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U2 small nuclear RNA auxiliary factor 1

U2AF35, U2AF1, hU2AF35
This gene belongs to the splicing factor SR family of genes. U2 auxiliary factor, comprising a large and a small subunit, is a non-snRNP protein required for the binding of U2 snRNP to the pre-mRNA branch site. This gene encodes the small subunit which plays a critical role in both constitutive and enhancer-dependent RNA splicing by directly mediating interactions between the large subunit and proteins bound to the enhancers. Alternatively spliced transcript variants encoding different isoforms have been identified. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: Retinoschisis, SAP 145, U2AF65, CAN, ASXL1
Papers on U2AF35
DLX4 hypermethylation is a prognostically adverse indicator in de novo acute myeloid leukemia.
New
Qian et al., Zhenjiang, China. In Tumour Biol, Feb 2016
DLX4 methylated patients showed significantly higher frequency of U2AF1 mutation compared with DLX4 unmethylated patients (P = 0.043).
Myelodysplastic syndromes: Contemporary review and how we treat.
Review
New
Tefferi et al., Rochester, United States. In Am J Hematol, Jan 2016
With the advent of next generation sequencing, recurrent somatic mutations in genes involved in epigenetic regulation (TET2, ASXL1, EZH2, DNMT3A, IDH1/2), RNA splicing (SF3B1, SRSF2, U2AF1, ZRSR2), DNA damage response (TP53), transcriptional regulation (RUNX1, BCOR, ETV6) and signal transduction (CBL, NRAS, JAK2) have been identified in MDS.
What's different about atypical CML and chronic neutrophilic leukemia?
New
Tyner et al., Portland, United States. In Hematology Am Soc Hematol Educ Program, Jan 2016
We also report a novel finding-our study reveals a high frequency of U2AF1 mutations at codon Q157 associated with CSF3R mutant myeloid neoplasms.
Exon-centric regulation of ATM expression is population-dependent and amenable to antisense modification by pseudoexon targeting.
New
Vorechovsky et al., Southampton, United Kingdom. In Sci Rep, Dec 2015
NSE levels were deregulated in leukemias and were influenced by the identity of U2AF35 residue 34.
Genetic landscape of recurrent ASXL1, U2AF1, SF3B1, SRSF2, and EZH2 mutations in 304 Chinese patients with myelodysplastic syndromes.
New
Li et al., Shanghai, China. In Tumour Biol, Nov 2015
A total of 304 Chinese MDS patients were screened for known mutations in five genes (ASXL1, U2AF1, SF3B1, SRSF2, and EZH2) using next-generation sequencing.
The spliceosome is a therapeutic vulnerability in MYC-driven cancer.
New
Impact
Westbrook et al., Houston, United States. In Nature, Oct 2015
Core spliceosomal factors (such as SF3B1 and U2AF1) associated with BUD31 are also required to tolerate oncogenic MYC.
A Pilot Study of the Telomerase Inhibitor Imetelstat for Myelofibrosis.
New
Impact
Pardanani et al., Rochester, United States. In N Engl J Med, Oct 2015
The rate of complete response was 38% among patients with a mutation in SF3B1 or U2AF1 versus 4% among patients without a mutation in these genes (P=0.04).
The molecular pathogenesis of the myelodysplastic syndromes.
Review
New
Boultwood et al., Oxford, United Kingdom. In Eur J Haematol, Jul 2015
The most common mutations found in MDS occur in genes involved in RNA splicing (including SF3B1, SRSF2, U2AF1, and ZRSR2) and epigenetic modification (including TET2, ASXL1, and DNMT3A).
Mutant U2AF1 Expression Alters Hematopoiesis and Pre-mRNA Splicing In Vivo.
New
Impact
Walter et al., Saint Louis, United States. In Cancer Cell, Jun 2015
Heterozygous somatic mutations in the spliceosome gene U2AF1 occur in ∼ 11% of patients with myelodysplastic syndromes (MDS), the most common adult myeloid malignancy.
The Activation-Induced Assembly of an RNA/Protein Interactome Centered on the Splicing Factor U2AF2 Regulates Gene Expression in Human CD4 T Cells.
Salomon et al., Los Angeles, United States. In Plos One, 2014
While knocking down the PIM, SYNCRIP, impacts a limited but immunologically important set of U2AF2-bound transcripts, knockdown of U2AF1 significantly impairs assembly of the majority of protein and mRNA components in the activation-induced interactome.
Integrating genetics and epigenetics in myelodysplastic syndromes: advances in pathogenesis and disease evolution.
Review
García-Manero et al., Madrid, Spain. In Br J Haematol, 2014
Recent studies are shedding light on the molecular basis of myelodysplasia and how mutations and epimutations can induce and promote this neoplastic process through aberrant transcription factor function (RUNX1, ETV6, TP53), kinase signalling (FLT3, NRAS, KIT, CBL) and epigenetic deregulation (TET2, IDH1/2, DNMT3A, EZH2, ASXL1, SF3B1, U2AF1, SRSF2, ZRSR2).
Splicing factor mutations and cancer.
Review
Ogawa et al., Kyoto, Japan. In Wiley Interdiscip Rev Rna, 2014
These mutations were heterozygous and mainly affected U2AF1 (U2AF35), SRSF2 (SC35), SF3B1 (SF3B155 or SAP155), and ZRSR2 (URP), which are engaged in the initial steps of RNA splicing, including 3' splice-site recognition, and occur in a large mutually exclusive pattern, suggesting a common impact of these mutations on RNA splicing.
Prognostic score including gene mutations in chronic myelomonocytic leukemia.
Impact
Solary et al., Villejuif, France. In J Clin Oncol, 2013
PATIENTS AND METHODS: We genotyped ASXL1 and up to 18 other genes including epigenetic (TET2, EZH2, IDH1, IDH2, DNMT3A), splicing (SF3B1, SRSF2, ZRSF2, U2AF1), transcription (RUNX1, NPM1, TP53), and signaling (NRAS, KRAS, CBL, JAK2, FLT3) regulators in 312 patients with CMML.
Cancer-Associated Perturbations in Alternative Pre-messenger RNA Splicing.
Review
Chabot et al., Sherbrooke, Canada. In Cancer Treat Res, 2012
Introns are identified by the binding of U1 snRNP to the 5' splice site and the U2AF65/U2AF35 complex to the 3' splice site.
Mapping the hallmarks of lung adenocarcinoma with massively parallel sequencing.
Impact
Meyerson et al., Cambridge, United States. In Cell, 2012
In addition, we identified statistically recurrent somatic mutations in the splicing factor gene U2AF1 and truncating mutations affecting RBM10 and ARID1A.
Frequency and prognostic impact of mutations in SRSF2, U2AF1, and ZRSR2 in patients with myelodysplastic syndromes.
GeneRIF
Heuser et al., Hannover, Germany. In Blood, 2012
In univariate analysis, mutated SRSF2 predicted shorter overall survival and more frequent acute myeloid leukemia progression compared with wild-type SRSF2, whereas mutated U2AF1, ZRSR2 had no impact on patient outcome.
Mutations in the spliceosome machinery, a novel and ubiquitous pathway in leukemogenesis.
GeneRIF
Maciejewski et al., Cleveland, United States. In Blood, 2012
U2AF1 and SRSF2 mutations are frequent in chronic myelomonocytic leukemia and advanced forms of MDS. U2AF1 and SRSF2 mutations are predictive for shorter survival.
hnRNP A1 proofreads 3' splice site recognition by U2AF.
GeneRIF
Valcárcel et al., Barcelona, Spain. In Mol Cell, 2012
hnRNP A1 forms a ternary complex with the U2AF heterodimer on AG-containing/uridine-rich RNAs, while it displaces U2AF from non-AG-containing/uridine-rich RNAs, an activity that requires the glycine-rich domain of hnRNP A1
Recurrent mutations in the U2AF1 splicing factor in myelodysplastic syndromes.
Impact
GeneRIF
Walter et al., Saint Louis, United States. In Nat Genet, 2012
Here we show that a missense mutation affecting the serine at codon 34 (Ser34) in U2AF1 was recurrently present in 13 out of 150 (8.7%) subjects with de novo MDS, and we found suggestive evidence of an increased risk of progression to sAML
A new mouse model for the trisomy of the Abcg1-U2af1 region reveals the complexity of the combinatorial genetic code of down syndrome.
GeneRIF
Herault et al., Orléans, France. In Hum Mol Genet, 2010
this study establishes definitely the contribution of the Abcg1-U2af1 orthologous region to the DS etiology and suggests new modulatory pathways for learning and memory.
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