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anti-Human SF3B1 Antibodies:
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Our findings suggest that the genetic profile of coexistent GNAQ (show GNAQ Antibodies) or GNA11 (show GNA11 Antibodies) mutations with BAP1 (show RNF2 Antibodies) or SF3B1 (show SF3B2 Antibodies) mutations can aid the histopathological diagnosis of blue nevus-like melanoma and distinguish blue nevus-like melanoma from conventional epidermal-derived melanomas.
Mutation in SF3B1 (show SF3B2 Antibodies) gene is associated with mucosal melanoma.
These data provide a catalog of copy-number associated gene dependencies and identify partial copy-loss of wild-type SF3B1 (show SF3B2 Antibodies) as a novel, non-driver cancer gene dependency.
although blocking the function of SF3b elicits a massive accumulation of unspliced pre-mRNAs in the nucleus, intron-containing transcripts can still bind the ALYREF (show THOC4 Antibodies) export factor and be transported to the cytoplasm, where they trigger an alternative nonsense-mediated decay pathway.
this study shows that DNMT3A (show DNMT3A Antibodies) mutations are present in a significant proportion of SF3B1mut patients with RARS (show RARS Antibodies) and its presence has a clearly negative impact on outcomes, determining a higher RBC (show CACNA1C Antibodies) transfusion dependency, higher risk of progression to AML (show RUNX1 Antibodies), and lower OS.
Somatic SF3B1 mutations are associated with metastatic NUT midline carcinoma.
Fanconi anemia (show PALB2 Antibodies) FANCD2 (show FANCD2 Antibodies) and FANCI (show FANCI Antibodies) proteins regulate the nuclear dynamics of splicing factors, such as SF3B1 (show SF3B2 Antibodies).
The frequently mutated SF3B1 (show SF3B2 Antibodies) residues contact the pre-mRNA splice site. Based on structural homology with other spliceosome subunits, and recent findings of altered RNA binding by mutant U2AF1 (show U2AF1 Antibodies) proteins, we suggest that affected U2AF1 (show U2AF1 Antibodies) residues also contact pre-mRNA.
The aberrantly spliced target genes and deregulated cellular pathways associated with the commonly mutated splicing factor (show SLU7 Antibodies) genes in myelodysplastic syndromes (SF3B1 (show SF3B2 Antibodies), SRSF2 (show SRSF2 Antibodies) and U2AF1 (show U2AF1 Antibodies)) are being identified, illuminating the molecular mechanisms underlying the disease. (Review)
These findings provide evidence of a multipotent lymphomyeloid Hematopoietic stem cell origin of SF3B1 (show SF3B2 Antibodies) mutations in myelodysplastic syndrome with ring sideroblasts patients.
Our findings demonstrate that, despite significant differences in affected transcripts, there is overlap in the phenotypes associated with SF3B1-K700E between human and mouse.
Sf3b1(K700E) mice develop macrocytic anemia (show TCN2 Antibodies) due to a terminal erythroid maturation defect, erythroid dysplasia, and long-term hematopoietic stem cell (LT-HSC (show FUT1 Antibodies)) expansion.
myocardial hypoxia actuates fructose metabolism in human and mouse models of pathological cardiac hypertrophy through hypoxia-inducible factor 1alpha (HIF1alpha (show HIF1A Antibodies)) activation of SF3B1 and SF3B1-mediated splice switching of KHK (show KHK Antibodies)-A to KHK (show KHK Antibodies)-C
Sf3b1 isrequired for the blastocyst formation.
SF3B1 plays an important role in the regulation of hematopoietic stem cells, whereas SF3B1 haploinsufficiency itself is not associated with the myelodysplastic syndrome phenotype with ring sideroblasts.
The level of Sf3b1 expression is critical for the proliferative capacity of hematopoietic stem cells. Depletion of Sf3b1 impairs proliferative capacity of hematopoietic stem cells but is not sufficient to induce myelodysplasia.
SF3B1 haploinsufficiency leads to formation of ring sideroblasts in myelodysplastic syndromes.
the active spliceosome, containing SAP155 phosphorylated by DYRKIA, performs pre-mRNA splicing in spermatogonia during testicular development
active spliceosome, containing phosphorylated SAP155, performs pre-mRNA splicing on chromatin concomitant with transcription during testicular development.
Sf3b1 and Polycomb (show CBX2 Antibodies) group (PcG) proteins interaction is essential for true PcG-mediated repression of Hox (show MSH2 Antibodies) genes.
Data indicate that splicing factor 3b (show SF3B14 Antibodies), subunit 1 (sf3b1) mutation causes aberrant splicing of sf3b1 resulting in functional and predicted non-functional transcripts and a 90% reduction in full-length Sf3b1 protein.
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.
, pre-mRNA processing 10
, pre-mRNA splicing factor SF3b, 155 kDa subunit
, spliceosome-associated protein 155
, splicing factor 3B subunit 1
, pre-mRNA-splicing factor SF3b 155 kDa subunit
, splicing factor 3b, subunit 1, 155 kDa
, transforming growth factor alpha regulated gene 4
, 146 kDa nuclear protein
, splicing factor 3b, subunit 1, 155kDa
, splicing factor 3B subunit 1-like
, splicing factor 3b, subunit 1, 155kD