Results 31 to 40 of about 19,190 (266)

Silencing SF3B1 promotes apoptosis and inhibits proliferation and invasion of human lung cancer cell line A549 [PDF]

open access: yesJichu yixue yu linchuang, 2023
Objective To explore the effect of splicing factor 3B subunit (SF3B1) on apoptosis, proliferation and invasion of human lung cancer cells. Methods Non-small cell lung cancer(NSCLC) patients in the General Hospital of Western Theater Command PLA from ...
ZHANG Xiaowan, KANG Xia, YAO Xiaoying, XIE Fang, LI Ying
doaj   +1 more source

Cancer-associated SF3B1 mutation K700E causes widespread changes in U2/branchpoint recognition without altering splicing. [PDF]

open access: yesProc Natl Acad Sci U S A
Myelodysplastic syndromes and other cancers are often associated with mutations in the U2 snRNP protein SF3B1. Common SF3B1 mutations, including K700E, disrupt SF3B1 interaction with the protein SUGP1 and induce aberrant activation of cryptic 3’ splice ...
Damianov A   +4 more
europepmc   +2 more sources

SF3B1 Mutations in Hematological Malignancies

open access: yesCancers, 2022
Recently, mutations in the genes involved in the spliceosome have attracted considerable interest in different neoplasms. Among these, SF3B1 mutations have acquired great interest, especially in myelodysplastic syndromes, as they identify a subgroup of patients who can benefit from personalized therapy. The SF3B1 gene encodes the largest subunit of the
Daniela Cilloni   +3 more
openaire   +3 more sources

SF3B1 mutant myelodysplastic syndrome: Recent advances [PDF]

open access: yesAdvances in Biological Regulation, 2021
The myelodysplastic syndromes (MDS) are common myeloid malignancies. Mutations in genes encoding different components of the spliceosome occur in more than half of all MDS patients. SF3B1 is the most frequently mutated splicing factor gene in MDS, and there is a strong association between SF3B1 mutations and the presence of ring sideroblasts in the ...
Pellagatti, A, Boultwood, J
openaire   +4 more sources

Pre-mRNA splicing-associated diseases and therapies

open access: yesRNA Biology, 2023
Precursor mRNA (pre-mRNA) splicing is an essential step in human gene expression and is carried out by a large macromolecular machine called the spliceosome.
Sierra L. Love   +3 more
doaj   +1 more source

SF3B1 hotspot mutations confer sensitivity to PARP inhibition by eliciting a defective replication stress response

open access: yesNature Genetics, 2023
SF3B1 hotspot mutations are associated with a poor prognosis in several tumor types and lead to global disruption of canonical splicing. Through synthetic lethal drug screens, we identify that SF3B1 mutant ( SF3B1 ^MUT) cells are selectively sensitive to
Philip Bland   +38 more
semanticscholar   +1 more source

The Effect of SF3B1 Mutation on the DNA Damage Response and Nonsense-Mediated mRNA Decay in Cancer

open access: yesFrontiers in Oncology, 2021
Recurrent mutations in splicing factor 3B subunit 1 (SF3B1) have been identified in several malignancies and are associated with an increased expression of 3’ cryptic transcripts as a result of alternative branchpoint recognition.
Alexander C. Leeksma   +25 more
doaj   +1 more source

SF3B1 thermostability as an assay for splicing inhibitor interactions. [PDF]

open access: yesJ Biol Chem
The spliceosome protein, SF3B1 associates with U2 snRNP during early spliceosome assembly for pre-mRNA splicing. Frequent somatic mutations in SF3B1 observed in cancer necessitates characterization of its role in identifying the branchpoint adenosine of introns. Remarkably, SF3B1 is the target of three distinct natural product drugs, each identified by
Amorello AN   +5 more
europepmc   +5 more sources

Localized inhibition of protein phosphatase 1 by NUAK1 promotes spliceosome activity and reveals a MYC-sensitive feedback control of transcription. [PDF]

open access: yes, 2020
Deregulated expression of MYC induces a dependence on the NUAK1 kinase, but the molecular mechanisms underlying this dependence have not been fully clarified.
Ade, C.P.   +18 more
core   +1 more source

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