| 2004 |
Snail mediates E-cadherin repression by recruiting a complex containing HDAC1, HDAC2, and mSin3A via its SNAG domain; this interaction is SNAG domain-dependent and results in histone H3/H4 deacetylation at the E-cadherin promoter. |
Co-immunoprecipitation, ChIP, TSA inhibitor experiments, overexpression studies |
Molecular and cellular biology |
High |
14673164
|
| 1999 |
The N-terminal repression domain of REST recruits Sin3A and histone deacetylase to neuronal gene promoters (GluR2 and type II sodium channel) in nonneuronal cells, establishing a mechanism for RE1/NRSE-mediated silencing. |
Multiple co-immunoprecipitation, reporter assay, ChIP-like promoter analysis |
Nature neuroscience |
High |
10491605
|
| 2008 |
PRMT1 methylates RUNX1 at arginine residues R206 and R210, which lie within the SIN3A-interaction region of RUNX1; this methylation abrogates RUNX1-SIN3A association, converting RUNX1 from a repressor to an activator. shRNA against PRMT1 enhances RUNX1-SIN3A association. |
Mass spectrometry, methyl-arginine-specific antibody, Co-IP, shRNA knockdown, ChIP |
Genes & development |
High |
18316480
|
| 2001 |
PSF (polypyrimidine tract-binding protein-associated splicing factor) acts as a corepressor by interacting with Sin3A and mediating silencing through recruitment of HDACs to the DNA-binding domains of nuclear hormone receptors TR and RXR, independently of N-CoR/SMRT. |
Biochemical pulldown, Co-immunoprecipitation, in vivo transcription assays |
Molecular and cellular biology |
Medium |
11259580
|
| 2017 |
Human THO complex physically interacts with the Sin3A histone deacetylase complex; this interaction suppresses co-transcriptional R-loop formation, DNA damage, and replication impairment. Depletion of either THO or Sin3A leads to histone hypo-acetylation, increased R-loop accumulation, and genomic instability. |
Co-immunoprecipitation, siRNA knockdown, immunofluorescence, DNA-RNA hybrid detection (DRIP), replication fork assays |
The EMBO journal |
High |
29074626
|
| 2003 |
Nkx3.2 forms an in vivo complex with HDAC1 and Smad1/Smad4 in a BMP-dependent manner; recruitment of the HDAC/Sin3A complex to Nkx3.2 requires Smad1/4 interaction, establishing that BMP-Smads potentiate transcriptional repression through Sin3A. |
Co-immunoprecipitation, reporter assay, dominant-negative Smad4 cell line rescue |
Molecular and cellular biology |
Medium |
14612411
|
| 2000 |
MBD2b binds directly to Sin3A; the minimal repression domain of MBD2b overlaps with its methyl-CpG-binding domain, and the interaction domain on Sin3A is the paired amphipathic helix 3 (PAH3) region. |
GST pulldown, co-immunoprecipitation, deletion mapping |
The Journal of biological chemistry |
Medium |
10950960
|
| 2013 |
EBNA3C physically interacts with Sin3A and recruits it to the CDKN2A (p14ARF) promoter through BATF/IRF4/SPI1/RUNX3 composite sites; conditional EBNA3C inactivation significantly decreased Sin3A binding at the p14ARF promoter, establishing Sin3A-mediated repression of p14ARF and p16INK4A. |
ChIP-seq, Co-immunoprecipitation, conditional inactivation |
Proceedings of the National Academy of Sciences of the United States of America |
Medium |
24344258
|
| 2018 |
SIN3A binds to promoters of hypoxia-repressed genes prior to hypoxia and participates in downregulation of 75% of hypoxia-repressed genes and induction of 47% of upregulated genes in endothelial cells; SIN3A occupancy is not altered by hypoxia itself but modulation of associated HDAC activity determines transcriptional output. |
siRNA knockdown, ChIP-seq, nascent RNA sequencing (4-thiouridine labeling) |
Nucleic acids research |
Medium |
29059365
|
| 2009 |
Estrogen-bound ERα recruits Sin3A to the proximal A promoter of ESR1, leading to loss of RNA polymerase II and repression; a direct estrogen-responsive interaction between Sin3A and ERα was identified; Sin3A siRNA knockdown specifically inhibits estrogen-induced repression of ESR1. |
ChIP, Co-immunoprecipitation, siRNA knockdown |
Molecular and cellular biology |
Medium |
19620290
|
| 2012 |
Sin3A directly interacts with STAT3, promotes STAT3 deacetylation, and is required for ISGF3-dependent (STAT1:STAT2:IRF9) gene transcription; Sin3A silencing results in prolonged nuclear retention of activated STAT3, enhanced STAT3 recruitment to the SOCS3 promoter, histone hyperacetylation, and enhanced STAT3-dependent transcription. Sin3A acts as a context-dependent ISGF3/STAT3 transcriptional switch. |
Genome-wide RNAi screen, Co-immunoprecipitation, ChIP, siRNA knockdown |
Proceedings of the National Academy of Sciences of the United States of America |
High |
22783022
|
| 2016 |
MeCP2 interacts with SIN3A; haploinsufficiency of SIN3A in vivo causes reduced cortical neurogenesis, altered neuronal identity, and aberrant corticocortical projections in the developing mouse brain following knockdown. |
In vivo functional knockdown (mouse), immunofluorescence, neuronal projection analysis |
Nature genetics |
Medium |
27399968
|
| 2005 |
Ebp1 interacts directly with Sin3A (C-terminal domain of Ebp1 with PAH4/HID domain of Sin3A); both Ebp1 and Sin3A co-occupy the PSA and E2F1 promoters; Sin3A enhances Ebp1-mediated repression of androgen receptor and E2F1-regulated genes. |
GST pulldown, Co-immunoprecipitation, ChIP, reporter assay |
Nucleic acids research |
Medium |
16254079
|
| 2004 |
Only a small, unstable fraction of MeCP2 interacts with Sin3A; purified rat brain MeCP2 behaves as an elongated monomer (~53 kDa) with no stably associated proteins, indicating MeCP2 is not an obligate Sin3A complex component. |
Size-exclusion chromatography, biophysical analysis (sedimentation), Co-immunoprecipitation from multiple tissues |
The Journal of biological chemistry |
Medium |
15322089
|
| 2007 |
AHPN/3-Cl-AHPC binds to the orphan nuclear receptor SHP, promoting SHP interaction with a corepressor complex containing Sin3A, N-CoR, HDAC4, and HSP90; formation of the SHP-Sin3A complex is essential for AHPN/3-Cl-AHPC-induced apoptosis, as SHP knockout or Sin3A knockdown compromises proapoptotic activity. |
Ligand-binding assay, Co-immunoprecipitation, siRNA/KO knockdown, apoptosis assay |
Cancer research |
Medium |
17210713
|
| 2011 |
The NMR solution structure of the mSin3A PAH3 domain complexed with the SAP30 Sin3-interaction domain (SID) was determined; PAH3 adopts a left-handed four-helix bundle; SAP30 SID binds via a tripartite motif to an interface of ~1400 Ų, accounting for constitutive association. The PAH3-SAP30 SID complex can bind nucleic acids, suggesting a role in targeting the complex to ribosomal RNA genes. |
NMR spectroscopy, solution structure determination, nucleic acid binding assays |
The Journal of biological chemistry |
High |
21676866
|
| 2006 |
SAP30L binds to the PAH3/HID region of Sin3A via residues 120–140, recruits Sin3A to the nucleolus via a functional nucleolar localization signal, and induces transcriptional repression; SAP30 also targets Sin3A to the nucleolus. |
Co-immunoprecipitation, deletion mapping, reporter assay, subcellular localization imaging |
Nucleic acids research |
Medium |
16820529
|
| 2004 |
The highly conserved region (HCR) of Sin3A, spanning ~134 amino acids and sharing >80% identity with Sin3B, interacts with the N-terminus of the corepressor Alien; this interaction is demonstrated both in vivo by ChIP (at the CYP24 promoter) and in vitro; HCR overexpression inhibits Alien-mediated repression and induces endogenous CYP24 expression. |
Co-immunoprecipitation, ChIP, reporter assay, GST pulldown |
Nucleic acids research |
Medium |
15173382
|
| 2003 |
The SIN3 interaction domain (SID) of Mad-family repressors and KLF proteins bind differentially to the PAH2 domain of Sin3A; computational and experimental analyses show two SID subtypes exhibit distinct PAH2 binding modes, providing structural insight into selective corepressor recruitment. |
Computational modeling, binding assays |
FEBS letters |
Low |
12885416
|
| 2006 |
The apo PAH2 domain of mSin3A is monomeric and folded at low micromolar concentrations but dimerizes at higher concentrations with concomitant partial unfolding, in contrast to mSin3B PAH2 behavior, suggesting paralog-specific structural differences relevant to coregulator interactions. |
NMR spectroscopy, analytical ultracentrifugation, biophysical analysis |
Journal of molecular biology |
Medium |
16813833
|
| 2011 |
Sin3A interacts with c-Myc and causes deacetylation of c-Myc protein, directly repressing c-Myc activity; in the absence of Sin3A, c-Myc genomic recruitment to the epidermal differentiation complex is enhanced; simultaneous deletion of c-Myc and Sin3A reverts the aberrant skin phenotype, establishing a negative feedback loop. |
Conditional knockout mouse, ChIP, Co-immunoprecipitation, epistasis (double knockout rescue) |
Nature cell biology |
High |
22101514
|
| 2011 |
Sin3a-null embryos suffer unresolved DNA damage and acute apoptosis specifically in the epiblast; Myc and E2F targets are downregulated in Sin3a-null ICMs; ES cells deleted for Sin3a show DNA double-strand break response, G2 arrest, and apoptosis, establishing Sin3a as essential for genomic integrity of pluripotent cells. |
Conditional knockout mouse, ES cell deletion, γH2AX staining, cell cycle analysis, gene expression profiling |
Developmental biology |
High |
22206758
|
| 2017 |
FOXN3 is physically associated with the SIN3A repressor complex in ER+ cells; the lncRNA NEAT1 is required for FOXN3 interactions with the SIN3A complex (shown by RNA immunoprecipitation); the FOXN3-NEAT1-SIN3A complex represses GATA3 and ER (ESR1) genes, forming a negative-feedback loop; NEAT1 is identified as a facultative component of the SIN3A complex. |
RNA immunoprecipitation-sequencing, ChIP-seq, Co-immunoprecipitation, in vitro/in vivo functional studies |
The Journal of clinical investigation |
High |
28805661
|
| 2018 |
LSD1 is an integral component of the SIN3A/HDAC complex; the LSD1/SIN3A/HDAC complex co-targets genes in p53 signaling and other pathways as shown by ChIP-on-chip; LSD1 and SIN3A coordinate to inhibit genes including CASP7, TGFB2, CDKN1A, HIF1A, TERT, and MDM2. |
Co-immunoprecipitation, ChIP-on-chip, siRNA knockdown |
Journal of molecular cell biology |
Medium |
29741645
|
| 2018 |
Sin3a interacts with Tet1 via a highly conserved SID in the PAH1 domain; two residues (Phe147, Phe182) in PAH1 are essential for Sin3a-Tet1 interaction; Sin3a-Tet1 complex activates transcription of Lefty1 and other target genes by promoting promoter DNA demethylation; this activity is required for ESC pluripotency. |
NMR spectroscopy, co-immunoprecipitation, ChIP-seq, MeDIP-seq, site-directed mutagenesis, reporter assay |
Nucleic acids research |
High |
29733394
|
| 2018 |
Tet1 contains a conserved SID that inserts into the PAH1 domain of Sin3A in a Type-II orientation similar to Sap25; mutagenesis of key SID residues abolishes the interaction and is absolutely required for Tet1 to repress transcription in cells. |
NMR spectroscopy, homology modelling, mutagenesis, Co-immunoprecipitation, transcription reporter assay |
Scientific reports |
High |
30279502
|
| 2014 |
CRL4B (CUL4B-containing ubiquitin ligase) physically interacts with the SIN3A-HDAC complex and co-occupies CDKN1A and CDKN1C promoters; CUL4B loss reduces SIN3A-HDAC retention on promoters, increases histone acetylation, and upregulates p21 and p57; the ubiquitylation function of CRL4B is not required for stable SIN3A-HDAC retention. |
Co-immunoprecipitation, ChIP, siRNA knockdown, histone acetylation assays |
Journal of cell science |
Medium |
25189618
|
| 2017 |
Sin3a is required for Sin3A/HDAC2 complex function in lung endoderm; loss of Sin3a in mouse early foregut endoderm causes embryonic lung epithelial progenitor cells to adopt a senescence-like state with permanent G1 arrest, mediated at least partially through upregulation of Cdkn1a and Cdkn2c; loss also disrupts epithelial-mesenchymal signaling. |
Conditional knockout mouse, cell cycle analysis, gene expression profiling |
Development (Cambridge, England) |
Medium |
28619823
|
| 2010 |
Sertoli cell-specific deletion of Sin3a reduces undifferentiated spermatogonia (Plzf, Gfra1, Oct4 markers downregulated), disrupts CXCL12/SDF1 and CXCR4 signaling, causes progressive spermatogenic failure, and suppresses teratoma formation from fetal germ cells in transplantation assays, establishing a non-cell-autonomous epigenetic role for Sin3a in niche function. |
Conditional knockout mouse (Sertoli-specific), marker analysis, transplantation assay |
Stem cells (Dayton, Ohio) |
Medium |
20572009
|
| 2014 |
Sin3a-associated Hdac1 and Hdac2 control hematopoietic stem cell homeostasis cell-autonomously; bone-marrow-specific deletion of Sin3a phenocopies loss of Hdac1/2, causing bone marrow failure, establishing that Sin3a-associated HDAC1/2 activity is essential for HSC homeostasis. |
Conditional knockout mouse (bone marrow specific), HSPC analysis, phenotypic rescue |
Haematologica |
Medium |
24763403
|
| 2011 |
Gon4l interacts with YY1, Sin3a, and HDAC1 as components of a single complex in mouse B cells (demonstrated by sequential immunoprecipitation); a conserved central domain of Gon4l is required for this complex assembly; Gon4l represses promoter activity in a manner correlated with its ability to interact with Sin3a and HDAC1. |
Co-immunoprecipitation, sequential immunoprecipitation, density gradient sedimentation, reporter assay |
The Journal of biological chemistry |
Medium |
21454521
|
| 2009 |
Mohawk recruits components of the Sin3A/HDAC co-repressor complex (Sin3A, Hdac1, Sap18) and a subset of general transcription factors; MRD1 (one of three repressor domains in Mohawk) is co-immunoprecipitated by Sap18; Mohawk represses target genes required for myogenic differentiation through this mechanism. |
Co-immunoprecipitation, point mutation analysis, reporter assay |
Developmental dynamics |
Medium |
19235719
|
| 2008 |
T-bet-dependent removal of HDAC-Sin3A complexes from the Ifng locus drives H4 acetylation accumulation and Th1 differentiation; in Th0 cells, HDAC-Sin3A complexes actively prevent H4 acetylation; loss of HDAC-Sin3A occurs during Th1 lineage commitment through T-bet-dependent mechanisms. |
ChIP, T-bet genetic analysis, Th1/Th0 differentiation assays |
Journal of immunology |
Medium |
19050254
|
| 2010 |
Sumoylation of ING2 at lysine 195 by SUMO1 enhances its association with Sin3a; sumoylated ING2 is required for Sin3A/HDAC complex recruitment to target gene promoters (e.g., TMEM71) and for regulation of their transcription. |
In vitro sumoylation assay, Co-immunoprecipitation, ChIP, reporter assay |
Oncogene |
Medium |
20676127
|
| 2008 |
PKCα/ERK signaling causes Sp1 phosphorylation, which leads to dissociation of the HDAC1/mSin3A repressor complex from Sp1 binding sites on the LHR promoter, histone H3 acetylation, and derepression of LHR transcription. |
Co-immunoprecipitation, ChIP, kinase inhibition, dominant-negative overexpression |
Molecular endocrinology |
Medium |
18372343
|
| 2001 |
TGIF directly interacts with Sin3A, thereby recruiting HDAC1 to androgen receptor (AR)-responsive promoters to repress AR-mediated transcription; this repression is TSA-sensitive and TGIF binds the DNA-binding domain of AR. |
Co-immunoprecipitation, reporter assay, TSA inhibition |
Molecular endocrinology |
Medium |
11682623
|
| 2019 |
STAT3 is constitutively acetylated in NPM-ALK+ ALCL cells; acetylated STAT3 constitutively binds the Sin3A complex and together occupies promoters of silenced tumor suppressor genes; SIN3A silencing causes re-expression of TSGs and induces ALCL apoptosis in vitro and reduces tumorigenic potential in vivo. STAT3-Sin3A association was also found in breast adenocarcinoma cells. |
Co-immunoprecipitation, ChIP, siRNA knockdown, in vivo xenograft, resveratrol pharmacology |
Cancer research |
Medium |
30692217
|
| 2017 |
ARID1A directly causes suppression of TERT expression and co-occupies the TERT promoter with the SIN3A repressor complex during retinoic acid-induced neuroblastoma differentiation; SIN3A co-occupancy is required for ARID1A-dependent TERT repression. |
ChIP-qPCR, TERT expression analysis, telomeric repeat amplification protocol, immunoblot |
Molecular carcinogenesis |
Medium |
31365169
|
| 2014 |
SIN3A is required for transcriptional induction of CYP1A1 by TCDD (aryl hydrocarbon receptor ligand); TCDD treatment increases SIN3A binding to both the proximal promoter and enhancer of Cyp1a1; ectopic human SIN3A rescues TCDD-induced EROD activity in Sin3A-depleted cells, establishing a positive (activating) role for SIN3A at an AhR target gene. |
siRNA knockdown, ectopic expression rescue, ChIP, EROD enzyme assay |
The Journal of biological chemistry |
Medium |
25305016
|
| 2017 |
Fam60a defines a variant Sin3a-Hdac complex present in ES cells that additionally contains Ogt and Tet1; Fam60a is essential for maintaining the complex on chromatin at H3K4me3-positive promoters; depletion of Fam60a phenocopies loss of Sin3a (reduced proliferation, extended G1, deregulation of lineage genes). |
Tandem endogenous immunoprecipitation with quantitative mass spectrometry, ChIP-seq, siRNA knockdown, phenotypic analysis |
The EMBO journal |
High |
28554894
|
| 2018 |
The HDAC2/Sin3A/MeCP2 corepressor complex acts as an endogenous inhibitor of CTGF at the CTGF promoter; ET-1 disrupts this complex through MAP kinase-mediated HDAC2 phosphorylation, releasing HDAC2/Sin3A/MeCP2 from the CTGF promoter and allowing AP-1-driven CTGF expression. |
Co-immunoprecipitation, ChIP, siRNA knockdown, overexpression, kinase inhibitors |
Journal of biomedical science |
Medium |
37312162
|
| 2017 |
HDAC2 and cofactor Sin3A deacetylate histones H3K14ac and H3K27ac at the ASS1 promoter during arginine starvation, facilitating PHD2-driven HIF-1α proteasomal degradation at the promoter and enabling ASS1 derepression. |
ChIP, Co-immunoprecipitation, knockdown, proteasome inhibitor studies |
Scientific reports |
Medium |
28883660
|
| 2020 |
Sin3A regulates hippocampal synaptic plasticity and long-term memory: postnatal neuronal deletion of Sin3a enhances hippocampal LTP and contextual fear memory; Sin3A loss increases Homer1 expression, alters mGluR1α and mGluR5 dependence of LTP, and increases ERK activation after learning. |
Conditional knockout mouse, electrophysiology (LTP), fear conditioning, ChIP, gene expression analysis |
JCI insight |
High |
32069266
|
| 2024 |
SIN3A complex histone deacetylase activity protects stalled replication forks from MUS81 endonuclease-mediated cleavage; Sin3A is enriched at replicating DNA under hydroxyurea treatment; Sin3A-depleted cells show increased replication fork stalling, H3 acetylation at stalled forks, MRE11-dependent DNA degradation, and impaired fork recovery—effects partially dependent on MUS81. |
iPOND (isolation of proteins on nascent DNA), ChIP, DNA fiber assays, siRNA knockdown, genetic epistasis (MUS81 co-depletion) |
Cell reports |
High |
38341854
|
| 2023 |
Nuclear complement C3b physically associates with the HDAC1/2-containing SIN3A complex; this interaction enhances SIN3A complex binding to the GADD45A promoter, reducing H3 acetylation and repressing GADD45A expression, thereby promoting paclitaxel resistance in NSCLC. |
Co-immunoprecipitation, ChIP, nuclear fractionation, siRNA knockdown, ectopic expression |
Cell death & disease |
Medium |
37291119
|
| 2019 |
Sin3a regulates the developmental progression through the morula-to-blastocyst transition via Hdac1: Sin3a depletion increases Trp53 acetylation (K379), reduces Cdx2 and Nanog, causes global DNA hypermethylation via increased nuclear DNMT1, and downregulates Hdac1; exogenous Hdac1 but not Hdac2 rescues the block. |
siRNA knockdown in mouse embryos, RNA-seq, Western blot, immunofluorescence, rescue by Hdac1 mRNA injection |
FASEB journal |
Medium |
31450981
|
| 2023 |
Tet2 recruits Sin3a to active enhancers in ESCs; Tet2 deficiency diminishes Sin3a at active enhancers and promoters; combined Tet1/2 loss (but not loss of their catalytic activities alone) reduces Sin3a at active enhancers, showing that Tet1/2 noncatalytic functions recruit Sin3a. |
ChIP-seq, Tet2 catalytic mutant and KO ESCs, Co-immunoprecipitation |
iScience |
Medium |
37456851
|
| 2018 |
SINHCAF/FAM60A links the SIN3A-HDAC complex to the hypoxia response by specifically repressing HIF-2α mRNA and protein expression; SINHCAF interacts with SP1 and recruits HDAC1 to the HIF-2α promoter to mediate this repression. |
Co-immunoprecipitation, ChIP, siRNA knockdown, angiogenesis assays |
The Biochemical journal |
Medium |
29784889
|
| 2015 |
Disruption of the SIN3A PAH2 domain interaction with PF1 (PHF12/SID-containing adaptor) using a competitive Tat-SID peptide blocks EMT and stem cell marker expression in TNBC; KLF9 is recruited to ITGA6 and ITGB1 promoters by SIN3A and mediates their repression; KLF9 knockdown re-establishes invasion. |
Peptide competition (Tat-SID), Co-immunoprecipitation, ChIP, siRNA knockdown, in vitro and in vivo invasion assays |
Oncotarget |
Medium |
26460951
|
| 2013 |
BIM is epigenetically silenced in NPM/ALK+ ALCL through recruitment of MeCP2 and the SIN3a/HDAC1/2 corepressor complex to the BIM locus; CpG methylation is required for MeCP2 corepressor complex recruitment; demethylation with 5-azacytidine detaches the complex and reacetylates histone tails. |
ChIP, DNA methylation analysis (5-azacytidine treatment), histone acetylation assays, siRNA knockdown |
Neoplasia (New York, N.Y.) |
Medium |
23633923
|
| 2011 |
Sin3A couples with MeCP2 at the GFAP promoter to suppress GFAP transcription; upon astrocyte differentiation, Sin3A-MeCP2 depart from the promoter coincident with STAT3 binding, CBP/p300 recruitment, and histone H3K9/K14 acetylation that drives GFAP expression. |
ChIP, immunofluorescence, siRNA knockdown, reporter assay |
PloS one |
Medium |
21779366
|
| 2022 |
Sin3A functions as a transcriptional coactivator cooperating with Tet1 to facilitate hydroxymethylation of epithelial gene promoters; disrupting the Sin3a-Tet1 interaction (via PAH1 mutants) significantly blocks mesenchymal-to-epithelial transition and iPSC generation. |
Co-immunoprecipitation, ChIP, hydroxymethylated DNA immunoprecipitation (hMeDIP), site-directed mutagenesis, RNA-seq |
Stem cell research & therapy |
Medium |
35073971
|
| 2020 |
SIN3A loss in pancreatic β-cells compromises survival, insulin-vesicle packaging, insulin secretion, and nutrient-induced Ca2+ influx; ChIP assays identify direct Sin3a target genes in β-cells modulating Ca2+/ion transport, cell survival, vesicle trafficking, and glucose metabolism. |
Conditional knockout mouse (endocrine progenitor), RNA-seq, ChIP, calcium imaging, insulin secretion assays |
Diabetes |
High |
32245798
|
| 2021 |
SIN3A depletion in porcine early embryos reduces CCNB1 (Cyclin B1) transcript levels and causes two-cell stage arrest; injection of CCNB1 mRNA partially rescues SIN3A-depleted embryos, establishing SIN3A regulation of CCNB1 as a key mechanism in porcine embryonic development. |
siRNA knockdown, RNA-seq, mRNA rescue injection, immunofluorescence |
Frontiers in cell and developmental biology |
Medium |
33692994
|
| 2023 |
Sin3A-deficient CD4+ T cells fail to properly upregulate Il17a, Il23r, and Il22 under Th17 skewing conditions; instead, IL-2+ and FOXP3+ cells accumulate; Sin3A deletion causes overt STAT3 activation, aberrant cytoplasmic RORγt accumulation, and enrichment of mTORC1 signaling genes. |
Conditional knockout mouse (CD4-Cre), flow cytometry, cytokine assays, gene expression analysis |
EMBO reports |
Medium |
36929576
|
| 1996 |
Mouse Sin3A physically associates with the strong repressive isoform of Mxi1 (Mxi1-SR); a mSin3A-Mxi1 fusion protein in which the mSin3-interacting domain of Mxi1 is replaced by full-length mSin3A exhibits repression equivalent to Mxi1-SR, demonstrating that the Mxi1 N-terminal repression domain functions solely to recruit mSin3A. |
Co-immunoprecipitation, fusion protein repression assay, transformation assay |
Oncogene |
Medium |
8649810
|
| 2004 |
Chick Dach1 interacts with the Smad complex and the corepressor Sin3a, acting as a repressor of BMP-mediated transcriptional control; this interaction regulates apical ectodermal ridge formation and proximodistal patterning in the limb. |
Co-immunoprecipitation, in vivo limb functional assays |
Development (Cambridge, England) |
Medium |
15280207
|
| 2012 |
Sin3a is required in the male germline for mitotic reentry of gonocytes; germline genetic inactivation of Sin3a causes rapid depletion of gonocytes coincident with cell cycle reentry, 2.5-fold increased histone H3 phosphorylation, prophase/metaphase block, near-complete germ cell loss, and altered Sertoli cell expression programs. |
Conditional knockout mouse (germline), histone phosphorylation analysis, gene expression profiling |
Developmental biology |
Medium |
22820070
|
| 2021 |
ZBTB25 and Sin3A associate with the HDAC1 silencing complex and are recruited to the IL-12B promoter in M. tuberculosis-infected macrophages to downregulate IL-12B expression; ZBTB25 knockdown prevents complex recruitment and enhances IL-12p40 release. |
Co-immunoprecipitation, ChIP, siRNA knockdown, cytokine assays |
mSphere |
Medium |
33627504
|