gopubmed logo
find other proteinsAll proteins
GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

SET nuclear oncogene

The protein encoded by this gene inhibits acetylation of nucleosomes, especially histone H4, by histone acetylases (HAT). This inhibition is most likely accomplished by masking histone lysines from being acetylated, and the consequence is to silence HAT-dependent transcription. The encoded protein is part of a complex localized to the endoplasmic reticulum but is found in the nucleus and inhibits apoptosis following attack by cytotoxic T lymphocytes. This protein can also enhance DNA replication of the adenovirus genome. Several transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Oct 2011] (from NCBI)
Top mentioned proteins: Histone, CAN, V1a, HAD, PP2A
Papers on SET
Transition state for the NSD2-catalyzed methylation of histone H3 lysine 36.
Schramm et al., United States. In Proc Natl Acad Sci U S A, Feb 2016
UNASSIGNED: Nuclear receptor SET domain containing protein 2 (NSD2) catalyzes the methylation of histone H3 lysine 36 (H3K36).
Molecular Evolution of the Substrate Specificity of Chloroplastic Aldolases/Rubisco Lysine Methyltransferases in Plants.
Alban et al., Grenoble, France. In Mol Plant, Feb 2016
This study provides insight into mechanisms by which SET-domain protein methyltransferases evolve new substrate specificity.
Molecular characterization and expression regulation of Smyd1a and Smyd1b in skeletal muscle of Chinese perch (Siniperca chuatsi).
Chu et al., Changsha, China. In Comp Biochem Physiol B Biochem Mol Biol, Feb 2016
UNASSIGNED: Smyd1 is a SET and MYND domain-containing protein, which functions as a histone methyltransferase for control of gene expression and regulates the skeletal and cardiac muscle differentiation.
Resetting the epigenome for heart regeneration.
Hudson et al., Brisbane, Australia. In Semin Cell Dev Biol, Feb 2016
BMP, bone morphogenetic protein; Bvht, Braveheart; CBP, CREB-binding protein; Cdkn, cyclin dependent kinase inhibitor; DOT1L, disruptor of telomeric silencing-1; DNMTs, DNA methyltransferases; eRNAs, enhancer RNAs; ESCs, embryonic stem cells; FGF, fibroblast growth factor; FOX, Forkhead box; Gcn5, general control of amino acid synthesis protein 5; HATs, histone acetyl transferases; HDACs, histone deacteylases; H3K27, histone 3, lysine 27; HMTs, histone methyltransferases; Jmj, Jumonji; JMJD3, Jumonji domain-containing protein 3; KDMs, histone lysine demethylases; lncRNAs, long non-coding RNAs; Mhrt, Myheart; miRNAs, microRNAs; Myh, myosin heavy chain; PRC2, polycomb repressive complex 2; PSCs, pluripotent stem cells; PTM, post-translational modification; SIRTs, Sirtuins; SMYD1, SET and MYND domain containing 1; Srf, serum response factor; TET, Ten-eleven translocation; TGF-β, transforming growth factor beta; TFs, transcription factors; UTX, ubiquitously transcribed tetratricopeptide repeat, X chromosome.
Sotos syndrome: An unusual presentation with intrauterine growth restriction, generalized lymphedema, and intention tremor.
Goel et al., Newcastle, Australia. In Am J Med Genet A, Feb 2016
UNASSIGNED: Sotos syndrome is a childhood overgrowth syndrome characterized clinically by a distinctive facial gestalt, advanced bone age, childhood overgrowth, and non-progressive developmental delay; and genetically by haploinsufficiency of the Nuclear receptor binding SET Domain 1 (NSD1) gene.
MMSET is dynamically regulated during cell-cycle progression and promotes normal DNA replication.
Lou et al., Rochester, United States. In Cell Cycle, Feb 2016
Multiple myeloma SET domain-containing protein (MMSET, a.k.a.
Tasimelteon for non-24-hour sleep-wake disorder in totally blind people (SET and RESET): two multicentre, randomised, double-masked, placebo-controlled phase 3 trials.
Polymeropoulos et al., Boston, United States. In Lancet, Dec 2015
In two consecutive placebo-controlled trials (SET and RESET), we assessed safety and efficacy (in terms of circadian entrainment and maintenance) of once-daily tasimelteon, a novel dual-melatonin receptor agonist.
Structural basis of histone H3K27 trimethylation by an active polycomb repressive complex 2.
Liu et al., Dallas, United States. In Science, Nov 2015
Eed is engulfed by a belt-like structure of Ezh2, and Suz12(VEFS) contacts both of these two subunits to confer an unusual split active SET domain for catalysis.
Mutation spectra of histone methyltransferases with canonical SET domains and EZH2-targeted therapy.
Katoh, Tokyo, Japan. In Epigenomics, Oct 2015
UNASSIGNED: Germline mutations in canonical SET-methyltransferases have been identified in autism and intellectual disability syndromes and gain-of-function somatic alterations in EZH2, MLL3, NSD1, WHSC1 (NSD2) and WHSC1L1 (NSD3) in cancer.
Alternative 3' UTRs act as scaffolds to regulate membrane protein localization.
Mayr et al., New York City, United States. In Nature, Jul 2015
In our model of 3' UTR-dependent protein localization, the long 3' UTR of CD47 acts as a scaffold to recruit a protein complex containing the RNA-binding protein HuR (also known as ELAVL1) and SET to the site of translation.
Molecular pathways in renal cell carcinoma: recent advances in genetics and molecular biology.
Srinivasan et al., New Brunswick, United States. In Curr Opin Oncol, May 2015
In addition, genes involved in chromatin remodeling such as polybromo 1 (PBRM1), SET domain containing 2 (SETD2), and BRCA-1-associated protein-1 (BAP1) have been shown to influence tumor biology and predict survival.
MLL leukemia and future treatment strategies.
Marschalek, Frankfurt am Main, Germany. In Arch Pharm (weinheim), Apr 2015
Vice versa, reciprocal X-MLL fusions exhibit a PHD domain (H3K4me3 reader domain), sequester the histone acetyltransferases CREBBP and MOF1 and bear a histone methyltransferase domain at their very C-terminus (SET domain).
From the Biology of PP2A to the PADs for Therapy of Hematologic Malignancies.
Perrotti et al., Houston, United States. In Front Oncol, 2014
Likewise, overexpression or aberrant expression of physiologic PP2A inhibitory molecules (e.g., SET and its associated SETBP1 and CIP2A) may turn off PP2A function and participate to leukemic progression.
Fructose-1,6-bisphosphatase opposes renal carcinoma progression.
Simon et al., Philadelphia, United States. In Nature, 2014
Recent large-scale sequencing analyses revealed the loss of several chromatin remodelling enzymes in a subset of ccRCC (these included polybromo-1, SET domain containing 2 and BRCA1-associated protein-1, among others), indicating that epigenetic perturbations are probably important contributors to the natural history of this disease.
SMYD3 links lysine methylation of MAP3K2 to Ras-driven cancer.
Gozani et al., Stanford, United States. In Nature, 2014
The largely cytoplasmic KMT SMYD3 (SET and MYND domain containing protein 3) is overexpressed in numerous human tumours.
Influence of the accessory protein SET on M3 muscarinic receptor phosphorylation and G protein coupling.
Lanier et al., Paris, France. In Mol Pharmacol, 2012
SET knockdown increased high-affinity binding of agonist in intact cells and membrane preparations.
Overexpression of SET is a recurrent event associated with poor outcome and contributes to protein phosphatase 2A inhibition in acute myeloid leukemia.
Odero et al., Pamplona, Spain. In Haematologica, 2012
SET overexpression is a key mechanism in the inhibition of PP2A in acute myeloid leukemia.
Accumulation of the SET protein in HEK293T cells and mild oxidative stress: cell survival or death signaling.
Curti et al., Ribeirão Preto, Brazil. In Mol Cell Biochem, 2012
Suggest that accumulated SET could act via Akt/PTEN either as cell survival signal or as oxidative stress sensor for cell death.
SET oncogene is upregulated in pediatric acute lymphoblastic leukemia.
Ozbek et al., İstanbul, Turkey. In Tumori, 2012
Results showed that SET is significantly overexpressed in pediatric acute lymphoblastic leukemia samples, and an increased level of SET might contribute to leukemic process.
Role of Template Activating Factor-I as a chaperone in linker histone dynamics.
Nagata et al., Tsukuba, Japan. In J Cell Sci, 2011
TAF-I is a key molecule that regulates linker histone-mediated chromatin assembly and disassembly
share on facebooktweetadd +1mail to friends