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Splicing factor 3b, subunit 1, 155kDa

SAP155, SF3b155, Sf3b1, Sap155p
This gene encodes subunit 1 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. The carboxy-terminal two-thirds of subunit 1 have 22 non-identical, tandem HEAT repeats that form rod-like, helical structures. Alternative splicing results in multiple transcript variants encoding different isoforms. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: SAP 145, P14, STEP, CAN, Fir
Papers on SAP155
[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.
Haploinsufficiency of Sf3b1 leads to compromised stem cell function but not to myelodysplasia.
Ogawa et al., Kyoto, Japan. In Leukemia, 2014
SF3B1 is a core component of the mRNA splicing machinery and frequently mutated in myeloid neoplasms with myelodysplasia, particularly in those characterized by the presence of increased ring sideroblasts.
Identification of four genes required for mammalian blastocyst formation.
Mager et al., Amherst Center, United States. In Zygote, 2014
Here we report the essential function of four RNA processing/splicing factors (Sf3b14, Sf3b1, Rpl7l1, and Rrp7a) and show that each of these genes is required for blastocyst formation in the mouse.
Splicing factor mutations and cancer.
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.
Cancer-relevant splicing factor CAPERα engages the essential splicing factor SF3b155 in a specific ternary complex.
Kielkopf et al., Rochester, United States. In J Biol Chem, 2014
Here we present structures of the CAPERα UHM bound to a representative SF3b155 ULM at 1.7 Å resolution and, for comparison, in the absence of ligand at 2.2 Å resolution.
Depletion of Sf3b1 impairs proliferative capacity of hematopoietic stem cells but is not sufficient to induce myelodysplasia.
Iwama et al., Chiba, Japan. In Blood, 2014
SF3B1 is mutated in 70% to 85% of refractory anemia with ringed sideroblasts (RARS) patients and is highly associated with the presence of RARS, although the pathological role of SF3B1 mutations in MDS-RARS has not been elucidated yet.
Alternative splicing of FBP-interacting repressor coordinates c-Myc, P27Kip1/cyclinE and Ku86/XRCC5 expression as a molecular sensor for bleomycin-induced DNA damage pathway.
Nomura et al., Chiba, Japan. In Oncotarget, 2014
FIR and FIRΔexon2 form homo- or heterodimers that complex with SAP155.
Non-transmissible Sendai virus vector encoding c-myc suppressor FBP-interacting repressor for cancer therapy.
Nomura et al., Chiba, Japan. In World J Gastroenterol, 2014
The molecular mechanism of the anti-tumor effect and c-Myc suppression by SeV/dF/FIR was examined using Spliceostatin A (SSA), a SAP155 inhibitor, or SAP155 siRNA which induce c-Myc by increasing FIR∆exon2 in HeLa cells.
Splicing factor 3b subunit 1 (Sf3b1) haploinsufficient mice display features of low risk Myelodysplastic syndromes with ring sideroblasts.
Tiu et al., San Francisco, United States. In J Hematol Oncol, 2013
BACKGROUND: The presence of somatic mutations in splicing factor 3b subunit 1 (SF3B1) in patients with Myelodysplastic syndromes with ring sideroblasts (MDS-RS) highlights the importance of the RNA-splicing machinery in MDS.
Interactions between SAP155 and FUSE-binding protein-interacting repressor bridges c-Myc and P27Kip1 expression.
Nomura et al., Chiba, Japan. In Mol Cancer Res, 2013
P27Kip1 (CDKN1B) arrests cells in G1, and SAP155 (SF3B1), a subunit of the essential splicing factor 3b (SF3b) subcomplex of the spliceosome, is required for proper P27 pre-mRNA splicing.
SAP155-mediated c-myc suppressor far-upstream element-binding protein-interacting repressor splicing variants are activated in colon cancer tissues.
Nomura et al., Chiba, Japan. In Cancer Sci, 2013
Recently, the knockdown of SAP155 pre-mRNA-splicing factor, a subunit of SF3b, was reported to disturb FIR pre-mRNA splicing and yield FIRΔexon2, an exon 2-spliced variant of FIR, which lacks c-myc repression activity.
The development and application of small molecule modulators of SF3b as therapeutic agents for cancer.
Potter et al., Memphis, United States. In Drug Discov Today, 2013
Several natural products have been demonstrated to bind to the SF3b1 subunit of this macromolecule and these agents modulate alternative RNA splicing.
Emerging roles of the spliceosomal machinery in myelodysplastic syndromes and other hematological disorders.
Tiu et al., Cleveland, United States. In Leukemia, 2012
Alterations in splicing factor 3 subunit b1 (SF3b1) were the first spliceosomal mutations described, immediately followed by identification of other splicing factor mutations, including U2 small nuclear RNA auxillary factor 1 (U2AF1) and serine arginine-rich splicing factor 2 (SRSF2).
Chronic lymphocytic leukemia with SF3B1 mutation.
Lopez-Otin et al., In N Engl J Med, 2012
mutational status of SF3B1 had a prognostic value for CLL that was independent of clinical stage or espression of ZAP70 or CD38
SAP155-mediated splicing of FUSE-binding protein-interacting repressor serves as a molecular switch for c-myc gene expression.
Nomura et al., Chiba, Japan. In Mol Cancer Res, 2012
Data indicate that altered FIR and c-myc pre-mRNA splicing, in addition to c-Myc expression by augmented FIR/FIRDeltaexon2-SAP155 complex, potentially contribute to colorectal cancer development.
Mutations in the spliceosome machinery, a novel and ubiquitous pathway in leukemogenesis.
Maciejewski et al., Cleveland, United States. In Blood, 2012
SF3B1 mutations are prevalent in low-risk MDS with ring sideroblasts, SF3B1 mutations are associated with a favorable prognosis.
SF3B1 mutations are prevalent in myelodysplastic syndromes with ring sideroblasts but do not hold independent prognostic value.
Tefferi et al., Rochester, United States. In Blood, 2012
SF3B1 mutations are prevalent in myelodysplastic syndromes with ring sideroblasts.
Exome sequencing identifies recurrent mutations of the splicing factor SF3B1 gene in chronic lymphocytic leukemia.
López-Otín et al., Oviedo, Spain. In Nat Genet, 2012
SF3B1, encoding a subunit of the spliceosomal U2 small nuclear ribonucleoprotein (snRNP), is somatically mutated in 9.7% of affected individuals.
Post-transcriptional spliceosomes are retained in nuclear speckles until splicing completion.
Lührmann et al., Göttingen, Germany. In Nat Commun, 2011
Here we determine the global extent of co- and post-transcriptional splicing in mammalian cells, and their respective subnuclear locations, using antibodies that specifically recognize phosphorylated SF3b155 (P-SF3b155) found only in catalytically activated/active spliceosomes.
Molecular architecture of the multiprotein splicing factor SF3b.
Stark et al., Göttingen, Germany. In Science, 2003
determined the three-dimensional structure of the human SF3b complex by single-particle electron cryomicroscopy at a resolution of less than 10 angstroms, allowing identification of protein domains with known structural folds
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