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

Additional sex combs like 2

ASXL2, KIAA1685, additional sex combs-like 2
ASXL2 is a human homolog of the Drosophila asx gene. Drosophila asx is an enhancer of trithorax (see MIM 159555) and polycomb (see MIM 610231) (ETP) gene that encodes a chromatin protein with dual functions in transcriptional activation and silencing (Katoh and Katoh, 2003 [PubMed 12888926]).[supplied by OMIM, Sep 2009] (from NCBI)
Top mentioned proteins: ASXL1, Polycomb, Histone, V1a, Ubiquitin
Papers on ASXL2
DNMT3A R882 Mutation with FLT3-ITD Positivity Is an Extremely Poor Prognostic Factor in Patients with Normal-Karyotype Acute Myeloid Leukemia after Allogeneic Hematopoietic Cell Transplantation.
New
Kim et al., Hwasun, South Korea. In Biol Blood Marrow Transplant, Jan 2016
A total of 115 patients who received allogeneic HCT for NK-AML were retrospectively evaluated for the FLT3-ITD, NPM1, CEBPA, DNMT3A, TET2, IDH1/2, WT1, NRAS, ASXL2, FAT1, DNAH11, and GATA2 mutations in diagnostic samples and analyzed for long-term outcomes after allogeneic HCT.
ASXL2 promotes proliferation of breast cancer cells by linking ERα to histone methylation.
New
Um et al., Seoul, South Korea. In Oncogene, Jan 2016
Selective expression of additional sex comb-like 2 (ASXL2) in ERα-positive breast cancer cells prompted us to investigate its role in chromatin modification required for ERα activation and breast carcinogenesis.
BAP1/ASXL1 recruitment and activation for H2A deubiquitination.
New
Sixma et al., Amsterdam, Netherlands. In Nat Commun, Dec 2015
This initial encounter-like complex is unproductive and needs to be activated by the DEUBAD domains of ASXL1, ASXL2 or ASXL3 to increase BAP1's affinity for ubiquitin on H2A, to drive the deubiquitination reaction.
The BAP1/ASXL2 Histone H2A Deubiquitinase Complex Regulates Cell Proliferation and Is Disrupted in Cancer.
New
Affar et al., Montréal, Canada. In J Biol Chem, Dec 2015
Here, we report that BAP1 forms two mutually exclusive complexes with the transcriptional regulators ASXL1 and ASXL2, which are necessary for maintaining proper protein levels of this DUB.
ASXL2 Regulates Glucose, Lipid, and Skeletal Homeostasis.
New
Zou et al., Saint Louis, United States. In Cell Rep, Jul 2015
ASXL2 is an ETP family protein that interacts with PPARγ.
Functional proteomics of the epigenetic regulators ASXL1, ASXL2 and ASXL3: a convergence of proteomics and epigenetics for translational medicine.
Review
New
Katoh, Tokyo, Japan. In Expert Rev Proteomics, Jun 2015
ASXL1, ASXL2 and ASXL3 are epigenetic scaffolds for BAP1, EZH2, NCOA1, nuclear receptors and WTIP.
A functional biological network centered on XRCC3: a new possible marker of chemoradiotherapy resistance in rectal cancer patients.
Nitti et al., Padova, Italy. In Cancer Biol Ther, 2014
Four genes were retained in the achieved model: ZNF160, XRCC3, HFM1 and ASXL2.
Frequent ASXL2 mutations in acute myeloid leukemia patients with t(8;21)/RUNX1-RUNX1T1 chromosomal translocations.
Jourdan et al., Orsay, France. In Blood, 2014
Here we identify somatic mutations in additional sex combs-like 2 (ASXL2) in 22.7% (25/110) of patients with t(8;21), but not in patients with inv(16)/t(16;16) (0/60) or RUNX1-mutated AML (0/26).
WTIP interacts with ASXL2 and blocks ASXL2-mediated activation of retinoic acid signaling.
Wang et al., Chicago, United States. In Biochem Biophys Res Commun, 2014
ASXL2 is highly expressed in the heart and is required for proper heart development and function.
Additional sex combs-like family genes are required for normal cardiovascular development.
Wang et al., Chicago, United States. In Genesis, 2014
Here we report the identification of ASXL2 and ASXL1, two homologous chromatin factors, as novel regulators of heart development.
The landscape of somatic mutations in epigenetic regulators across 1,000 paediatric cancer genomes.
Downing et al., Memphis, United States. In Nat Commun, 2013
The most frequently mutated genes are H3F3A, PHF6, ATRX, KDM6A, SMARCA4, ASXL2, CREBBP, EZH2, MLL2, USP7, ASXL1, NSD2, SETD2, SMC1A and ZMYM3.
Recurrent inactivation of STAG2 in bladder cancer is not associated with aneuploidy.
Impact
Real et al., Madrid, Spain. In Nat Genet, 2013
A discovery exome sequencing screen (n = 17), followed by a prevalence screen (n = 60), identified new genes mutated in this tumor coding for proteins involved in chromatin modification (MLL2, ASXL2 and BPTF), cell division (STAG2, SMC1A and SMC1B) and DNA repair (ATM, ERCC2 and FANCA).
Functional and cancer genomics of ASXL family members.
Review
Katoh, Tokyo, Japan. In Br J Cancer, 2013
Additional sex combs-like (ASXL)1, ASXL2 and ASXL3 are human homologues of the Drosophila Asx gene that are involved in the regulation or recruitment of the Polycomb-group repressor complex (PRC) and trithorax-group (trxG) activator complex.
The ASXL-BAP1 axis: new factors in myelopoiesis, cancer and epigenetics.
Review
Dey et al., New York City, United States. In Leukemia, 2013
BAP1, a nuclear-localized deubiquitinase, has been shown to interact with a number of proteins, including ASXL1 and/or ASXL2, but the functional importance of this interaction has remained elusive.
Loss of the tumor suppressor BAP1 causes myeloid transformation.
Impact
Dixit et al., San Francisco, United States. In Science, 2012
Knockin mice expressing BAP1 with a 3xFlag tag revealed that BAP1 interacts with host cell factor-1 (HCF-1), O-linked N-acetylglucosamine transferase (OGT), and the polycomb group proteins ASXL1 and ASXL2 in vivo.
Additional sex comb-like (ASXL) proteins 1 and 2 play opposite roles in adipogenesis via reciprocal regulation of peroxisome proliferator-activated receptor {gamma}.
GeneRIF
Um et al., Seoul, South Korea. In J Biol Chem, 2011
ASXL1 represses, whereas ASXL2 increases, the expression of adipogenic genes, most of which are PPARgamma targets
Violating the splicing rules: TG dinucleotides function as alternative 3' splice sites in U2-dependent introns.
GeneRIF
Platzer et al., Jena, Germany. In Genome Biol, 2006
the apparent occurrence of an unusual TG 3' splice site in intron 2 is discussed
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