human Sin3B/HDAC1 complex for down-regulation of its target promoters in response to genotoxic stress. PloS one 32 22028823
2018 The HDAC-Associated Sin3B Protein Represses DREAM Complex Targets and Cooperates with APC/C to Promote Quiescence. Cell reports 30 30517867
2014 Sin3b interacts with Myc and decreases Myc levels. The Journal of biological chemistry 26 24951594
2021 Haploinsufficiency of the Sin3/HDAC corepressor complex member SIN3B causes a syndromic intellectual disability/autism spectrum disorder. American journal of human genetics 25 33811806
2014 Sin3B mediates collagen type I gene repression by interferon gamma in vascular smooth muscle cells. Biochemical and biophysical research communications 24 24709079
2023 Mechanism of assembly, activation and lysine selection by the SIN3B histone deacetylase complex. Nature communications 23 37137925
2008 Sin3B: an essential regulator of chromatin modifications at E2F target promoters during cell cycle withdrawal. Cell cycle (Georgetown, Tex.) 23 18469515
2014 Transcriptional repression of Sin3B by Bmi-1 prevents cellular senescence and is relieved by oncogene activation. Oncogene 18 25263442
2019 SIN3B promotes integrin αV subunit gene transcription and cell migration of hepatocellular carcinoma. Journal of molecular cell biology 17 30215728
2016 The chromatin-associated Sin3B protein is required for hematopoietic stem cell functions in mice. Blood 15 27806947
2024 SIN3B Loss Heats up Cold Tumor Microenvironment to Boost Immunotherapy in Pancreatic Cancer. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 11 39316363
2017 Chromatin-Associated Protein SIN3B Prevents Prostate Cancer Progression by Inducing Senescence. Cancer research 11 28807943
2016 Negative autoregulation of BMP dependent transcription by SIN3B splicing reveals a role for RBM39. Scientific reports 11 27324164
2017 Zebrafish sin3b mutants are viable but have size, skeletal, and locomotor defects. Developmental dynamics : an official publication of the American Association of Anatomists 10 28850761
2017 The potential of targeting Sin3B and its associated complexes for cancer therapy. Expert opinion on therapeutic targets 9 28956957
2013 Interaction between the transcriptional corepressor Sin3B and voltage-gated sodium channels modulates functional channel expression. Scientific reports 9 24077057
2008 The human SIN3B corepressor forms a nucleolar complex with leukemia-associated ETO homologues. BMC molecular biology 6 18205948
2014 SIN3B, the SASP, and pancreatic cancer. Molecular & cellular oncology 5 27308374
2015 pH might play a role in regulating the function of paired amphipathic helices domains of human Sin3B by altering structure and thermodynamic stability. Biochemistry. Biokhimiia 3 25869359
2015 Stress-mediated Sin3B activation leads to negative regulation of subset of p53 target genes. Bioscience reports 3 26181367
2024 Chromatin accessibility and cell cycle progression are controlled by the HDAC-associated Sin3B protein in murine hematopoietic stem cells. Epigenetics & chromatin 2 38254205
2023 The Sin3B chromatin modifier restricts cell cycle progression to dictate hematopoietic stem cell differentiation. bioRxiv : the preprint server for biology 1 36747851
2023 Chromatin-Associated SIN3B Protects Cancer Cells from Genotoxic Stress-Induced Apoptosis and Dictates DNA Damage Repair Pathway Choice. Molecular cancer research : MCR 1 37314748
2025 Knockout of SIN3B modulates transcriptional programs and cell survival in cutaneous melanoma. Pharmacological research 0 40393534

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