Affinage

SUV39H1

Histone-lysine N-methyltransferase SUV39H1 · UniProt O43463

Length
412 aa
Mass
47.9 kDa
Annotated
2026-04-28
100 papers in source corpus 58 papers cited in narrative 57 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

SUV39H1 is a histone H3 lysine 9 (H3K9) methyltransferase that catalyzes di- and trimethylation of H3K9 at pericentric heterochromatin, telomeres, and retrotransposons, serving as a central architect of constitutive heterochromatin and transcriptional silencing essential for genome stability, chromosome segregation, and differentiation (PMID:11701123, PMID:14702045, PMID:24981170). Its chromodomain reads pre-existing H3K9me2/3 and binds chromatin-associated RNA (including satellite repeat transcripts), creating a positive-feedback loop that allosterically stimulates SET-domain catalytic activity and spreads the repressive mark across nucleosomal arrays (PMID:26807716, PMID:23285239, PMID:28760200, PMID:28760201). SUV39H1 recruits HP1 proteins, HDACs, and DNA methyltransferases (DNMT3A/3B) to establish multi-layered silencing, and is itself regulated by SIRT1-mediated deacetylation (activating), MDM2/USP7-controlled ubiquitination (destabilizing/stabilizing), SET7/9 methylation (inhibiting), and CDK2 phosphorylation (promoting S-phase chromatin dissociation) (PMID:18004385, PMID:21504832, PMID:26971997, PMID:23509280, PMID:24728993, PMID:12867029, PMID:11788710). Beyond histone substrates, SUV39H1 methylates non-histone proteins including RAG2, SET8, DOT1L, and mycobacterial HupB, and is recruited by diverse transcription factors (Snail, MyoD, RUNX1, EVI1) to silence lineage-specific gene programs controlling muscle differentiation, immune gene expression, viral latency, and T cell exhaustion (PMID:28169523, PMID:29170282, PMID:22562246, PMID:16858404, PMID:16652147, PMID:19776757, PMID:34, PMID:37934007).

Mechanistic history

Synthesis pass · year-by-year structured walk · 21 steps
  1. 2000 High

    Initial structure–function dissection established that SUV39H1 localizes to heterochromatin via its N-terminal chromodomain, represses transcription through its SET domain, and is a phosphoprotein regulated across the cell cycle — revealing it as an enzymatic chromatin silencer rather than a passive structural component.

    Evidence Deletion-mutant transfections, immunofluorescence, GAL4-reporter assays, phosphorylation analysis in HeLa cells

    PMID:10671371 PMID:10779362 PMID:10848615

    Open questions at the time
    • Catalytic substrate not yet identified at this point
    • Phosphorylation sites not mapped
    • Mechanism of transcriptional repression unknown
  2. 2001 High

    Double-null mouse studies demonstrated that Suv39h1/h2 are the principal H3K9 trimethylases at pericentric heterochromatin, and that loss of this mark causes chromosomal instability, tumor predisposition, and meiotic defects — establishing the biological necessity of H3K9me3 for genome integrity.

    Evidence Suv39h double-null mouse knockout with cytogenetics, immunofluorescence, tumor monitoring

    PMID:11701123

    Open questions at the time
    • Relative contributions of Suv39h1 vs Suv39h2 not separated
    • Whether catalytic-dead alleles phenocopy null unclear
  3. 2002 High

    Identification of SUV39H1 physical interactions with HDAC1/2/3 and Polycomb group proteins (HPC2) revealed that SUV39H1 acts as a scaffold coordinating histone deacetylation and Polycomb-mediated repression at heterochromatin.

    Evidence Co-IP, GST pulldown, immunofluorescence, HMTase activity assays

    PMID:11788710 PMID:12101246

    Open questions at the time
    • Stoichiometry of complexes unknown
    • Whether HDAC and PcG interactions are mutually exclusive unclear
  4. 2003 High

    A direct physical and functional link between SUV39H1-mediated H3K9me3 and DNA methylation was established: Suv39h recruits DNMT3A/3B via HP1 to pericentric heterochromatin, and loss of H3K9me3 disrupts DNA methylation at satellite repeats but not vice versa, demonstrating a hierarchical epigenetic pathway.

    Evidence ChIP, DNA methylation analysis, co-IP, and GST pulldowns in Suv39h- and Dnmt-null mouse ES cells

    PMID:12711675 PMID:12867029

    Open questions at the time
    • Whether this hierarchy holds at all genomic loci unclear
    • Role of DNMT1 vs DNMT3 in downstream pathway not fully resolved
  5. 2003 High

    Suv39h was shown to govern H3K9me2/3 at telomeres and to constrain telomere length, extending its heterochromatin maintenance role beyond pericentromeres.

    Evidence ChIP, telomere length measurement in Suv39h double-null primary cells

    PMID:14702045

    Open questions at the time
    • Whether telomere elongation is due to direct telomerase derepression or indirect effects unknown
  6. 2005 High

    Live-cell FRAP revealed a substantial immobile fraction of SUV39H1 at heterochromatin dependent on the SET domain, demonstrating a structural anchoring role beyond catalytic transit — and showing that HP1 binding is transient and partly dispensable for SUV39H1 recruitment.

    Evidence FRAP and FRET in living HeLa cells with deletion mutants

    PMID:16103223

    Open questions at the time
    • Nature of the SET-domain anchoring interaction unknown
    • Whether RNA contributes to the immobile fraction not yet tested
  7. 2006 High

    SUV39H1 was found to be recruited by lineage-specific transcription factors (MyoD, RUNX1, Cabin1-MEF2) to silence differentiation genes, establishing it as a facultative repressor beyond constitutive heterochromatin.

    Evidence Co-IP, ChIP, siRNA, reporter assays in muscle cells, hematopoietic cells, and T cells

    PMID:16652147 PMID:16858404 PMID:17172641

    Open questions at the time
    • Mechanism selecting SUV39H1 vs other H3K9 HMTs at specific promoters unclear
    • Genome-wide target maps for each TF context not available
  8. 2007 High

    SIRT1 was identified as a direct activator of SUV39H1: deacetylation of K266 in the SET domain stimulates catalytic activity, linking NAD+ metabolism to heterochromatin maintenance.

    Evidence In vitro deacetylation assay, K266 mutagenesis, ChIP, immunofluorescence

    PMID:18004385

    Open questions at the time
    • Full acetylation site landscape of SUV39H1 not mapped
    • Whether other sirtuins can substitute unknown
  9. 2007 High

    SUV39H1 and HP1γ were shown to deposit H3K9me3 on the integrated HIV-1 LTR, establishing SUV39H1 as a mediator of viral latency whose removal reactivates proviral transcription.

    Evidence ChIP, RNAi, reporter assays, primary PBMCs from HIV-1-infected donors

    PMID:17245432

    Open questions at the time
    • Recruitment mechanism to HIV-1 LTR not identified
    • Whether SUV39H1 inhibition alone is sufficient for latency reversal in vivo unknown
  10. 2010 High

    SUV39H1 was found to coexist with G9a, GLP, and SETDB1 in a megacomplex, with interdependent protein stability, revealing cooperative H3K9 methyltransferase function rather than isolated enzyme action.

    Evidence Co-IP/mass spectrometry, immunoblot in null cell lines, ChIP

    PMID:20129054

    Open questions at the time
    • Stoichiometry and assembly order of the megacomplex unknown
    • Whether all four HMTs act simultaneously at the same nucleosome unclear
  11. 2011 High

    The MDM2–USP7 ubiquitin axis was shown to control SUV39H1 protein stability via K87 polyubiquitination, with p53 activation tipping the balance toward degradation — connecting p53 signaling to heterochromatin dynamics.

    Evidence Ubiquitination assays, protein half-life measurement, co-IP, calorie restriction model

    PMID:21504832 PMID:26971997

    Open questions at the time
    • Whether other E3 ligases contribute to basal SUV39H1 turnover unclear at this point
  12. 2012 High

    Crystal structure of the SUV39H1 chromodomain confirmed specific recognition of H3K9me2/3 and revealed a distinctive extended C-terminal helix, providing the structural basis for its reader function.

    Evidence X-ray crystallography with binding assays

    PMID:23285239

    Open questions at the time
    • Full-length structure including SET domain not resolved
    • Chromodomain–nucleosome complex structure unavailable
  13. 2013 High

    Multiple regulatory post-translational modifications were mapped: SET7/9 methylates K105/K123 to inhibit activity (DNA damage response), A-type lamins stabilize SUV39H1 (with pathological excess in progeria), and Pin1 promotes phospho-dependent degradation — revealing SUV39H1 as a signaling hub.

    Evidence In vitro methylation/mass spectrometry, progeria mouse models, ubiquitination assays

    PMID:23509280 PMID:23695662 PMID:23934277

    Open questions at the time
    • Crosstalk among multiple PTMs not systematically dissected
    • Whether K105/K123 methylation occurs physiologically outside DNA damage unclear
  14. 2014 High

    CDK2-mediated S391 phosphorylation was shown to dissociate SUV39H1 from chromatin during S phase, enabling heterochromatin replication by JMJD2A demethylase access — establishing cell-cycle-dependent regulation of H3K9me3 at replication forks.

    Evidence In vitro kinase assay, phospho-specific antibodies, cell synchronization, ChIP, replication timing assay

    PMID:24728993

    Open questions at the time
    • Whether phospho-SUV39H1 is re-recruited after replication fork passage unknown
    • Mechanism of JMJD2A preference for phospho-evicted loci not defined
  15. 2014 High

    Genome-wide ChIP-seq in Suv39h-null ES cells revealed that ~5% of the epigenome is covered by Suv39h-dependent H3K9me3, predominantly at intact LINE and ERV retrotransposons — defining the genomic substrate beyond centromeres and telomeres.

    Evidence ChIP-seq in Suv39h double-null mouse ES cells with bioinformatic analysis

    PMID:24981170

    Open questions at the time
    • Whether retrotransposon silencing is maintained by Suv39h in differentiated cells or handed off to DNA methylation not fully resolved
  16. 2016 High

    Reconstitution on designer chromatin revealed a two-step allosteric activation: chromodomain reading of H3K9me3 stimulates SET domain catalysis on adjacent nucleosomes, explaining the positive-feedback mechanism for heterochromatin spreading.

    Evidence In vitro methyltransferase assay on defined multidomain chromatin templates with mutagenesis

    PMID:26807716

    Open questions at the time
    • Whether spreading is limited by boundary elements in this reconstitution unclear
    • Contribution of RNA to allosteric activation not tested in this system
  17. 2016 High

    A catalysis-independent function was discovered: SUV39H1's N-terminal domain promotes HP1α sumoylation via Ubc9, accelerating de novo heterochromatin formation — separating structural/scaffolding from enzymatic roles.

    Evidence In vitro sumoylation assay, domain tethering at pericentromeres, immunofluorescence

    PMID:27426629

    Open questions at the time
    • Physiological contribution of SUV39H1-mediated sumoylation vs H3K9me3 not quantified
    • Whether other SUMOylation substrates exist at heterochromatin unknown
  18. 2017 High

    Three independent studies converged on RNA as an essential chromatin-anchoring signal: SUV39H1's chromodomain binds satellite repeat RNAs and RNA:DNA hybrids; RNase treatment or RNA knockdown abolishes SUV39H1 chromatin association, establishing an RNA-dependent recruitment mechanism.

    Evidence RNA immunoprecipitation, in vitro nucleic acid binding, FRAP, RNaseA/H treatment, satellite RNA knockdown in mouse ES cells

    PMID:28760199 PMID:28760200 PMID:28760201

    Open questions at the time
    • Sequence specificity of RNA binding not defined
    • Whether RNA binding and H3K9me3 reading are simultaneous or sequential unclear
  19. 2017 High

    SUV39H1 was shown to methylate non-histone substrates (RAG2, SET8, DOT1L, and mycobacterial HupB), broadening its role from a histone-only modifier to a general lysine methyltransferase with immunological and antimicrobial functions.

    Evidence In vitro methylation assays, cell-based confirmation, mycobacterial infection model

    PMID:28169523 PMID:29170282

    Open questions at the time
    • Full non-histone substrate repertoire not systematically surveyed
    • In vivo relevance of RAG2 methylation for VDJ recombination not demonstrated
  20. 2018 High

    SirT6-mediated cysteine monoubiquitination in the PRE-SET domain was identified as a novel mechanism to evict SUV39H1 from specific gene promoters (IκBα), attenuating NF-κB signaling — demonstrating locus-specific removal as a regulatory strategy.

    Evidence Co-IP, ubiquitination assay, ChIP, NF-κB reporter, mutagenesis

    PMID:29317652

    Open questions at the time
    • Enzyme catalyzing cysteine ubiquitination not identified
    • Breadth of cysteine monoubiquitination across the proteome unknown
  21. 2024 High

    CRISPR disruption of SUV39H1 in CAR T cells enhanced persistence, memory transcription factor accessibility, and antitumor efficacy upon serial tumor rechallenge — translating epigenetic control of T cell exhaustion into a therapeutic strategy.

    Evidence CRISPR KO in human CAR T cells, scRNA-seq, scATAC-seq, in vivo tumor models; independently replicated

    PMID:37934001 PMID:37934007

    Open questions at the time
    • Long-term safety of SUV39H1-deleted T cells in patients unknown
    • Whether heterochromatin instability accumulates in edited T cells over time untested

Open questions

Synthesis pass · forward-looking unresolved questions
  • A full-length structural model of SUV39H1 on a nucleosomal substrate — integrating chromodomain reader, SET domain writer, RNA-binding surface, and allosteric connectivity — remains unresolved, as does the logic governing locus-specific recruitment by different transcription factor partners versus constitutive heterochromatin maintenance.
  • No full-length or nucleosome-bound structure available
  • Locus-selectivity determinants for TF-directed vs constitutive targeting unknown
  • Systematic non-histone substrate profiling in vivo lacking

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0016740 transferase activity 7 GO:0140110 transcription regulator activity 4 GO:0003723 RNA binding 3 GO:0042393 histone binding 2
Localization
GO:0005694 chromosome 7 GO:0005634 nucleus 3
Pathway
R-HSA-4839726 Chromatin organization 7 R-HSA-74160 Gene expression (Transcription) 4 R-HSA-1266738 Developmental Biology 3 R-HSA-1640170 Cell Cycle 3 R-HSA-168256 Immune System 3
Partners
DNMT3AG9AHDAC1HP1AMBD1MDM2SIRT1USP7
Complex memberships
G9a/GLP/SETDB1/SUV39H1 megacomplexMDM2–USP7–SUV39H1 trimeric complexSUV39H1–HP1–DNMT3A/3B silencing complex

Evidence

Reading pass · 57 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2001 Murine Suv39h1 and Suv39h2 histone methyltransferases (HMTases) govern H3K9 trimethylation at pericentric heterochromatin; loss of both enzymes in double-null mice leads to severely impaired viability, chromosomal instabilities, increased tumor risk, and perturbed chromosome interactions during male meiosis, establishing a crucial role for pericentric H3K9 methylation in genome stability. Suv39h double-null mouse knockout; immunofluorescence; cytogenetics Cell High 11701123
2000 SUV39H1 transiently accumulates at centromeric positions during mitosis (specifically prometaphase), dissociating at the meta-to-anaphase transition; its chromo domain plus the first 44 N-terminal amino acids direct specific accumulation at heterochromatin, while the C-terminal SET domain mediates redistribution of HP1β and induction of mitotic defects. SUV39H1 is a phosphoprotein with additional phosphorylated isoforms detected in mitotic extracts. Immunofluorescence; cell cycle fractionation; transfection of SUV39H1 deletion mutants; phosphoprotein analysis Journal of cell science High 10671371
2000 SUV39H1 represses transcription in a GAL4-tethered assay in a SET domain-dependent manner, localizes to nuclear heterochromatin bodies, suppresses cell growth when overexpressed, and is phosphorylated at the G1/S transition; the oncogenic antiphosphatase Sbf1 interacts with the SET domain and stabilizes phosphorylated SUV39H1, antagonizing its growth-suppressive and chromatin-silencing activities. Transient transcriptional reporter assay; immunofluorescence; co-immunoprecipitation; cell growth assay; phosphorylation analysis Molecular and cellular biology High 10848615
2000 Structure-function analysis revealed that forced expression of full-length SUV39H1 redistributes endogenous HP1β and induces associations with inter- and metaphase chromatin via the C-terminal SET domain; the HP1 interaction surface maps to the first 44 N-terminal amino acids plus the adjacent chromo domain. Overexpression causes severe mitotic progression defects and chromosome segregation errors, and disperses the G2-specific focal distribution of phospho-H3S10. Transfection of deletion mutants; immunofluorescence; co-immunoprecipitation Molecular and cellular biology High 10779362
2003 Suv39h-mediated H3K9 trimethylation at pericentric heterochromatin is required to direct Dnmt3b (via HP1α interaction) to major satellite repeats for DNA methylation; in Suv39h double-null ES cells, Dnmt3b fails to localize to heterochromatic foci and DNA methylation at pericentric satellite repeats is altered, while H3K9me3 at pericentric heterochromatin is not impaired in Dnmt-deficient cells. ChIP; immunofluorescence; DNA methylation analysis; Suv39h and Dnmt knockout mouse ES cells Current biology High 12867029
2003 Endogenous Dnmt3a associates with SUV39H1 in vitro and in vivo via the PHD-like motif of Dnmt3a; SUV39H1 also binds Dnmt1; HP1β binds directly to Dnmt1 and Dnmt3a; SUV39H1 can purify DNA methyltransferase activity from nuclear extracts, establishing a direct physical connection between H3K9 methyltransferase and DNA methyltransferase machinery. Co-IP; GST pulldown; in vitro binding; nuclear extract purification Nucleic acids research High 12711675
2003 MBD1 directly interacts with SUV39H1 and HP1 through its methyl-CpG binding domain (MBD) in vitro and in cells; SUV39H1 enhances MBD1-mediated transcriptional repression via the MBD domain; MBD1 also links to HDACs through SUV39H1, resulting in coordinated histone methylation and deacetylation for gene silencing. GST pulldown; co-IP; reporter assay; ChIP Journal of biological chemistry High 12711603
2003 Suv39h1 and Suv39h2 govern di- and trimethylation of H3K9 at telomeric heterochromatin; primary cells from SUV39H double-null mice have abnormally long telomeres with reduced H3K9me2/3 and decreased binding of HP1 proteins (Cbx1, Cbx3, Cbx5), demonstrating epigenetic regulation of telomere length. ChIP; telomere length measurement; immunofluorescence; Suv39h double-null mouse Nature genetics High 14702045
2003 The chromo shadow domain of HP1α directly interacts with the N-terminal 39 amino acids of SUV39H1 in yeast two-hybrid and GST pulldown assays; self-dimerization of the chromo shadow domain is required for this interaction, as the IY165/168EE mutation abrogated both self-interaction and SUV39H1 binding. Yeast two-hybrid; GST pulldown; mutagenesis Biochemical and biophysical research communications High 12565857
2002 SUV39H1 physically interacts with HDAC1, HDAC2, and HDAC3 by co-immunoprecipitation; the N-terminal domain of SUV39H1 (not requiring enzymatic activity) is sufficient for transcriptional repression and binds the core HDAC complex (HDAC1, HDAC2, RbAp48, RbAp46), suggesting SUV39H1 recruits HDACs for heterochromatin silencing and Rb-mediated repression. Co-IP; reporter assay; domain deletion analysis Nucleic acids research High 11788710
2004 Suv39h histone methyltransferase is required for H3K9 methylation at Rb/E2F target promoters specifically in terminally differentiating cells (but not cycling cells); siRNA knockdown of Suv39h prevents H3K9 methylation and permanent silencing of S-phase genes upon differentiation, and Suv39h-depleted myoblasts fail to express muscle differentiation markers. ChIP; siRNA knockdown; gene expression analysis in differentiating vs cycling cells The EMBO journal High 14765126
2007 SIRT1 directly interacts with, recruits, and deacetylates SUV39H1 at lysine 266 within its catalytic SET domain; SIRT1-mediated deacetylation stimulates SUV39H1 H3K9 methyltransferase activity, leading to increased H3K9me3 and proper HP1 localization at heterochromatin. Loss of SIRT1 greatly reduces SUV39H1-dependent H3K9me3. Co-IP; in vitro deacetylation assay; mutagenesis; ChIP; immunofluorescence Nature High 18004385
2011 SirT1 controls global levels of Suv39h1 protein by increasing its half-life through inhibition of Suv39h1 lysine 87 polyubiquitination by the E3-ubiquitin ligase MDM2; oxidative stress and calorie restriction upregulate SirT1, which in turn stabilizes Suv39h1 to ensure genome integrity. Ubiquitination assay; protein stability (half-life) measurement; in vivo calorie restriction model; co-IP Molecular cell High 21504832
2013 SET7/9 methyltransferase interacts with SUV39H1 (via SUV39H1's chromodomain-containing region) in response to DNA damage and specifically methylates SUV39H1 at lysines 105 and 123, as confirmed by mass spectrometry and methyl-specific antibodies; this methylation dramatically downregulates SUV39H1 methyltransferase activity, decreasing H3K9me3 and causing heterochromatin relaxation and genome instability. Co-IP; GST pulldown; in vitro methylation assay; mass spectrometry; Western blot with site-specific antibodies; MNase sensitivity assay PNAS High 23509280
2013 A-type lamins interact with SUV39H1, and prelamin A/progerin exhibits enhanced binding to SUV39H1, protecting it from proteasomal degradation and consequently increasing H3K9me3 levels; depletion of Suv39h1 restores DNA repair capacity, delays senescence in progeroid cells, and extends lifespan of Zmpste24-/- mice by ~60%. Co-IP; protein stability assay; Suv39h1 depletion in mouse model; DNA repair assay; lifespan measurement Nature communications High 23695662
2013 MDM2 acts as an E3 ubiquitin ligase that ubiquitinates SUV39H1, promoting its degradation; USP7 deubiquitinase forms a trimeric complex with MDM2 and SUV39H1, protecting SUV39H1 from MDM2-mediated ubiquitination in unstressed cells. Upon p53 activation, this protection is lost, leading to SUV39H1 degradation and relaxation of H3K9me3 at p53 target promoters. Co-IP; ubiquitination assay; ChIP; protein stability assay; domain mapping Cell reports High 26971997
2010 A subset of H3K9 methyltransferases — G9a, GLP, SETDB1, and Suv39h1 — coexist in the same megacomplex; in Suv39h or G9a null cells, the remaining HKMTs are destabilized at the protein level, indicating interdependence. All four HKMTs are recruited to major satellite repeats and cooperate in regulation of G9a target genes. Co-IP; mass spectrometry; immunoblot in null cell lines; ChIP Molecular cell High 20129054
2012 Crystal structure of the human SUV39H1 chromodomain was determined by X-ray crystallography; the chromodomain specifically recognizes histone H3K9me2/3 but has a distinct longer C-terminal helix compared to other chromodomains. X-ray crystallography; binding assay PLoS ONE High 23285239
2016 Suv39h1 uses a two-step activation switch: H3K9me3 recognition by its chromodomain allosterically promotes methylation activity and anchors the enzyme to chromatin (positive feedback); this mechanism was dissected using designer multidomain chromatin templates and confirmed in cells using nucleic acid and methyl-binding mutants. Reconstituted designer chromatin substrates; in vitro methyltransferase assay; mutagenesis; cell-based chromatin assay Nature chemical biology High 26807716
2016 Suv39h1 promotes HP1α sumoylation in vitro and in vivo through its N-terminal domain (aa1-167), which is distinct from its catalytic KMT domain and mediates binding to the SUMO E2 enzyme Ubc9; tethering this domain to pericentric heterochromatin accelerates de novo HP1α targeting, establishing a KMT-independent function for Suv39h1 in heterochromatin formation via the SUMO pathway. In vitro sumoylation assay; co-IP; domain tethering experiments; immunofluorescence Nature communications High 27426629
2017 SUV39H1 associates with α-satellite RNA transcripts and purified SUV39H1 directly binds nucleic acids through its chromodomain; nucleic acid-binding mutants destabilize SUV39H1 association with chromatin in mitotic and interphase cells (effects recapitulated by RNase treatment or RNA Pol inhibition) and cause defects in heterochromatin function, revealing RNA-mediated stabilization of SUV39H1 at constitutive heterochromatin. RNA immunoprecipitation; purified protein nucleic acid binding assay; FRAP; RNase treatment; mutagenesis; immunofluorescence eLife High 28760200
2017 Suv39h1's chromodomain binds nucleic acids (preferentially RNA over DNA) independently of H3K9me3 recognition; Suv39h1 binds major satellite RNAs in vivo, and knockdown of major satellite RNAs lowers Suv39h1 retention at pericentromeres. Both nucleic acid-binding and H3K9me-binding activities of the chromodomain are required for pericentric heterochromatin assembly. In vitro nucleic acid binding assay; RNA immunoprecipitation; knockdown of satellite RNA; mutagenesis; ChIP eLife High 28760201
2017 Suv39h1 and Suv39h2 exclusively associate with poly-nucleosomes from native mouse ES cell chromatin; this association is attenuated by RNaseH and entirely lost by RNaseA treatment, indicating that RNA (including RNA:DNA hybrids formed by major satellite repeat transcripts) mediates stable chromatin interaction of Suv39h enzymes. Native nucleosome purification; RNaseA/H treatment; RNA secondary structure analysis eLife High 28760199
2005 FRAP analysis in living cells shows a substantial immobile fraction of SUV39H1 at pericentromeric heterochromatin, indicating a structural role in addition to catalytic activity; the SET domain mediates this stable binding; HP1 transiently interacts with SUV39H1 at heterochromatin, and SUV39H1 recruitment to heterochromatin is at least partly independent of HP1. FRAP; FRET; live-cell imaging; deletion mutant analysis Journal of cell biology High 16103223
2006 Suv39h1 interacts with MyoD in proliferating muscle cells and its HMT activity associated with MyoD diminishes during differentiation; the Suv39h1-MyoD complex occupies the myogenin promoter with concurrent H3K9 methylation; increased Suv39h1 represses MyoD-dependent muscle gene expression in an HMT activity-dependent manner, and siRNA abrogation of Suv39h1 activates muscle gene expression by MyoD. Co-IP; ChIP; siRNA knockdown; reporter assay; differentiation assay The EMBO journal High 16858404
2009 DBC1 (Deleted in Breast Cancer 1) binds directly to the SUV39H1 catalytic domain, disrupts the SUV39H1-SIRT1 complex, and inhibits SUV39H1's ability to methylate histone H3 in vitro and in vivo; knockdown of endogenous DBC1 increases cellular H3K9 methylation. Co-IP; in vitro methylation assay; DBC1 knockdown; Western blot for H3K9me Journal of biological chemistry High 19218236
2014 CDK2 phosphorylates Suv39H1 at Ser391; phosphorylation levels peak at S phase and are maintained through S-G2-M phase; phosphorylation promotes dissociation of Suv39H1 from chromatin, enhanced occupancy of JMJD2A demethylase on heterochromatin, and early replication of heterochromatin. Phospho-defective Suv39H1 causes altered replication timing and increased sensitivity to replication stress. In vitro kinase assay; phospho-specific antibodies; cell synchronization; ChIP; BrdU incorporation assay; mutagenesis Nucleic acids research High 24728993
2017 SUV39H1 methylates the mycobacterial histone-like protein HupB; this trimethylation reduces the cell adhesion capability of mycobacterial bacilli and their survival inside host cells; SUV39H1 was found associated with mycobacterial bacilli during infection, and reduced mycobacterial biofilm formation was observed in the presence of SUV39H1. In vitro methylation assay; infection assay; confocal microscopy; biofilm assay; mouse infection model The EMBO journal High 29170282
2017 SUV39H1 methylates non-histone proteins RAG2, SET8, and DOT1L (confirmed in cells); methylation of SET8 allosterically stimulates its H4K20 monomethylation activity; methylation of RAG2 alters its subnuclear localization, suggesting SUV39H1 regulates VDJ recombination. Peptide and protein methylation assay; cell-based confirmation; subnuclear localization by immunofluorescence; substrate specificity profiling ACS chemical biology High 28169523
2018 DCAF13 functions as an adaptor for CRL4 E3 ubiquitin ligase that targets SUV39H1 for polyubiquitination and proteasomal degradation; Dcaf13 knockout embryos arrest at the 8-to-16-cell stage with high H3K9me3 levels; this degradation facilitates H3K9me3 removal and zygotic gene expression during preimplantation development. Ubiquitination assay; Dcaf13 knockout mouse; embryo development phenotyping; Western blot The EMBO journal High 30111536
2018 SirT6 binds to Suv39h1 and induces monoubiquitination of conserved cysteines in the PRE-SET domain of Suv39h1; following NF-κB activation, Suv39h1 is released from the IκBα locus, suppressing the NF-κB pathway. SirT6-mediated cysteine monoubiquitination thus attenuates NF-κB signaling through chromatin eviction of Suv39h1. Co-IP; ubiquitination assay; ChIP; mutagenesis; NF-κB reporter assay Nature communications High 29317652
2014 Suv39h-dependent H3K9me3 selectively accumulates at intact long interspersed nuclear elements (LINEs) and endogenous retroviruses (ERVs) in mouse ES cells (covering ~5% of the epigenome); transcriptional repression of intact LINEs in ESCs is governed by Suv39h, while committed cells use DNA methylation for this repression. Genome-wide ChIP-seq in Suv39h double-null ES cells; bioinformatic analysis; comparison with Dnmt-null cells Molecular cell High 24981170
2002 Vertebrate Polycomb homologs HPC2 and XPc2 interact with SUV39H1 both in vitro (GST pulldown) and in vivo (co-IP); overexpression of SUV39H1 induces nuclear relocalization of HPC/HPH PcG proteins to pericentromeric heterochromatin (1q12) with increased H3K9 methylation; endogenous HPC2 is associated with H3K9 HMTase activity. GST pulldown; co-IP; immunofluorescence; HMTase activity assay Molecular and cellular biology High 12101246
2006 Suv39h1 histone methyltransferase activity specifically increases IgA class switch recombination (Smu-Sα recombination) in a transfected plasmid switch substrate assay; B cells from Suv39h1-deficient mice show an isotype-specific reduction in IgA switching without effects on germline Iα-Cα transcripts. Plasmid switch substrate transfection assay; Suv39h1-null mouse B cells; isotype-specific switching measurement; HMTase activity mutant analysis Journal of immunology High 16818776
2007 SUV39H1 and HP1γ are recruited to the HIV-1 LTR in a transcription-dependent manner and mediate chromatin-based transcriptional silencing of integrated HIV-1 via H3K9me3; knockdown of HP1γ by RNAi reactivates HIV-1 expression in multiple cellular models including PBMCs from HIV-1-infected donors. ChIP; RNAi knockdown; reporter assay; primary patient cell assay The EMBO journal High 17245432
2009 CTIP2 recruits SUV39H1 to the p21(WAF1) gene promoter to cooperatively silence p21 transcription via H3K9me3; the specific SUV39H1 inhibitor chaetocin represses H3K9me3 at the p21 promoter, stimulates p21 expression, and induces cell cycle arrest. ChIP; co-IP; chaetocin pharmacological inhibition; reporter assay Oncogene High 19581932
2012 Snail interacts with SUV39H1 through the SNAG domain of Snail and the SET domain of SUV39H1; Snail recruits SUV39H1 to the E-cadherin promoter for H3K9me3-dependent transcriptional repression and DNA methylation; SUV39H1 knockdown restores E-cadherin expression by blocking H3K9me3 and DNA methylation, inhibiting cell migration and invasion. Co-IP; domain mutagenesis; ChIP; siRNA knockdown; cell migration/invasion assay Oncogene High 22562246
2013 CRL4B (Cullin4B-Ring E3 ligase) associates with SUV39H1, HP1, and DNMT3A; CRL4B, through catalyzing H2AK119 monoubiquitination, facilitates SUV39H1-mediated H3K9me3 and DNA methylation; CUL4B depletion results in loss of H2AK119ub, H3K9me3, and DNA methylation with derepression of tumor suppressor IGFBP3. Co-IP; ChIP; ubiquitination assay; CUL4B knockdown Oncogene High 24292684
2006 RUNX1 repression domain 2 (RD2) directly contacts SUV39H1 via two binding motifs; endogenous Suv39h1 associates with a Runx1-regulated repression element in MEL cells by ChIP; RD2 also contacts HDAC1 and HDAC3 through overlapping motifs, and both interactions are required for full RUNX1-mediated repression. Co-IP; domain mapping; ChIP; reporter assay Oncogene High 16652147
2009 EVI-1 physically interacts with SUV39H1 and G9a; EVI-1 forms an active complex with SUV39H1 that retains methyltransferase activity in vitro; catalytically inactive SUV39H1 abrogates EVI-1-mediated transcriptional repression; RNAi knockdown of SUV39H1 or G9a significantly reduces colony-forming activity of Evi-1-expressing progenitors. Co-IP; in vitro methyltransferase assay; dominant-negative mutant; RNAi; colony assay Leukemia High 19776757
2006 Cabin1 physically binds to SUV39H1 through its 501-900 amino acid region (distinct from its HDAC-recruiting domain); SUV39H1 enhances Cabin1-mediated repression of MEF2 transcriptional activity; Cabin1 immunoprecipitate methylates histone H3; both SUV39H1 and Cabin1 occupy MEF2 target promoters in a calcium-dependent manner. Co-IP; in vitro HMTase activity assay; ChIP; reporter assay Journal of biological chemistry High 17172641
2010 RFX1 co-immunoprecipitates with SUV39H1 at the CD11a and CD70 promoters in healthy CD4+ T cells; RFX1 expression correlates with H3K9me3 levels at these promoters; overexpression or knockdown of RFX1 directly alters H3K9me3 and gene expression, demonstrating that RFX1 recruits SUV39H1 to regulate autoimmune gene silencing. Co-IP; ChIP; RFX1 overexpression/knockdown; RT-PCR Arthritis research & therapy Medium 21192791
2014 Suv39h1 interacts with AP-2α and G9a on the C/EBPα promoter during adipogenesis; G9a mediates H3K9me2, providing the substrate for Suv39h1-catalyzed H3K9me3; Suv39h1 knockdown markedly increases C/EBPα expression and promotes adipogenesis, while ectopic Suv39h1 delays C/EBPα expression and impairs adipocyte differentiation. Co-IP; ChIP; siRNA knockdown; overexpression; differentiation assay Molecular and cellular biology High 24732798
2013 Pin1 interacts with SUV39H1 in a phosphorylation-dependent manner and promotes ubiquitination-mediated degradation of SUV39H1, reducing H3K9me3; conversely, depletion of Pin1 elevates SUV39H1 levels and H3K9me3, inhibiting tumorigenicity. Co-IP; ubiquitination assay; Pin1 knockdown/overexpression; protein stability assay; xenograft model FASEB journal Medium 23934277
2019 IFI16 forms a complex with SUV39H1 and GLP (another H3K9 methyltransferase) and recruits them to the KSHV genome during infection and latency; resulting H3K9me2/me3 serves as a docking site for HP1α, leading to epigenetic silencing of KSHV lytic genes. Co-IP; ChIP; IFI16 knockdown; immunofluorescence eLife High 31682228
2020 SUV39H1 deficiency modulates H3K9me3 status at the DPP4 promoter, resulting in upregulation of DPP4 expression that contributes to ferroptosis (iron accumulation and lipid peroxidation) disrupting ccRCC cell growth in vitro and in vivo. siRNA knockdown; ChIP; ferroptosis assay; xenograft model Acta pharmaceutica Sinica B Medium 33643820
2016 KAT7/HBO1 acetyltransferase interacts with the CENP-A assembly factor M18BP1; Suv39h1 overexpression in KAT7 knockout HeLa cells enhances chromosome misalignment and micronuclei formation; tethering KAT7 to alphoid DNA removes H3K9me3 and stimulates CENP-A assembly, demonstrating that Suv39h1-mediated H3K9me3 can antagonize CENP-A deposition and centromere function. Co-IP; KAT7 knockout; Suv39h1 overexpression; CENP-A ChIP; tethering assay; microscopy Developmental cell High 27270040
2016 SUV39H1 expression in hematopoietic stem cells is regulated by microRNA miR-125b; miR-125b targets SUV39H1 mRNA; overexpression of miR-125b or inhibition of SUV39H1 in young HSCs induces loss of B cell potential, while enforced SUV39H1 expression improves B cell generation from elderly HSCs. miRNA target validation; overexpression/knockdown; HSC differentiation assay; ChIP Stem cell reports Medium 27304919
2012 SUV39H1 orchestrates temporal dynamics of centromeric H3K9 methylation during mitosis; inhibition of SUV39H1 methyltransferase activity perturbs chromosome congression, causes a brief increase in Aurora B kinase activity, enriches microtubule depolymerase MCAK at centromeres, destabilizes kinetochore-microtubule attachments, reduces tension across sister kinetochores, and leads to chromosome misalignment. FRET-based methylation sensors in living HeLa cells; immunofluorescence; chaetocin inhibition; Aurora B and MCAK localization assays Journal of molecular cell biology High 22831836
2017 SUV39H1 cooperates with HP1γ to catalyze H3K9me3 on the SIRT1 promoter and represses SIRT1 transcription in cardiomyocytes under ischemic/oxidative stress; SUV39H1 knockout mice are protected from myocardial infarction; ischemic stress leads to rapid upregulation of SUV39H1 paralleling SIRT1 downregulation. ChIP; SUV39H1 KO mouse; Co-IP; chaetocin pharmacological inhibition; cardiac injury assay Nature communications High 28361889
2011 Suv39h1 occupies the HTLV-1 LTR after Tax induction (by ChIP); Tax interacts with SUV39H1 in vitro dependent on the C-terminal SET domain of SUV39H1; Tax does not affect SUV39H1 methyltransferase activity but tethers it to a Tax-containing nuclear complex; SUV39H1 represses Tax transactivation of HTLV-1 LTR in a methyltransferase activity-dependent manner. In vitro binding assay; co-IP; ChIP; reporter assay; HMTase activity assay Retrovirology Medium 16409643
2015 Oct4P4 lncRNA forms a complex with SUV39H1 to direct H3K9me3 and HP1α to the promoter of the ancestral Oct4 gene, leading to gene silencing and reduced mESC self-renewal; the lncRNA provides targeting specificity for SUV39H1-mediated silencing. RNA immunoprecipitation; ChIP; lncRNA overexpression/knockdown; mESC differentiation assay Nature communications High 26158551
2019 CIITA interacts with and enlists SUV39H1 to the eNOS promoter in response to IFN-γ; IFN-γ augments SUV39H1 expression and promotes H3K9me3 deposition at the eNOS promoter; silencing of SUV39H1 abrogates IFN-γ-induced eNOS repression. Co-IP; ChIP; SUV39H1 siRNA; reporter assay Biochimica et biophysica acta. Gene regulatory mechanisms Medium 30716531
2020 HPV E7 oncoprotein upregulates SUV39H1, which then promotes H3K9me3-mediated epigenetic silencing at the promoters of innate immune sensor genes RIG-I, cGAS, and STING; pharmacological or genetic inhibition of SUV39H1 restores innate immune gene expression and IFN-β/λ1 production. ChIP; SUV39H1 siRNA/inhibitor (chaetocin); qRT-PCR; ELISA for IFN Journal of virology High 31776268
2018 SUV39H1/DNMT3A cooperatively methylate the RB1 promoter (H3K9me3 facilitating CpG methylation via interaction between SUV39H1 and DNMT3A); reduced RB abundance impairs E2F1 inhibition, leading to increased PIN1 and melanoma tumorigenesis via RAF1-MEK-ERK signaling. Co-IP (SUV39H1-DNMT3A); ChIP; siRNA knockdown; xenograft model FASEB journal Medium 29750576
2024 Genetic disruption of SUV39H1 in CAR T cells enhances early expansion, long-term persistence, and antitumor efficacy; persisting SUV39H1-edited CAR T cells show improved expression and chromatin accessibility of memory transcription factors, reduced inhibitory receptor expression, and limited exhaustion upon multiple tumor rechallenges. CRISPR-mediated SUV39H1 knockout in CAR T cells; scRNA-seq; scATAC-seq; in vivo tumor rechallenge models Cancer discovery High 37934001 37934007
2024 Suv39h1 binds to the HMOX1 (heme oxygenase 1) promoter and represses its transcription in hepatic stellate cells; Suv39h1 inhibition or HSC/myofibroblast-specific deletion of Suv39h1 ameliorates liver fibrosis; HMOX1 depletion blunts the effects of Suv39h1 inhibition on HSC-myofibroblast transition. ChIP; conditional KO mouse (Lrat-Cre and Postn-CreERT2); chaetocin pharmacological inhibition; in vitro and in vivo fibrosis models Gut High 38176898

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2001 Loss of the Suv39h histone methyltransferases impairs mammalian heterochromatin and genome stability. Cell 1400 11701123
2003 Suv39h-mediated histone H3 lysine 9 methylation directs DNA methylation to major satellite repeats at pericentric heterochromatin. Current biology : CB 952 12867029
2003 The DNA methyltransferases associate with HP1 and the SUV39H1 histone methyltransferase. Nucleic acids research 571 12711675
2003 Epigenetic regulation of telomere length in mammalian cells by the Suv39h1 and Suv39h2 histone methyltransferases. Nature genetics 440 14702045
2007 SIRT1 regulates the histone methyl-transferase SUV39H1 during heterochromatin formation. Nature 357 18004385
2008 PRC1 and Suv39h specify parental asymmetry at constitutive heterochromatin in early mouse embryos. Nature genetics 275 18311137
2010 A subset of the histone H3 lysine 9 methyltransferases Suv39h1, G9a, GLP, and SETDB1 participate in a multimeric complex. Molecular cell 269 20129054
2007 Suv39H1 and HP1gamma are responsible for chromatin-mediated HIV-1 transcriptional silencing and post-integration latency. The EMBO journal 264 17245432
2014 Suv39h-dependent H3K9me3 marks intact retrotransposons and silences LINE elements in mouse embryonic stem cells. Molecular cell 257 24981170
2003 Methyl-CpG binding domain 1 (MBD1) interacts with the Suv39h1-HP1 heterochromatic complex for DNA methylation-based transcriptional repression. The Journal of biological chemistry 209 12711603
2012 Interaction with Suv39H1 is critical for Snail-mediated E-cadherin repression in breast cancer. Oncogene 169 22562246
2004 A Suv39h-dependent mechanism for silencing S-phase genes in differentiating but not in cycling cells. The EMBO journal 167 14765126
2000 Structure-function analysis of SUV39H1 reveals a dominant role in heterochromatin organization, chromosome segregation, and mitotic progression. Molecular and cellular biology 166 10779362
2017 Major satellite repeat RNA stabilize heterochromatin retention of Suv39h enzymes by RNA-nucleosome association and RNA:DNA hybrid formation. eLife 147 28760199
2002 Functional and physical interaction between the histone methyl transferase Suv39H1 and histone deacetylases. Nucleic acids research 136 11788710
2017 RNA-dependent stabilization of SUV39H1 at constitutive heterochromatin. eLife 135 28760200
2006 Zebra fish Dnmt1 and Suv39h1 regulate organ-specific terminal differentiation during development. Molecular and cellular biology 126 16980612
2013 Depleting the methyltransferase Suv39h1 improves DNA repair and extends lifespan in a progeria mouse model. Nature communications 120 23695662
2011 Stabilization of Suv39H1 by SirT1 is part of oxidative stress response and ensures genome protection. Molecular cell 116 21504832
2008 Gestational choline supply regulates methylation of histone H3, expression of histone methyltransferases G9a (Kmt1c) and Suv39h1 (Kmt1a), and DNA methylation of their genes in rat fetal liver and brain. The Journal of biological chemistry 106 19001366
2006 Histone methyltransferase Suv39h1 represses MyoD-stimulated myogenic differentiation. The EMBO journal 104 16858404
2009 p21(WAF1) gene promoter is epigenetically silenced by CTIP2 and SUV39H1. Oncogene 101 19581932
2000 Mitotic phosphorylation of SUV39H1, a novel component of active centromeres, coincides with transient accumulation at mammalian centromeres. Journal of cell science 100 10671371
2013 CRL4B promotes tumorigenesis by coordinating with SUV39H1/HP1/DNMT3A in DNA methylation-based epigenetic silencing. Oncogene 99 24292684
2010 Ring1B and Suv39h1 delineate distinct chromatin states at bivalent genes during early mouse lineage commitment. Development (Cambridge, England) 94 20573702
2009 Reexpression of epigenetically silenced AML tumor suppressor genes by SUV39H1 inhibition. Oncogene 93 19881540
2013 Methylation of SUV39H1 by SET7/9 results in heterochromatin relaxation and genome instability. Proceedings of the National Academy of Sciences of the United States of America 91 23509280
2000 Set domain-dependent regulation of transcriptional silencing and growth control by SUV39H1, a mammalian ortholog of Drosophila Su(var)3-9. Molecular and cellular biology 90 10848615
2016 A two-state activation mechanism controls the histone methyltransferase Suv39h1. Nature chemical biology 89 26807716
2015 Epigenetic silencing of Oct4 by a complex containing SUV39H1 and Oct4 pseudogene lncRNA. Nature communications 88 26158551
2014 Histone lysine methyltransferase SUV39H1 is a potent target for epigenetic therapy of hepatocellular carcinoma. International journal of cancer 88 24844570
2003 Self-interaction of heterochromatin protein 1 is required for direct binding to histone methyltransferase, SUV39H1. Biochemical and biophysical research communications 88 12565857
2017 The histone H3K9 methyltransferase SUV39H links SIRT1 repression to myocardial infarction. Nature communications 86 28361889
2016 Age-Associated Decrease of the Histone Methyltransferase SUV39H1 in HSC Perturbs Heterochromatin and B Lymphoid Differentiation. Stem cell reports 85 27304919
2017 Impact of nucleic acid and methylated H3K9 binding activities of Suv39h1 on its heterochromatin assembly. eLife 80 28760201
2020 SUV39H1 deficiency suppresses clear cell renal cell carcinoma growth by inducing ferroptosis. Acta pharmaceutica Sinica. B 79 33643820
2018 ALDH2 protects against high fat diet-induced obesity cardiomyopathy and defective autophagy: role of CaM kinase II, histone H3K9 methyltransferase SUV39H, Sirt1, and PGC-1α deacetylation. International journal of obesity (2005) 79 29535452
2016 KAT7/HBO1/MYST2 Regulates CENP-A Chromatin Assembly by Antagonizing Suv39h1-Mediated Centromere Inactivation. Developmental cell 79 27270040
2009 Inhibition of SUV39H1 methyltransferase activity by DBC1. The Journal of biological chemistry 77 19218236
2015 The SUV39H1 inhibitor chaetocin induces differentiation and shows synergistic cytotoxicity with other epigenetic drugs in acute myeloid leukemia cells. Blood cancer journal 76 25978433
2002 Selective interactions between vertebrate polycomb homologs and the SUV39H1 histone lysine methyltransferase suggest that histone H3-K9 methylation contributes to chromosomal targeting of Polycomb group proteins. Molecular and cellular biology 75 12101246
2010 RFX1 regulates CD70 and CD11a expression in lupus T cells by recruiting the histone methyltransferase SUV39H1. Arthritis research & therapy 67 21192791
2018 DCAF13 promotes pluripotency by negatively regulating SUV39H1 stability during early embryonic development. The EMBO journal 65 30111536
2024 Disruption of SUV39H1-Mediated H3K9 Methylation Sustains CAR T-cell Function. Cancer discovery 64 37934007
2009 EVI-1 interacts with histone methyltransferases SUV39H1 and G9a for transcriptional repression and bone marrow immortalization. Leukemia 64 19776757
2005 A glue for heterochromatin maintenance: stable SUV39H1 binding to heterochromatin is reinforced by the SET domain. The Journal of cell biology 63 16103223
2018 Automethylation-induced conformational switch in Clr4 (Suv39h) maintains epigenetic stability. Nature 62 30051891
2012 Crystal structure of the human SUV39H1 chromodomain and its recognition of histone H3K9me2/3. PloS one 62 23285239
2020 Human Papillomavirus E7 Oncoprotein Subverts Host Innate Immunity via SUV39H1-Mediated Epigenetic Silencing of Immune Sensor Genes. Journal of virology 61 31776268
2006 RUNX1 associates with histone deacetylases and SUV39H1 to repress transcription. Oncogene 61 16652147
2003 SUV39H1 interacts with AML1 and abrogates AML1 transactivity. AML1 is methylated in vivo. Oncogene 60 12917624
2019 Interplay among H3K9-editing enzymes SUV39H1, JMJD2C and SRC-1 drives p66Shc transcription and vascular oxidative stress in obesity. European heart journal 58 29077881
2011 Anti-leukemia activity of chaetocin via death receptor-dependent apoptosis and dual modulation of the histone methyl-transferase SUV39H1. Leukemia 57 21979880
2017 The KMT1A-GATA3-STAT3 Circuit Is a Novel Self-Renewal Signaling of Human Bladder Cancer Stem Cells. Clinical cancer research : an official journal of the American Association for Cancer Research 53 28765327
2011 Genetic examination of SETD7 and SUV39H1/H2 methyltransferases and the risk of diabetes complications in patients with type 1 diabetes. Diabetes 53 21896933
2007 The Suv39h-HP1 histone methylation pathway is dispensable for enrichment and protection of cohesin at centromeres in mammalian cells. Chromosoma 53 18075750
2019 SUV39H1 Represses the Expression of Cytotoxic T-Lymphocyte Effector Genes to Promote Colon Tumor Immune Evasion. Cancer immunology research 52 30610059
2019 IFI16, a nuclear innate immune DNA sensor, mediates epigenetic silencing of herpesvirus genomes by its association with H3K9 methyltransferases SUV39H1 and GLP. eLife 50 31682228
2018 SIRT6-dependent cysteine monoubiquitination in the PRE-SET domain of Suv39h1 regulates the NF-κB pathway. Nature communications 50 29317652
2001 Over-expression of the SUV39H1 histone methyltransferase induces altered proliferation and differentiation in transgenic mice. Mechanisms of development 49 11520670
2008 A novel interaction between the proto-oncogene Evi1 and histone methyltransferases, SUV39H1 and G9a. FEBS letters 46 18619962
2019 Class II transactivator (CIITA) mediates IFN-γ induced eNOS repression by enlisting SUV39H1. Biochimica et biophysica acta. Gene regulatory mechanisms 45 30716531
2016 USP7 Enforces Heterochromatinization of p53 Target Promoters by Protecting SUV39H1 from MDM2-Mediated Degradation. Cell reports 45 26971997
2008 EVI1 recruits the histone methyltransferase SUV39H1 for transcription repression. Journal of cellular biochemistry 45 18655152
2019 Alpinetin improves intestinal barrier homeostasis via regulating AhR/suv39h1/TSC2/mTORC1/autophagy pathway. Toxicology and applied pharmacology 43 31676321
2017 Metformin inhibits SUV39H1-mediated migration of prostate cancer cells. Oncogenesis 43 28459432
2011 Epigenetic regulation of surfactant protein A gene (SP-A) expression in fetal lung reveals a critical role for Suv39h methyltransferases during development and hypoxia. Molecular and cellular biology 43 21402781
2024 SUV39H1 Ablation Enhances Long-term CAR T Function in Solid Tumors. Cancer discovery 42 37934001
2015 Inhibition of histone methyltransferases SUV39H1 and G9a leads to neuroprotection in an in vitro model of cerebral ischemia. Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism 42 25966950
2022 CD8+T cell responsiveness to anti-PD-1 is epigenetically regulated by Suv39h1 in melanomas. Nature communications 41 35768432
2014 Suv39h1 mediates AP-2α-dependent inhibition of C/EBPα expression during adipogenesis. Molecular and cellular biology 41 24732798
2021 Structure, Activity and Function of the Suv39h1 and Suv39h2 Protein Lysine Methyltransferases. Life (Basel, Switzerland) 39 34357075
2016 Survival in Quiescence Requires the Euchromatic Deployment of Clr4/SUV39H by Argonaute-Associated Small RNAs. Molecular cell 39 27984744
2016 Histone H2AK119 and H2BK120 mono-ubiquitination modulate SET7/9 and SUV39H1 in type 1 diabetes-induced renal fibrosis. The Biochemical journal 38 27582499
2020 SUV39H1-DNMT3A-mediated epigenetic regulation of Tim-3 and galectin-9 in the cervical cancer. Cancer cell international 36 32699524
2014 A role for SUV39H1-mediated H3K9 trimethylation in the control of genome stability and senescence in WI38 human diploid lung fibroblasts. Aging 36 25063769
2012 SUV39H1 orchestrates temporal dynamics of centromeric methylation essential for faithful chromosome segregation in mitosis. Journal of molecular cell biology 36 22831836
2020 CD74 knockout protects against LPS-induced myocardial contractile dysfunction through AMPK-Skp2-SUV39H1-mediated demethylation of BCLB. British journal of pharmacology 35 31877229
2011 Hydrogen peroxide induces Sp1 methylation and thereby suppresses cyclin B1 via recruitment of Suv39H1 and HDAC1 in cancer cells. Free radical biology & medicine 35 22036763
2006 SUV39H1 interacts with HTLV-1 Tax and abrogates Tax transactivation of HTLV-1 LTR. Retrovirology 35 16409643
2020 SUV39H1 regulates human colon carcinoma apoptosis and cell cycle to promote tumor growth. Cancer letters 34 32061753
2022 LncRNA HOTAIR promotes the proliferation and invasion/metastasis of breast cancer cells by targeting the miR-130a-3p/Suv39H1 axis. Biochemistry and biophysics reports 32 35619625
2018 SUV39H1/DNMT3A-dependent methylation of the RB1 promoter stimulates PIN1 expression and melanoma development. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 32 29750576
2016 The methyltransferase Suv39h1 links the SUMO pathway to HP1α marking at pericentric heterochromatin. Nature communications 32 27426629
2013 Prolyl isomerase Pin1 negatively regulates the stability of SUV39H1 to promote tumorigenesis in breast cancer. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 32 23934277
2006 The histone methyltransferase Suv39h1 increases class switch recombination specifically to IgA. Journal of immunology (Baltimore, Md. : 1950) 32 16818776
2016 ThPOK represses CXXC5, which induces methylation of histone H3 lysine 9 in Cd40lg promoter by association with SUV39H1: implications in repression of CD40L expression in CD8+ cytotoxic T cells. Journal of leukocyte biology 31 26896487
2014 Aberrant histone methylation and the effect of Suv39H1 siRNA on gastric carcinoma. Oncology reports 31 24737085
2007 Post-translational modifications of histones H3 and H4 associated with the histone methyltransferases Suv39h1 and G9a. Genome biology 31 18096052
2020 SUV39H1 regulates the progression of MLL-AF9-induced acute myeloid leukemia. Oncogene 30 33037410
2018 Functional Role of SUV39H1 in Human Renal Tubular Epithelial Cells Under High-glucose Ambiance. Inflammation 30 28852907
2018 Epigenetic silenced miR-125a-5p could be self-activated through targeting Suv39H1 in gastric cancer. Journal of cellular and molecular medicine 30 30117667
2017 The SUV39H1 Protein Lysine Methyltransferase Methylates Chromatin Proteins Involved in Heterochromatin Formation and VDJ Recombination. ACS chemical biology 30 28169523
2013 The histone methyltransferase SUV39H1 suppresses embryonal rhabdomyosarcoma formation in zebrafish. PloS one 30 23705022
2011 Histone methyltransferase KMT1A restrains entry of alveolar rhabdomyosarcoma cells into a myogenic differentiated state. Cancer research 30 21493592
2006 Cabin1 represses MEF2 transcriptional activity by association with a methyltransferase, SUV39H1. The Journal of biological chemistry 30 17172641
2017 Histone methyltransferase SUV39H1 participates in host defense by methylating mycobacterial histone-like protein HupB. The EMBO journal 28 29170282
2014 CDK2-dependent phosphorylation of Suv39H1 is involved in control of heterochromatin replication during cell cycle progression. Nucleic acids research 28 24728993
2012 H3K9 trimethylation precedes DNA methylation during sheep oogenesis: HDAC1, SUV39H1, G9a, HP1, and Dnmts are involved in these epigenetic events. The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society 26 23019017
2024 Histone methyltransferase Suv39h1 regulates hepatic stellate cell activation and is targetable in liver fibrosis. Gut 22 38176898