SF3B1


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SF3B1

A gene on chromosome 2q33.1 that encodes subunit 1 of the splicing factor SF3B, which is required for “A” complex assembly by the stable binding of U2 snRNP to the branchpoint sequence in pre-mRNA. Binding of the SF3A/SF3B complex upstream of the branch site may anchor U2 snRNP to pre-mRNA. SF3B1 may be involved in assembling the “E” complex.
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With this approach, they identified many components of the spliceosome, of which SF3B1 is a key component.
The SF3B1 biomarker is included in our GeneReadTM DNAseq Leukemia V2 gene panel for next-generation sequencing," said Vincent Fert, QIAGEN s Personalized Healthcare Program Leader.
QIAGEN licensed the SF3B1 biomarker in an ongoing expansion of the oncohematology offering for clinical research and diagnostics.
Somatic SF3B1 mutation in myelodysplasia with ring sideroblasts.
Clinical significance of SF3B1 mutations in myelodysplastic syndromes and myelodysplastic/myeloproliferative neoplasms.
Patients with mutations in the SF3B1 gene frequently had a specific abnormality of red blood cells in their bone marrow, called ring sideroblasts, researchers said.
We believe that by identifying SF3B1, and working to characterize the underlying biology of this disease, we will be able to build improved diagnosis and treatment protocols.
Title: Total synthesis of 6-deoxypladienolide D and assessment of splicing inhibitory activity in a mutant SF3B1 cancer cell line Date and time: Wednesday, April 22, 2015, 8:00 AM - 12:00 PM
Mutations of SF3B1 gene, to be targeted by new test, indicate favorable prognosis for patients with bone marrow disorders known as myelodysplastic syndromes
QIAGEN sees potential for developing companion diagnostics to guide treatment with new anti-cancer compounds under development that target the SF3B1 gene
a biopharmaceutical company specializing in the discovery and development of precision medicines for oncology, announced today that it has named its lead investigational drug candidate for its program that targets SF3B1, a component of the human genetic splicing machinery that has been implicated and shown to be frequently mutated in multiple cancers.
Our research has shed significant light into the mechanism of SF3B1 mutations and their role in aberrant splicing and irregular epigenetic controls.