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Splicing factor 3b, subunit 2, 145kDa

SAP 145, SF3B2, SF3B1
This gene encodes subunit 2 of the splicing factor 3b protein complex. Splicing factor 3b, together with splicing factor 3a and a 12S RNA unit, forms the U2 small nuclear ribonucleoproteins complex (U2 snRNP). The splicing factor 3b/3a complex binds pre-mRNA upstream of the intron's branch site in a sequence-independent manner and may anchor the U2 snRNP to the pre-mRNA. Splicing factor 3b is also a component of the minor U12-type spliceosome. Subunit 2 associates with pre-mRNA upstream of the branch site at the anchoring site. Subunit 2 also interacts directly with subunit 4 of the splicing factor 3b complex. Subunit 2 is a highly hydrophilic protein with a proline-rich N-terminus and a glutamate-rich stretch in the C-terminus. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: p53, p300, iMpact, ASXL1, HAD
Papers on SAP 145
Functional Genomic Screening Reveals Splicing of the EWS-FLI1 Fusion Transcript as a Vulnerability in Ewing Sarcoma.
Caplen et al., Nashville, United States. In Cell Rep, Feb 2016
We also demonstrate the sensitivity of EWS-FLI1 fusion transcripts to the loss of function of the U2 snRNP component, SF3B1.
Interchangeable SF3B1 inhibitors interfere with pre-mRNA splicing at multiple stages.
Jurica et al., Santa Cruz, United States. In Rna, Feb 2016
UNASSIGNED: The protein SF3B1 is a core component of the spliceosome, the large ribonucleoprotein complex responsible for pre-mRNA splicing.
Myelodysplastic syndromes: Contemporary review and how we treat.
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.
Prognostic indices in chronic lymphocytic leukaemia: where do we stand how do we proceed?
Rosenquist et al., Uppsala, Sweden. In J Intern Med, Jan 2016
NOTCH1, SF3B1 and BIRC3).
Chronic lymphocytic leukemia (CLL) - Then and Now.
Jain et al., Houston, United States. In Am J Hematol, Jan 2016
More recently, stereotypy of BCR (B cell receptor) and whole exome sequencing (WES) based discovery of specific mutations such as NOTCH1, TP53, SF3B1, XPO-1, BIRC3, ATM and RPS15 further refined the current prognostication system in CLL.
Deep sequencing of uveal melanoma identifies a recurrent mutation in PLCB4.
Hayward et al., Brisbane, Australia. In Oncotarget, Jan 2016
UNASSIGNED: Next generation sequencing of uveal melanoma (UM) samples has identified a number of recurrent oncogenic or loss-of-function mutations in key driver genes including: GNAQ, GNA11, EIF1AX, SF3B1 and BAP1.
SF3B1 and EIF1AX mutations occur in primary leptomeningeal melanocytic neoplasms; yet another similarity to uveal melanomas.
Prinsen et al., Nijmegen, Netherlands. In Acta Neuropathol Commun, Dec 2015
However, it is currently unknown whether these LMNs harbor mutations in BAP1, SF3B1 and/or EIF1AX like uveal melanomas as well.
The spliceosome is a therapeutic vulnerability in MYC-driven cancer.
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.
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).
[Alternative Splicing Detection as a Biomarker for Cancer Diagnosis: A Novel Progressive Mechanism of Acute Lymphoblastic Leukemia with Alternative Splicing as a Biomarker Candidate].
Nomura et al., In Rinsho Byori, Sep 2015
Recently, somatic mutations of the SF3B1 (SAP155) gene, a subunit of the SF3B spliceosome complex, were found in myelodysplastic leukemia.
HIF-driven SF3B1 induces KHK-C to enforce fructolysis and heart disease.
Krek et al., Zürich, Switzerland. In Nature, Jul 2015
Here we show that myocardial hypoxia actuates fructose metabolism in human and mouse models of pathological cardiac hypertrophy through hypoxia-inducible factor 1α (HIF1α) activation of SF3B1 and SF3B1-mediated splice switching of KHK-A to KHK-C.
Idiopathic dysplasia of undetermined/uncertain significance (IDUS) initially presenting erythroblastosis and hyperferritinemia.
Yatomi et al., Tokyo, Japan. In Rinsho Ketsueki, 2014
The SF3B1 mutation was identified in this patient, suggesting that he might be at a stage prior to myelodysplastic syndrome.
[Molecular Prognostic Markers and Their Clinical Relevance in Chronic Lymphocytic Leukemia].
Pospíšilová et al., In Klin Onkol, 2014
The most relevant candidates are mutations in SF3B1, NOTCH1 and BIRC3 genes, which are now intensively studied with respect to their clinical importance.
Age-related mutations associated with clonal hematopoietic expansion and malignancies.
Ding et al., Saint Louis, United States. In Nat Med, 2014
Remarkably, 83% of these mutations were from 19 leukemia and/or lymphoma-associated genes, and nine were recurrently mutated (DNMT3A, TET2, JAK2, ASXL1, TP53, GNAS, PPM1D, BCORL1 and SF3B1).
Exome sequencing identifies recurrent somatic mutations in EIF1AX and SF3B1 in uveal melanoma with disomy 3.
Zeschnigk et al., Essen, Germany. In Nat Genet, 2013
Using exome sequencing, we identified recurrent somatic mutations in EIF1AX and SF3B1, specifically occurring in uveal melanomas with disomy 3, which rarely metastasize.
Proteomic and protein interaction network analysis of human T lymphocytes during cell-cycle entry.
Thomas et al., London, United Kingdom. In Mol Syst Biol, 2011
Inhibiting the induction of two proteins involved in two of the most significantly upregulated cellular processes, ribosome biogenesis (eIF6) and hnRNA splicing (SF3B2/SF3B4), showed that human T cells can enter the cell cycle without growing in size.
Human immunodeficiency virus type 1 Vpr induces G2 checkpoint activation by interacting with the splicing factor SAP145.
Yasuda et al., Minneapolis, United States. In Mol Cell Biol, 2006
Data show that Vpr induces checkpoint activation and G(2) arrest by binding to the CUS1 domain of SAP145 and interfering with the functions of the SAP145 and SAP49 proteins, two subunits of the multimeric splicing factor 3b (SF3b).
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