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

SET domain containing 2

Huntington's disease (HD), a neurodegenerative disorder characterized by loss of striatal neurons, is caused by an expansion of a polyglutamine tract in the HD protein huntingtin. This gene encodes a protein belonging to a class of huntingtin interacting proteins characterized by WW motifs. This protein is a histone methyltransferase that is specific for lysine-36 of histone H3, and methylation of this residue is associated with active chromatin. This protein also contains a novel transcriptional activation domain and has been found associated with hyperphosphorylated RNA polymerase II. [provided by RefSeq, Aug 2008] (from NCBI)
Top mentioned proteins: SET, Histone, JAK2, CAN, POLYMERASE
Papers using Set2 antibodies
ChIPOTle: a user-friendly tool for the analysis of ChIP-chip data
Brunet Anne et al., In Nature, 2004
... Genetically wildtype descendents from set-2 mutant parents have extended lifespan for several generations ...
Papers on Set2
Novel pyrrole carboxamide inhibitors of JAK2 as potential treatment of myeloproliferative disorders.
Donati et al., Nerviano, Italy. In Bioorg Med Chem, Jun 2015
A series of compounds was synthesized leading to the identification of the potent and orally bioavailable JAK2 inhibitor 16 (NMS-P830), which showed an encouraging tumour growth inhibition in SET-2 xenograft tumour model, with evidence for JAK2 pathway suppression demonstrated by in vivo pharmacodynamic effects.
Pro-Apoptotic Activity of Ruxolitinib Alone and in Combination with Hydroxyurea, Busulphan, and PI3K/mTOR Inhibitors in JAK2-Positive Human Cell Lines.
Treliński et al., Łódź, Poland. In Adv Clin Exp Med, Mar 2015
OBJECTIVES: This study assessed the potential cytotoxicity of RX against JAK2-positive human cell lines (SET-2 and HEL), either alone or in combination with hydroxyurea, busulphan, rapamycin or LY294002.
The Bone Marrow-Mediated Protection of Myeloproliferative Neoplastic Cells to Vorinostat and Ruxolitinib Relies on the Activation of JNK and PI3K Signalling Pathways.
Almeida et al., Lisbon, Portugal. In Plos One, 2014
Here, we show that bone marrow (BM) stromal cells (HS-5) protected MPN-derived cell lines (SET-2; HEL and UKE-1) and MPN patient-derived BM cells from the cytotoxic effects of Ruxolitinib and the HDACi Vorinostat.
Identification and Analysis of the SET-Domain Family in Silkworm, Bombyx mori.
Cui et al., Chongqing, China. In Biomed Res Int, 2014
Firstly, 24 genes containing SET domain from silkworm genome were characterized and 17 of them belonged to six subfamilies of SUV39, SET1, SET2, SUV4-20, EZ, and SMYD.
The SET-2/SET1 histone H3K4 methyltransferase maintains pluripotency in the Caenorhabditis elegans germline.
Palladino et al., Lyon, France. In Cell Rep, 2014
In Caenorhabditis elegans, SET-2/SET1, WDR-5.1, and ASH-2 are differentially required for germline H3K4 methylation.
Pyrrole-3-carboxamides as potent and selective JAK2 inhibitors.
Donati et al., Nerviano, Italy. In Bioorg Med Chem, 2014
Compound 28 displayed significant tumour growth inhibition in SET-2 xenograft tumour model, with a mechanism of action confirmed in vivo by typical modulation of known biomarkers, and with a favourable pharmacokinetic and safety profile.
Therapeutic efficacy of an Fc-enhanced TCR-like antibody to the intracellular WT1 oncoprotein.
Scheinberg et al., New York City, United States. In Clin Cancer Res, 2014
ESKM was more potent in vivo against JMN mesothelioma, and effective against SET2 AML and fresh ALL xenografts.
Eaf5/7/3 form a functionally independent NuA4 submodule linked to RNA polymerase II-coupled nucleosome recycling.
Côté et al., Québec, Canada. In Embo J, 2014
Loss of Eaf5/7/3 partially suppresses intragenic cryptic transcription arising in set2 mutants, supporting a role in nucleosome destabilization.
Changes in corticospinal excitability during an acute bout of resistance exercise in the elbow flexors.
Avela et al., Jyväskylä, Finland. In Eur J Appl Physiol, 2013
Motor evoked potential (MEP) were 138.7 ± 52.7 % (p < 0.05), 130.4 ± 44.7 and 113.1 ± 31.4 % after SET1, SET2 and SET3, respectively, when compared to pre-exercise value.
Chd1 co-localizes with early transcription elongation factors independently of H3K36 methylation and releases stalled RNA polymerase II at introns.
Iyer et al., Austin, United States. In Epigenetics Chromatin, 2013
We also found that deletion of the histone methyltransferase for H3K36 (SET2) did not affect either Chd1 occupancy or nucleosome organization genome-wide.
Set2 methylation of histone H3 lysine 36 suppresses histone exchange on transcribed genes.
Workman et al., Kansas City, United States. In Nature, 2012
Set2 functions both to suppress the incorporation of acetylated histones and to signal for the deacetylation of these histones in transcribed genes. By suppressing spurious cryptic transcripts from initiating within ORFs, this pathway is essential to maintain the accuracy of transcription by RNA polymerase II.
Arabidopsis trithorax-related3/SET domain GROUP2 is required for the winter-annual habit of Arabidopsis thaliana.
Amasino et al., Madison, United States. In Plant Cell Physiol, 2012
The novel-class H3K4 methyltransferase, ATXR3, is a transcriptional activator that plays a role in the FLC activation and establishing the winter-annual habit.
Metallo-GTPase HypB from Helicobacter pylori and its interaction with nickel chaperone protein HypA.
Sun et al., Hong Kong, Hong Kong. In J Biol Chem, 2012
The unique N terminus of H. pylori HypB was identified to participate in the interaction with H. pylori HypA.
RNA polymerase II carboxyl-terminal domain phosphorylation regulates protein stability of the Set2 methyltransferase and histone H3 di- and trimethylation at lysine 36.
Strahl et al., Chapel Hill, United States. In J Biol Chem, 2012
RNA polymerase II carboxyl-terminal domain phosphorylation regulates protein stability of the Set2 methyltransferase and histone H3 di- and trimethylation at lysine 36.
Transgenerational epigenetic inheritance of longevity in Caenorhabditis elegans.
Brunet et al., Stanford, United States. In Nature, 2011
The histone H3 lysine 4 trimethylation (H3K4me3) complex, composed of ASH-2, WDR-5 and the histone methyltransferase SET-2, regulates Caenorhabditis elegans lifespan.
Effects of metal on the biochemical properties of Helicobacter pylori HypB, a maturation factor of [NiFe]-hydrogenase and urease.
Zamble et al., Toronto, Canada. In J Bacteriol, 2011
Mutation of Cys106 and His107, which are located between two major GTPase motifs, results in undetectable Ni(II) binding, and the Zn(II) affinity is weakened by 2 orders of magnitude.
Members of the H3K4 trimethylation complex regulate lifespan in a germline-dependent manner in C. elegans.
Brunet et al., Stanford, United States. In Nature, 2010
Deficiencies in members of the ASH-2 complex-ASH-2 itself, WDR-5 and the H3K4 methyltransferase SET-2-extend worm lifespan.
Prevention of early flowering by expression of FLOWERING LOCUS C requires methylation of histone H3 K36.
Shen et al., Strasbourg, France. In Nat Cell Biol, 2005
Here we show that loss-of-function of SET DOMAIN GROUP 8 (SDG 8), which encodes a homologue of the yeast SET2 histone methyltransferase, results in reduced dimethylation of histone H3K36, particularly in chromatin associated with the FLC promoter and the first intron, regions that contain essential cis-elements for transcription.
Cotranscriptional set2 methylation of histone H3 lysine 36 recruits a repressive Rpd3 complex.
Krogan et al., Boston, United States. In Cell, 2005
Rpd3C(S) mutants exhibit phenotypes remarkably similar to those of Set2, a histone methyltransferase associated with elongating RNA polymerase II.
Histone H3 methylation by Set2 directs deacetylation of coding regions by Rpd3S to suppress spurious intragenic transcription.
Workman et al., Kansas City, United States. In Cell, 2005
Mutants in the RNA polymerase II-associated SET2 histone methyltransferase also displayed these defects.
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