Affinage

SUV39H2

Histone-lysine N-methyltransferase SUV39H2 · UniProt Q9H5I1

Length
410 aa
Mass
46.7 kDa
Annotated
2026-06-10
42 papers in source corpus 21 papers cited in narrative 23 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

SUV39H2 (KMT1B) is a SET domain histone methyltransferase that establishes and maintains H3K9 di- and trimethylation at heterochromatin, where these marks recruit HP1 proteins and govern chromatin compaction and genome stability (PMID:11094092, PMID:14702045). The enzyme reads a long H3 substrate motif spanning residues T6–K14, with strict dependence on R8, S10, T11 and G12; it prefers unmodified H3K9 and adds the first two methyl groups processively while trimethylation proceeds slowly, and catalytic competence requires an intact SET-domain active site (PMID:25459750). At telomeric heterochromatin SUV39H1/H2 loss collapses H3K9me2/me3 into H3K9me1, abolishes HP1 (Cbx1/3/5) binding, and deregulates telomere length (PMID:14702045); in embryonic stem cells the H3K9me3 it deposits sustains HP1 occupancy that gates pioneer-factor access and exit from pluripotency. SUV39H2 acts as a transcriptional repressor by trimethylating H3K9 at defined promoters, silencing SLIT1 in colorectal cancer (PMID:29458143), SIRT1 and PPARγ in liver and macrophages (PMID:28244120, PMID:28232186), Vnn1 in hepatocytes (PMID:38401627), DUSP6 in gastric cancer (PMID:36806557), and the protocadherin-β (Pcdhb) cluster in developing brain (PMID:34262135). Beyond histones it methylates non-histone substrates: trimethylation of LSD1-K322 blocks LSD1 polyubiquitination and stabilizes the protein (PMID:26183527), and mono-methylation of PPP1CA-K141 disrupts its interaction with TFEB to impair autophagy (PMID:37605006). SUV39H2 activity is constrained by autoregulatory automethylation at K392, which weakens substrate binding (PMID:26988914), and is tuned by alternative splicing of exon 3, which alters stability, localization, and activity (PMID:25605796). Through promoter H3K9 trimethylation SUV39H2 controls cell-fate programs in epidermal stem/progenitor maintenance via the Wnt/p63/adhesion axis (PMID:33604655), trophoblast stem-cell self-renewal downstream of CDX2 (PMID:33556426), and adult hippocampal neuronal differentiation (PMID:35096813). A catalytically inactivating SET-domain mutation (N324K) causes hereditary nasal parakeratosis in dogs (PMID:24098150), and a loss-of-function variant (A211S) with reduced methyltransferase activity is associated with autism-spectrum disorder, modeled by behavioral and Pcdhb-derepression phenotypes in Suv39h2 knockout mice (PMID:34262135).

Mechanistic history

Synthesis pass · year-by-year structured walk · 16 steps
  1. 2000 High

    Established that Suv39h2 is a distinct H3K9-selective methyltransferase enriched at heterochromatin and the meiotic XY body, defining its catalytic identity and chromatin compartment.

    Evidence In vitro HMTase assay and immunolocalization during spermatogenesis, FISH mapping

    PMID:11094092

    Open questions at the time
    • Functional consequence of XY-body localization for meiotic silencing not tested
    • Distinction of Suv39h2-specific from Suv39h1-redundant roles unresolved
  2. 2003 High

    Showed that Suv39h1/h2 generate H3K9me2/me3 at telomeres to recruit HP1 and constrain telomere length, linking the enzyme to heterochromatin integrity.

    Evidence Reciprocal ChIP in SUV39DN double-knockout primary cells plus telomere length analysis

    PMID:14702045

    Open questions at the time
    • Cannot separate Suv39h2 from Suv39h1 contribution
    • Mechanism linking H3K9me loss to telomere elongation not defined
  3. 2014 High

    Defined the substrate readout and kinetic mechanism of methyl transfer, explaining how SUV39H2 achieves specificity and how a disease mutation abolishes activity.

    Evidence Peptide SPOT arrays, kinetic in vitro methylation, active-site mutagenesis, circular dichroism

    PMID:25459750

    Open questions at the time
    • Structural basis of T6–K14 motif recognition not solved
    • Crosstalk with S10/T11 phosphorylation in vivo not addressed
  4. 2013 Medium

    Linked SUV39H2 catalytic loss to a Mendelian skin-differentiation disease, implicating H3K9 methylation in keratinocyte terminal differentiation.

    Evidence GWAS, whole-genome sequencing, large cohort genotyping, epidermal histopathology in Labrador Retrievers

    PMID:24098150

    Open questions at the time
    • Target loci controlling differentiation not identified in this study
    • Mechanism inferred from histopathology rather than chromatin assays
  5. 2015 Medium

    Extended SUV39H2 function to non-histone methylation, showing that LSD1-K322 trimethylation stabilizes LSD1 against proteasomal degradation.

    Evidence In vitro methylation, co-IP, mass spectrometry, siRNA with protein/mRNA quantification

    PMID:26183527

    Open questions at the time
    • Reciprocal validation and structural detail of K322 methylation absent
    • Downstream LSD1 target effects shown only indirectly
  6. 2015 Medium

    Demonstrated that exon 3 alternative splicing is a regulatory switch controlling SUV39H2 stability, localization, and activity, diversifying its transcriptional output.

    Evidence Isoform RT-PCR, stability/localization/activity assays, genome-wide expression profiling

    PMID:25605796

    Open questions at the time
    • Physiological signals controlling isoform choice unknown
    • Isoform-specific target loci not mapped
  7. 2016 Medium

    Identified an autoregulatory automethylation at K392 that dampens substrate binding, revealing intrinsic negative feedback on the enzyme.

    Evidence In vitro and in-cell automethylation detection, co-IP binding assays

    PMID:26988914

    Open questions at the time
    • Stoichiometry and dynamics of K392 automethylation in vivo unknown
    • Demethylase that reverses the mark not identified
  8. 2016 Medium

    Refuted a proposed H2AX-K134 methylation activity, narrowing the confirmed substrate repertoire of SUV39H2.

    Evidence In vitro methylation with H2AX protein/peptides and functional positive controls

    PMID:27177470

    Open questions at the time
    • Does not exclude context-dependent or cofactor-requiring methylation in cells
    • Single-lab negative result
  9. 2017 Medium

    Showed SUV39H2 directly represses SIRT1 and PPARγ via promoter H3K9me3, linking it to NF-κB-driven inflammation and hepatic steatosis.

    Evidence Promoter ChIP, Suv39h2 knockout mouse NASH/MCD models, expression analysis

    PMID:28232186 PMID:28244120

    Open questions at the time
    • Recruitment mechanism to specific promoters unknown
    • Direct vs secondary effects on NF-κB acetylation not fully separated
  10. 2018 Medium

    Established SUV39H2 as a pro-tumorigenic repressor in cancer through promoter H3K9me3 silencing of SLIT1, validated by functional rescue, and identified small-molecule inhibitors.

    Evidence Promoter ChIP, knockdown/overexpression, in vivo proliferation/metastasis and xenograft assays, in vitro inhibitor characterization

    PMID:29458143 PMID:30159125

    Open questions at the time
    • Inhibitor selectivity over SUV39H1 and other KMTs not fully defined
    • Recruitment to oncogenic target promoters unexplained
  11. 2021 High

    Connected SUV39H2 loss-of-function to ASD through behavioral deficits and Pcdhb-cluster derepression, defining a neurodevelopmental gene-regulatory role.

    Evidence Variant HMTase assay, Suv39h2 KO mouse behavior, H3K9me3 ChIP at Pcdhb promoters, RNA-seq

    PMID:34262135

    Open questions at the time
    • Causal link between Pcdhb derepression and behavior not established
    • Human variant penetrance not assessed
  12. 2021 High

    Defined SUV39H2 as a maintainer of stem/progenitor fate across epidermis, trophoblast, and adult neurogenesis by repressing differentiation- and Wnt-axis loci through H3K9me3.

    Evidence Loss-of-function dog model, cross-species keratinocyte assays, siRNA in trophoblast stem cells, retroviral RNAi and chaetocin in dentate gyrus, locus-specific ChIP

    PMID:33556426 PMID:33604655 PMID:35096813

    Open questions at the time
    • Neurogenesis study cannot fully separate Suv39h1 from Suv39h2
    • Upstream signals deploying SUV39H2 to fate genes incompletely mapped
  13. 2023 Medium

    Showed SUV39H2 mono-methylates PPP1CA-K141 to block TFEB dephosphorylation, coupling the enzyme to autophagy and cellular senescence control.

    Evidence Proteomics, in vitro methylation, co-IP, nuclear translocation and autophagy flux assays, in vivo IVD model

    PMID:37605006

    Open questions at the time
    • Structural basis and stoichiometry of K141 methylation not resolved
    • In vivo relevance beyond IVD model untested
  14. 2023 Medium

    Placed SUV39H2 within an m6A-regulated axis where it silences DUSP6 to enhance ATM-dependent homologous recombination and chemoresistance.

    Evidence MeRIP-seq, RNA stability, DUSP6 promoter ChIP, ATM phosphorylation and HR repair assays, in vivo tumor model

    PMID:36806557

    Open questions at the time
    • Direct mechanism linking DUSP6 repression to ATM activation not detailed
    • Generality beyond gastric cancer unknown
  15. 2025 Medium

    Revealed SUV39H2 as a host antiviral restriction factor that H3K9me3-silences oncolytic HSV-1 promoters, antagonized by ICP0-driven proteasomal degradation.

    Evidence Genome-wide CRISPR screen, viral-promoter ChIP, knockdown/overexpression, inhibitor in vitro/in vivo, proteasome inhibition

    PMID:40849299

    Open questions at the time
    • Whether SUV39H2 restricts other viruses untested
    • Recruitment to viral promoters not mechanistically defined
  16. 2025 Low

    Probed SUV39H2 contribution to centromeric H3K9me3 completion and constraint of CENP-A spreading, refining the heterochromatin-enzyme division of labor.

    Evidence siRNA/CRISPRi depletion of SUV39H1/2 and SETDB1, H3K9me ChIP-seq, CENP-A localization (preprint)

    Open questions at the time
    • SUV39H2-specific role inferred from combined SUV39H1/2 depletion
    • Preprint, not peer-reviewed

Open questions

Synthesis pass · forward-looking unresolved questions
  • How SUV39H2 is selectively recruited to its diverse genomic and non-histone targets, and what distinguishes its functions from the highly homologous SUV39H1, remain unresolved.
  • No defined targeting/recruitment mechanism for specific promoters
  • No structure of full-length enzyme with substrate
  • Functional non-redundancy with SUV39H1 not systematically delineated

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0016740 transferase activity 4 GO:0140110 transcription regulator activity 4 GO:0140096 catalytic activity, acting on a protein 2 GO:0042393 histone binding 1
Localization
GO:0000228 nuclear chromosome 3 GO:0005634 nucleus 2
Pathway
R-HSA-74160 Gene expression (Transcription) 4 R-HSA-1266738 Developmental Biology 3 R-HSA-4839726 Chromatin organization 3
Partners
CBX1CBX3CBX5LSD1PPP1CAPPP1R9BTFEB

Evidence

Reading pass · 23 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2000 Suv39h2 encodes a histone H3 lysine 9-selective methyltransferase (HMTase) that shares 59% identity with Suv39h1 but differs by the presence of a highly basic N terminus. Immunolocalization during spermatogenesis showed enriched distribution at heterochromatin from leptotene to round spermatid stage, and specific accumulation with sex chromosome chromatin (XY body) undergoing meiotic silencing. In vitro HMTase activity assay, immunolocalization/immunofluorescence during spermatogenesis, FISH chromosomal mapping Molecular and cellular biology High 11094092
2003 Suv39h1 and Suv39h2 govern H3K9 di- and trimethylation at telomeric heterochromatin. Loss of both enzymes (SUV39DN cells) results in reduced di/trimethylated H3K9 and increased monomethylated H3K9 at telomeres, concomitant with reduced binding of HP1 homologs (Cbx1, Cbx3, Cbx5) at telomeres and abnormal telomere elongation. Chromatin immunoprecipitation (ChIP) in SUV39DN double-knockout primary cells, telomere length analysis Nature genetics High 14702045
2014 SUV39H2 recognizes a long substrate motif on histone H3 comprising residues T6–K14, with highly specific readout of R8, S10, T11, and G12. Modification of R8 or phosphorylation of S10/T11 reduces/abolishes activity. The enzyme prefers unmethylated H3K9me0 as substrate over H3K9me1/me2 and introduces the first two methyl groups processively; the trimethylation step is much slower. The N324K missense mutation in the SET domain (causing inherited nasal skin disease in Labrador Retrievers) renders SUV39H2 catalytically inactive and causes slight structural changes detected by circular dichroism. Peptide SPOT array methylation, in vitro methylation assays with SET domain, circular dichroism spectroscopy, active-site mutagenesis Biochimica et biophysica acta High 25459750
2013 A missense variant (c.972T>G, p.N324K) in the catalytically active SET domain of SUV39H2 causes hereditary nasal parakeratosis (HNPK) in Labrador Retrievers with autosomal recessive inheritance. The phenotype reflects delayed terminal differentiation of keratinocytes rather than hyperproliferation, implicating SUV39H2-mediated H3K9 methylation in epigenetic regulation of keratinocyte differentiation. GWAS, whole genome sequencing, cohort genotyping (>500 dogs), histopathological analysis of epidermis PLoS genetics Medium 24098150
2015 SUV39H2 trimethylates LSD1 on lysine 322 (a non-histone substrate). This methylation suppresses LSD1 polyubiquitination and proteasomal degradation, thereby stabilizing LSD1 protein. SUV39H2 knockdown decreases LSD1 protein levels without affecting LSD1 mRNA, and SUV39H2 overexpression indirectly affects LSD1 target gene expression. In vitro methylation assay, co-immunoprecipitation, mass spectrometry, siRNA knockdown with protein and mRNA quantification Oncotarget Medium 26183527
2015 Alternative splicing of SUV39H2 exon 3 is a determinant of protein stability, sub-nuclear localization, and HMTase activity. Inclusion of exon 3 changes SUV39H2 function, and genome-wide expression analysis showed that the two splice isoforms differentially regulate target gene expression. RT-PCR isoform analysis across tissues/cell lines, functional assays (stability, nuclear localization by imaging, HMTase activity assay), genome-wide expression profiling Nucleic acids research Medium 25605796
2016 SUV39H2 undergoes automethylation at lysine 392 both in vitro and in cells. Automethylation impairs SUV39H2 binding affinity to substrate proteins (histone H3 and LSD1), and hyper-automethylated SUV39H2 shows reduced methyltransferase activity toward these substrates. In vitro methylation assay, co-immunoprecipitation binding assays, in-cell automethylation detection Oncotarget Medium 26988914
2016 NEGATIVE FINDING: SUV39H2 (and its homolog SUV39H1) failed to methylate H2AX at K134 or any other lysine in vitro using H2AX protein and peptides under conditions where positive controls were functional. This challenges the prior report that SUV39H2 methylates H2AX-K134 to stimulate γ-H2AX during DNA damage response. In vitro methylation reactions with H2AX protein and peptides, positive control validation FEBS letters Medium 27177470
2017 Suv39h2 binds to the Sirt1 gene promoter in hepatocytes and represses Sirt1 transcription by catalyzing H3K9 trimethylation at that locus. Suv39h2 deficiency normalizes Sirt1 expression, allowing NF-κB/p65 to become hypoacetylated, dampening NF-κB-dependent proinflammatory transcription. In macrophages, Suv39h2-mediated repression of PPARγ transcription favors a proinflammatory M1 phenotype. ChIP assay at Sirt1 promoter, Suv39h2 knockout mouse model (NASH), gene expression analysis, cell culture knockdown/overexpression Hepatology (Baltimore, Md.) Medium 28244120
2017 Suv39h2 represses SIRT1 expression in hepatocytes by stimulating H3K9 trimethylation at the SIRT1 promoter, contributing to steatosis pathogenesis. This was confirmed in a methionine-and-choline deficient diet mouse model where Suv39h2 KO mice showed improved steatosis and upregulated SIRT1. ChIP at SIRT1 promoter, Suv39h2 knockout mouse (MCD diet model), qPCR, histological staining Biochemical and biophysical research communications Medium 28232186
2018 SUV39H2 directly binds to the SLIT1 promoter and suppresses SLIT1 transcription by catalyzing H3K9 trimethylation at that locus in colorectal cancer cells. Rescue assays confirmed SLIT1 can antagonize SUV39H2-driven proliferation and metastasis. ChIP assay at SLIT1 promoter, siRNA knockdown, overexpression, in vitro and in vivo proliferation/metastasis assays, rescue experiments Cancer letters Medium 29458143
2018 A series of imidazo[1,2-a]pyridine compounds inhibit SUV39H2 methyltransferase activity in vitro. The compound OTS193320 decreases global H3K9 trimethylation in breast cancer cells and triggers apoptosis. A further optimized compound OTS186935 inhibits tumor growth in xenograft models (MDA-MB-231 and A549) and reduces γ-H2AX levels when combined with doxorubicin. In vitro methyltransferase inhibition assay, cell viability assay, global H3K9me3 quantification, in vivo xenograft mouse model Oncotarget Medium 30159125
2021 A rare loss-of-function variant A211S in SUV39H2 found in ASD individuals shows strongly reduced H3K9 methyltransferase activity in vitro. Suv39h2 KO mice display hyperactivity and reduced behavioral flexibility. Suv39h2 deficiency causes elevated expression of protocadherin β (Pcdhb) cluster genes in embryonic brain due to loss of H3K9me3 at Pcdhb gene promoters, which persists into adulthood in the cerebellum. In vitro HMTase activity assay of variant protein, Suv39h2 KO mouse behavioral assays, ChIP-seq/ChIP for H3K9me3 at Pcdhb promoters, RNA-seq Molecular psychiatry High 34262135
2021 SUV39H2 maintains epidermal stem and progenitor cells by placing H3K9me3 repressive marks on promoters of genes encoding components of the Wnt/p63/adhesion axis. Loss of SUV39H2 function relieves this repression, causing enhanced Wnt activity that drives premature progenitor cell cycle exit, exhaustion of stem cell growth potential, and compromised epidermal differentiation and genome stability. Spontaneous loss-of-function dog model (monogenic inheritance), pharmacological Wnt activation in primary keratinocytes (canine, human, mouse), H3K9me3 ChIP at specific promoters, cell cycle and differentiation assays The Journal of cell biology High 33604655
2021 SUV39H2 transcript and protein are highly expressed in rat trophoblast stem (TS) cells in the stem state and decline upon differentiation. SUV39H2 knockdown arrests TS cell proliferation and activates trophoblast differentiation. SUV39H2 regulates H3K9 methylation status at loci with differentiation-dependent gene expression. SUV39H2 is a downstream target of caudal type homeobox 2 (CDX2), a master regulator of trophoblast lineage development. Loss-of-function (siRNA) in rat TS cells and ex vivo blastocysts, H3K9 methylation ChIP at specific loci, ChIP for CDX2 at SUV39H2 locus, differentiation marker assays Biochimica et biophysica acta. General subjects Medium 33556426
2021 In the adult hippocampus, Suv39h1 and Suv39h2 are highly expressed at early neurogenic stages and decline upon differentiation. Pharmacological inhibition (chaetocin) reduces H3K9me3 and decreases neuronal differentiation while increasing proliferation of adult hippocampal progenitors. Retrovirus-mediated knockdown of Suv39h1/2 in newborn cells of adult mouse dentate gyrus impairs neuronal differentiation of progenitor cells. Pharmacological inhibition (chaetocin), retrovirus-mediated RNAi in adult mouse dentate gyrus, immunohistochemistry for H3K9me3 and differentiation markers Frontiers in cell and developmental biology Medium 35096813
2021 SUV39H2 positively regulates LSD1 expression, and LSD1 in turn negatively regulates CDH1 (E-cadherin) expression in osteosarcoma. SUV39H2 overexpression or LSD1 overexpression promotes EMT (reduced E-cadherin, upregulated Vimentin and N-cadherin) and migration, effects reversed by CDH1 restoration. Loss- and gain-of-function assays, immunofluorescence for EMT markers, in vivo osteosarcoma mouse model, rescue experiments Cancer cell international Low 33397384
2023 SUV39H2 methylates PPP1CA (protein phosphatase 1 catalytic subunit alpha) at K141 (mono-methylation). This methylation disrupts PPP1CA interaction with TFEB, blocking TFEB dephosphorylation and nuclear translocation, leading to autophagy deficiency and NPC senescence. PPP1R9B (a PP1 regulatory subunit) binds PPP1CA and facilitates TFEB targeting, and this interaction is also disrupted by K141 methylation. Proteomic analysis identified SUV39H2 as the writer of this mark. Proteomic analysis, in vitro methylation assay, co-immunoprecipitation, nuclear translocation assays, autophagy flux assays, cellular senescence assays, in vivo IVD model Cell death and differentiation Medium 37605006
2023 METTL3-mediated m6A modification of SUV39H2 mRNA promotes its stability in an IGF2BP2-dependent manner in gastric cancer cells. SUV39H2 represses DUSP6 transcription via H3K9 trimethylation at the DUSP6 locus, increasing ATM phosphorylation and promoting homologous recombination repair, thereby inhibiting cisplatin sensitivity. m6A-seq/MeRIP, RNA stability assay, ChIP at DUSP6 locus, ATM phosphorylation assays, HR repair assay, siRNA knockdown, in vivo tumor model Cancer letters Medium 36806557
2024 Suv39h2 represses Vanin-1 (Vnn1) transcription in hepatocytes exposed to free fatty acids. Hepatocyte-specific Suv39h2 deletion (Suv39h2f/f × Alb-Cre) de-represses Vanin-1, and Vanin-1 knockdown normalizes lipid accumulation in Suv39h2-null hepatocytes, placing the Suv39h2-Vanin-1 axis in hepatic lipid metabolism. Conditional hepatocyte-specific Suv39h2 KO mouse, RNA-seq, Vanin-1 knockdown rescue assay, lipid accumulation assays Life sciences Medium 38401627
2025 SUV39H2 catalyzes H3K9me3 at viral promoter regions (of ICP0, ICP4, ICP8) of oncolytic HSV-1, repressing viral gene transcription. oHSV-1 infection induces proteasomal degradation of SUV39H2 through viral protein ICP0, relieving this repression and allowing viral replication. CRISPR/Cas9 genome-wide library screen, ChIP at viral promoters, siRNA knockdown and overexpression functional assays, SUV39H2 inhibitor (OTS186935) in vitro/in vivo, proteasomal pathway inhibition Cell death discovery Medium 40849299
2024 In Suv39h2 KO mouse embryonic stem cells, rapid depletion of remaining H3K9me3 KMTs reveals that both passive dilution and active removal contribute to H3K9me3 decay within 12–24 hours. HP1 rapidly dissociates from heterochromatin upon KMT depletion, and a threshold level of HP1 limits pioneer factor binding, chromatin opening, and exit from pluripotency. Engineered Suv39h2 KO ESCs with auxin-inducible degron for remaining KMTs, ChIP-seq for H3K9me3, ATAC-seq, live imaging of HP1 dynamics, time-course experiments bioRxivpreprint Medium
2025 At human centromeres, SUV39H1/2 complete H3K9 trimethylation (while SETDB1 is required for H3K9 dimethylation at core centromeres). Depleting all three enzymes results in aberrantly high H3K9me3 driven by G9a/GLP methyltransferases that promiscuously deposit H3K9me3 within the centromere core, causing CENP-A expansion into pericentromeres. siRNA/CRISPRi depletion of SUV39H1, SUV39H2, and SETDB1; H3K9me ChIP-seq; CENP-A localization assays bioRxivpreprint Low

Source papers

Stage 0 corpus · 42 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2003 Epigenetic regulation of telomere length in mammalian cells by the Suv39h1 and Suv39h2 histone methyltransferases. Nature genetics 440 14702045
2000 Isolation and characterization of Suv39h2, a second histone H3 methyltransferase gene that displays testis-specific expression. Molecular and cellular biology 259 11094092
2017 The histone methyltransferase Suv39h2 contributes to nonalcoholic steatohepatitis in mice. Hepatology (Baltimore, Md.) 53 28244120
2018 SUV39H2 promotes colorectal cancer proliferation and metastasis via tri-methylation of the SLIT1 promoter. Cancer letters 46 29458143
2015 SUV39H2 methylates and stabilizes LSD1 by inhibiting polyubiquitination in human cancer cells. Oncotarget 45 26183527
2014 Activity and specificity of the human SUV39H2 protein lysine methyltransferase. Biochimica et biophysica acta 45 25459750
2021 Structure, Activity and Function of the Suv39h1 and Suv39h2 Protein Lysine Methyltransferases. Life (Basel, Switzerland) 40 34357075
2013 A mutation in the SUV39H2 gene in Labrador Retrievers with hereditary nasal parakeratosis (HNPK) provides insights into the epigenetics of keratinocyte differentiation. PLoS genetics 30 24098150
2015 Alternative splicing regulates the expression of G9A and SUV39H2 methyltransferases, and dramatically changes SUV39H2 functions. Nucleic acids research 29 25605796
2023 Lysine methylation of PPP1CA by the methyltransferase SUV39H2 disrupts TFEB-dependent autophagy and promotes intervertebral disc degeneration. Cell death and differentiation 28 37605006
2023 N6-methyadenosine modified SUV39H2 regulates homologous recombination through epigenetic repression of DUSP6 in gastric cancer. Cancer letters 27 36806557
2020 microRNA-let-7e in serum-derived exosomes inhibits the metastasis of non-small-cell lung cancer in a SUV39H2/LSD1/CDH1-dependent manner. Cancer gene therapy 27 33299140
2019 The Oncogenic Potential of SUV39H2: A Comprehensive and Perspective View. Journal of Cancer 27 30719171
2006 Novel polymorphisms in the SUV39H2 histone methyltransferase and the risk of lung cancer. Carcinogenesis 27 16774942
2018 Identification of SUV39H2 as a potential oncogene in lung adenocarcinoma. Clinical epigenetics 24 30348215
2018 Development of novel SUV39H2 inhibitors that exhibit growth suppressive effects in mouse xenograft models and regulate the phosphorylation of H2AX. Oncotarget 23 30159125
2016 Automethylation of SUV39H2, an oncogenic histone lysine methyltransferase, regulates its binding affinity to substrate proteins. Oncotarget 22 26988914
2021 A loss-of-function variant in SUV39H2 identified in autism-spectrum disorder causes altered H3K9 trimethylation and dysregulation of protocadherin β-cluster genes in the developing brain. Molecular psychiatry 21 34262135
2022 H3K9 Methyltransferases Suv39h1 and Suv39h2 Control the Differentiation of Neural Progenitor Cells in the Adult Hippocampus. Frontiers in cell and developmental biology 19 35096813
2015 Targeting Suppressor of Variegation 3-9 Homologue 2 (SUV39H2) in Acute Lymphoblastic Leukemia (ALL). Translational oncology 18 26500027
2019 Histone methyltransferase SUV39H2 regulates cell growth and chemosensitivity in glioma via regulation of hedgehog signaling. Cancer cell international 17 31636512
2012 Downregulation of histone methyltransferase genes SUV39H1 and SUV39H2 increases telomere length in embryonic stem-like cells and embryonic fibroblasts in pigs. The Journal of reproduction and development 12 23018532
2021 Histone methyltransferase SUV39H2 regulates LSD1-dependent CDH1 expression and promotes epithelial mesenchymal transition of osteosarcoma. Cancer cell international 11 33397384
2021 SUV39H2 epigenetic silencing controls fate conversion of epidermal stem and progenitor cells. The Journal of cell biology 11 33604655
2017 Aberrant levels of SUV39H1 and SUV39H2 methyltransferase are associated with genomic instability in chronic lymphocytic leukemia. Environmental and molecular mutagenesis 10 28833505
2021 SUV39H2 controls trophoblast stem cell fate. Biochimica et biophysica acta. General subjects 9 33556426
2018 Histone methyltransferase SUV39H2 serves oncogenic roles in osteosarcoma. Oncology reports 9 30542727
2016 Investigation of H2AX methylation by the SUV39H2 protein lysine methyltransferase. FEBS letters 9 27177470
2018 A splice site variant in the SUV39H2 gene in Greyhounds with nasal parakeratosis. Animal genetics 8 29423952
2024 Histone methyltransferase SUV39H2 regulates apoptosis and chemosensitivity in prostate cancer through AKT/FOXO signaling pathway. Medical oncology (Northwood, London, England) 7 38170382
2021 SUV39H2/KMT1B Inhibits the cardiomyocyte senescence phenotype by down-regulating BTG2/PC3. Aging 7 34559682
2017 Suv39h2 deficiency ameliorates diet-induced steatosis in mice. Biochemical and biophysical research communications 7 28232186
2017 Reduced Histone H3 Lysine 9 Methylation Contributes to the Pathogenesis of Latent Autoimmune Diabetes in Adults via Regulation of SUV39H2 and KDM4C. Journal of diabetes research 6 28396876
2019 Elevated SUV39H2 attributes to the progression of nasopharyngeal carcinoma via regulation of NRIP1. Biochemical and biophysical research communications 5 30709585
2024 Histone Methyltransferase SUV39H2 Supports Nasopharyngeal Carcinoma Cell Metastasis by Regulation of SIRT1. Environmental toxicology 4 38994737
2024 Ablation of histone methyltransferase Suv39h2 in hepatocytes attenuates NASH in mice. Life sciences 3 38401627
2023 BRD4770 inhibits vascular smooth muscle cell proliferation via SUV39H2, but not EHMT2 to protect against neointima formation. Human cell 3 37306883
2025 CRISPR/Cas9 screening identifies SUV39H2 as a key regulator of oHSV-1 resistance in oral squamous cell carcinoma. Cell death discovery 2 40849299
2026 Role of SUV39H2 in shaping the malignant phenotype of triple-negative breast cancer. Frontiers in oncology 1 41551146
2026 Inhibition of SUV39H1 and SUV39H2 promotes zygotic genome activation and improves the developmental competence of porcine somatic cell nuclear transfer embryos. Theriogenology 0 41638075
2025 SUV39H2 is a vulnerability in glioblastoma stem cells enhanced by co-targeting SUV39H1. Epigenomics 0 41047764
2025 Synthetic lethality from the combination of a histone methyltransferase SUV39H2 inhibitor and a poly (ADP-ribose) polymerase inhibitor for uterine leiomyosarcoma. BMC cancer 0 41402789

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