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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

SET domain, bifurcated 1

SETDB1, ESET
This gene encodes a histone methyltransferase which regulates histone methylation, gene silencing, and transcriptional repression. This gene has been identified as a target for treatment in Huntington Disease, given that gene silencing and transcription dysfunction likely play a role in the disease pathogenesis. Alternatively spliced transcript variants of this gene have been described.[provided by RefSeq, Jun 2011] (from NCBI)
Top mentioned proteins: Histone, SET, V1a, CAN, TIF1beta
Papers on SETDB1
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.
H3K4/H3K9me3 Bivalent Chromatin Domains Targeted by Lineage-Specific DNA Methylation Pauses Adipocyte Differentiation.
New
Sakai et al., Tokyo, Japan. In Mol Cell, Dec 2015
We show lineage-specific gene-body DNA methylation recruits H3K9 methyltransferase SETDB1, which methylates H3K9 immediately downstream of transcription start sites marked with H3K4me3 to establish the bivalent domain.
Left-Right Axis Differentiation and Functional Lateralization: a Haplotype in the Methyltransferase Encoding Gene SETDB2 Might Mediate Handedness in Healthy Adults.
New
Akkad et al., Bochum, Germany. In Mol Neurobiol, Dec 2015
Here, we investigated the relation of genetic variation in SETDB2-and its paralogue SETDB1-with different handedness phenotypes in 950 healthy adult participants.
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.
Prognostic value of ERCC1, RRM1, BRCA1 and SETDB1 in early stage of non-small cell lung cancer.
New
Carretero et al., Alzira, Spain. In Clin Transl Oncol, Dec 2015
Moreover, SETDB1 has been recently proposed as a bona fide oncogene in lung tumourigenesis and related with metastasis.
Systematic identification of factors for provirus silencing in embryonic stem cells.
New
Impact
Loh et al., Singapore, Singapore. In Cell, Oct 2015
Histone chaperones (Chaf1a/b), sumoylation factors (Sumo2/Ube2i/Sae1/Uba2/Senp6), and chromatin modifiers (Trim28/Eset/Atf7ip) are key determinants that establish provirus silencing.
GENE SILENCING. Epigenetic silencing by the HUSH complex mediates position-effect variegation in human cells.
New
Impact
Lehner et al., Melbourne, Australia. In Science, Jul 2015
Our results suggest that the HUSH complex is recruited to genomic loci rich in H3K9me3, where subsequent recruitment of the methyltransferase SETDB1 is required for further H3K9me3 deposition to maintain transcriptional silencing.
Histone H3.3 is required for endogenous retroviral element silencing in embryonic stem cells.
New
Impact
Banaszynski et al., Cambridge, United Kingdom. In Nature, Jul 2015
Recent studies have demonstrated that a subset of transposable elements, endogenous retroviral elements (ERVs) containing long terminal repeats (LTRs), are silenced through trimethylation of histone H3 on lysine 9 (H3K9me3) by ESET (also known as SETDB1 or KMT1E) and a co-repressor complex containing KRAB-associated protein 1 (KAP1; also known as TRIM28) in mouse embryonic stem cells.
SETDB1 in Early Embryos and Embryonic Stem Cells.
Review
Kang, Taejŏn, South Korea. In Curr Issues Mol Biol, 2014
The histone methyltransferase SETDB1 contributes to the silencing of local chromatin and the target specificity appears to be determined through various proteins that SETDB1 interacts with.
An epigenetic regulator: methyl-CpG-binding domain protein 1 (MBD1).
Review
Chan et al., Hong Kong, Hong Kong. In Int J Mol Sci, 2014
MBD1 acts as an epigenetic regulator via different mechanisms, such as the formation of the MCAF1/MBD1/SETDB1 complex or the MBD1-HDAC3 complex.
On your histone mark, SET, methylate!
Review
Binda, Newcastle, South Africa. In Epigenetics, 2013
Two very interesting examples of this cross-talk between methyl-lysine sites are found in the SET (Su(var)3-9, Enhancer-of-zeste, Trithorax) domain-containing lysine methyltransferases SET7 and SETDB1, whereby the histone H3 trimethylated on lysine 4 (H3K4 (me3) ) modification prevents methylation by SETDB1 on H3 lysine 9 (H3K9) and the histone H3 trimethylated on lysine 9 (H3K9 (me3) ) modification prevents methylation by SET7 on H3K4.
Step-wise methylation of histone H3K9 positions heterochromatin at the nuclear periphery.
Impact
Gasser et al., Basel, Switzerland. In Cell, 2012
The two HMTs target H3K9 in a consecutive fashion: MET-2, a SETDB1 homolog, mediates mono- and dimethylation, and SET-25, a previously uncharacterized HMT, deposits H3K9me3.
Dynamics of Setdb1 expression in early mouse development.
GeneRIF
Kang et al., Taejŏn, South Korea. In Gene Expr Patterns, 2012
Observations highlight the significance of Setdb1 in early mouse development; Setdb1 signals were observed diffusely in the nucleus from the two-cell stage onward and, by the blastocyst, took a punctate form, away from nucleolus.
Epigenetic involvement of Alien/ESET complex in thyroid hormone-mediated repression of E2F1 gene expression and cell proliferation.
GeneRIF
Baniahmad et al., Tianjin, China. In Biochem Biophys Res Commun, 2012
these data indicate that Alien/ESET complex is involved in TRbeta1-mediated transcription repression of E2F1 and provide a molecular basis of thyroid hormone-induced repression of proliferation.
Dual functions of histone-lysine N-methyltransferase Setdb1 protein at promyelocytic leukemia-nuclear body (PML-NB): maintaining PML-NB structure and regulating the expression of its associated genes.
GeneRIF
Kang et al., Taejŏn, South Korea. In J Biol Chem, 2011
Setdb1 performs dual, but inseparable, functions at PML-NBs to maintain the structural integrity of PML-NBs and to control PML-NB-associated genes transcriptionally
Genome-wide association study identifies a new melanoma susceptibility locus at 1q21.3.
Impact
Hayward et al., Brisbane, Australia. In Nat Genet, 2011
locus span a region with ten genes, and plausible candidate genes for melanoma susceptibility include ARNT and SETDB1.
DNA methylation and SETDB1/H3K9me3 regulate predominantly distinct sets of genes, retroelements, and chimeric transcripts in mESCs.
Impact
GeneRIF
Lorincz et al., Vancouver, Canada. In Cell Stem Cell, 2011
The SETDB1 plays a previously unappreciated yet critical role in inhibiting aberrant gene transcription by suppressing the expression of proximal ERVs.
The histone methyltransferase SETDB1 is recurrently amplified in melanoma and accelerates its onset.
Impact
GeneRIF
Zon et al., Boston, United States. In Nature, 2011
studies establish SETDB1 as an oncogene in melanoma and underscore the role of chromatin factors in regulating tumorigenesis
Molecular coupling of DNA methylation and histone methylation.
Review
Cheng et al., Atlanta, United States. In Epigenomics, 2010
The H3K9 methyltransferase SETDB1 contains a putative MBD that potentially links the H3K4 methylation reaction to methylated DNA or may do so through the interaction with the MBD containing protein MBD1.
Wnt and PPARgamma signaling in osteoblastogenesis and adipogenesis.
Review
Kato et al., Tokyo, Japan. In Nat Rev Rheumatol, 2009
Signaling via the canonical Wnt-beta-catenin pathway inhibits PPARgamma mRNA expression, whereas signaling via the noncanonical Wnt pathway results in activation of a histone methyltransferase SETDB1 that represses PPARgamma transactivation through histone H3K9 methylation of target genes.
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