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Suppressor of variegation 3-9 homolog 1

SUV39H1, Suv39h
This gene is a member of the suppressor of variegation 3-9 homolog family and encodes a protein with a chromodomain and a C-terminal SET domain. This nuclear protein moves to the centromeres during mitosis and functions as a histone methyltransferase, methylating Lys-9 of histone H3. Overall, it plays a vital role in heterochromatin organization, chromosome segregation, and mitotic progression. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: Histone, Haptoglobin, CAN, G9a, SET
Papers using SUV39H1 antibodies
SMART
Supplier
Kashanchi Fatah et al., In Retrovirology, 1991
... Anti-ESET(SETDB1) and anti-SUV39H1 antibodies were purchased from Cell Signaling (Danvers, MA) ...
Papers on SUV39H1
IL-4 Inhibits the Biogenesis of an Epigenetically Suppressive PIWI-Interacting RNA To Upregulate CD1a Molecules on Monocytes/Dendritic Cells.
New
Zhang et al., Guangzhou, China. In J Immunol, Feb 2016
Further, we revealed that the td-piR(Glu)/PIWIL4 complex recruited SETDB1, SUV39H1, and heterochromatin protein 1β to the CD1A promoter region and facilitated H3K9 methylation.
Control of genetic stability by a new heterochromatin compaction pathway involving the Tip60 histone acetyltransferase.
New
Escaffit et al., Toulouse, France. In Mol Biol Cell, Jan 2016
In mammals, it relies on methylation of histone H3K9 by Suv39H enzymes, which provides a docking site for HP1 proteins, therefore mediating heterochromatin compaction.
Conserved factor Dhp1/Rat1/Xrn2 triggers premature transcription termination and nucleates heterochromatin to promote gene silencing.
New
Grewal et al., Bethesda, United States. In Proc Natl Acad Sci U S A, Jan 2016
Remarkably, our results reveal that Dhp1 interacts with the Clr4/Suv39h methyltransferase complex and acts directly to nucleate heterochromatin.
Cancer-predisposition gene KLLN maintains pericentric H3K9 trimethylation protecting genomic stability.
New
Eng et al., Cleveland, United States. In Nucleic Acids Res, Jan 2016
Interestingly, we show that KLLN interacts with DBC1, with consequent abrogation of DBC1 inhibition of SUV39H1, a H3K9 methyltransferase, suggesting the mode of KLLN regulating H3K9me3.
Histone acetylation and methylation significantly change with severity of atherosclerosis in human carotid plaques.
New
Pelisek et al., München, Germany. In Cardiovasc Pathol, Dec 2015
The expression of histone acetyltransferases (GNAT group: GCN5L, P300/CBP group: P300, MYST group: MYST1 and MYST2) and histone methyltransferases (H3K4: MLL2/4, SET7/9, and hSET1A; H3K9: SUV39H1, SUV39H2, ESET/SETDB1, and EHMT1; H3K27: EZH2 and G9a) was analyzed by SYBR-green-based real-time polymerase chain reaction.
The Daxx/Atrx Complex Protects Tandem Repetitive Elements during DNA Hypomethylation by Promoting H3K9 Trimethylation.
New
Impact
Songyang et al., Guangzhou, China. In Cell Stem Cell, Oct 2015
Mechanistically, Daxx/Atrx-mediated repression seems to involve Suv39h recruitment and H3K9 trimethylation.
Stem Cell Depletion by Global Disorganization of the H3K9me3 Epigenetic Marker in Aging.
Review
New
Larrick et al., Sunnyvale, United States. In Rejuvenation Res, Aug 2015
Although WRN plays a role in DNA repair, WRN exerted its effects on aging via maintaining heterochromatin, evidenced by reduced levels of interacting chromatin regulators heterochromatin protein 1α (HP1α), suppressor of variegation 3-9 homolog 1 (SUV39H1), and lamina-associated polypeptide 2β (LAP2β) as well as modified histone H3K9me3.
Aging stem cells. A Werner syndrome stem cell model unveils heterochromatin alterations as a driver of human aging.
New
Impact
Belmonte et al., Beijing, China. In Science, Jul 2015
We show that WRN associates with heterochromatin proteins SUV39H1 and HP1α and nuclear lamina-heterochromatin anchoring protein LAP2β.
Epigenetics. Epigenetic inheritance uncoupled from sequence-specific recruitment.
New
Impact
Moazed et al., Boston, United States. In Science, May 2015
The putative JmjC domain H3K9 demethylase, Epe1, and the chromodomain of the H3K9 methyltransferase, Clr4/Suv39h, play opposing roles in maintaining silent H3K9me domains.
DOT1L inhibits SIRT1-mediated epigenetic silencing to maintain leukemic gene expression in MLL-rearranged leukemia.
New
Impact
Armstrong et al., New York City, United States. In Nat Med, Apr 2015
DOT1L inhibits chromatin localization of a repressive complex composed of SIRT1 and the H3K9 methyltransferase SUV39H1, thereby maintaining an open chromatin state with elevated H3K9 acetylation and minimal H3K9 methylation at MLL fusion target genes.
Multiple endocrine neoplasia type 1 (MEN1) and type 4 (MEN4).
Review
Thakker, Oxford, United Kingdom. In Mol Cell Endocrinol, 2014
Thus, menin by forming a subunit of the mixed lineage leukemia (MLL) complexes that trimethylate histone H3 at lysine 4 (H3K4), facilitates activation of transcriptional activity in target genes such as cyclin-dependent kinase (CDK) inhibitors; and by interacting with the suppressor of variegation 3-9 homolog family protein (SUV39H1) to mediate H3K methylation, thereby silencing transcriptional activity of target genes.
Epigenetic regulation of EMT: the Snail story.
Review
Zhou et al., Lexington, United States. In Curr Pharm Des, 2013
Histone deacetylation may promote subsequent recruitment of PRC2 to methylate H3K27, while H3K4 demethylation favors the association of H3K9 methyltransferases G9a and Suv39H1.
Prdm3 and Prdm16 are H3K9me1 methyltransferases required for mammalian heterochromatin integrity.
Impact
Jenuwein et al., Freiburg, Germany. In Cell, 2012
Although the Suv39h methyltransferases (KMTs) are known to ensure pericentric H3K9me3 methylation, the mechanisms that initiate and maintain mammalian heterochromatin organization remain elusive.
[Epigenetic regulation of histone H3 lysine 9 methylation in leukemia].
Review
Ma et al., Zhangzhou, China. In Zhongguo Shi Yan Xue Ye Xue Za Zhi, 2012
SUV39H1, the first described histone H3 lysine 9 methyltransferase takes part in heterochromatin formation and gene transcription regulation.
Hydrogen peroxide induces Sp1 methylation and thereby suppresses cyclin B1 via recruitment of Suv39H1 and HDAC1 in cancer cells.
GeneRIF
Hung et al., Tainan City, Taiwan. In Free Radic Biol Med, 2012
The methylation of Sp1 increased the recruitment of Su(var) 3-9 homologue 1(Suv39H1)to the cyclin B1 promoter, resulting in deacetylation and methylation of histone H3 and subsequent downregulation of cyclin B1.
Epigenetic and epigenomic mechanisms shape sarcoma and other mesenchymal tumor pathogenesis.
Review
Bennani-Baiti, Vienna, Austria. In Epigenomics, 2011
The epigenetic activities of histone-modifying and chromatin-remodeling enzymes such as SUV39H1/KMT1A, EZH2/KMT6A and BMI1 are central to epigenetic-regulated transformation, a property we coin oncoepigenic.
Genetic examination of SETD7 and SUV39H1/H2 methyltransferases and the risk of diabetes complications in patients with type 1 diabetes.
GeneRIF
FinnDiane Study Group et al., Helsinki, Finland. In Diabetes, 2011
genetic association studies in a Finnish population with type I diabetes: No associations were found between SNPs in SUV39H1 and the diabetic complications studied.
Histone 3 lysine 9 (H3K9) methyltransferase recruitment to the interleukin-2 (IL-2) promoter is a mechanism of suppression of IL-2 transcription by the transforming growth factor-β-Smad pathway.
GeneRIF
Yoshimura et al., Tokyo, Japan. In J Biol Chem, 2011
Smads recruit H3K9 methyltransferases Suv39h1 to the IL-2 promoter, thereby inducing suppressive histone methylation and inhibiting T cell receptor-mediated IL-2 transcription.
Epigenetic regulation of surfactant protein A gene (SP-A) expression in fetal lung reveals a critical role for Suv39h methyltransferases during development and hypoxia.
GeneRIF
Mendelson et al., Dallas, United States. In Mol Cell Biol, 2011
findings suggest that Suv39H1 and Suv39H2 are key hypoxia-induced methyltransferases; their decline in fetal lung during late gestation is critical for epigenetic changes resulting in the developmental induction of SP-A
Stabilization of Suv39H1 by SirT1 is part of oxidative stress response and ensures genome protection.
GeneRIF
Vaquero et al., Barcelona, Spain. In Mol Cell, 2011
SirT1 preserves heterochromatin structure: it modulates Suv39h1 protein levels in stress conditions by preventing MDM2-mediated polyubiquitination at K87.
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