Results 51 to 60 of about 12,272 (217)

Inhibition of SF3b1 by pladienolide B evokes cycle arrest, apoptosis induction and p73 splicing in human cervical carcinoma cells

open access: yesArtificial Cells, Nanomedicine, and Biotechnology, 2019
Pladienolide B is a potent cancer cell growth inhibitor that targets the SF3b1 subunit of the spliceosome. There is considerable interest in the compound as a tool to study SF3b1 function in cancer.
Qianjing Zhang   +10 more
doaj   +1 more source

Transcriptome sequencing reveals potential mechanism of cryptic 3' splice site selection in SF3B1-mutated cancers. [PDF]

open access: yesPLoS Computational Biology, 2015
Mutations in the splicing factor SF3B1 are found in several cancer types and have been associated with various splicing defects. Using transcriptome sequencing data from chronic lymphocytic leukemia, breast cancer and uveal melanoma tumor samples, we ...
Christopher DeBoever   +9 more
doaj   +1 more source

Structure-activity relationship study of splicing modulators on Hsh155/SF3B1 through chemical synthesis and yeast genetics [PDF]

open access: yes
Meayamycins are synthetic analogs of the natural product FR901464 and exhibit potent anticancer activity against human cancers. They bind SF3B1 and PHF5A, components of the human spliceosome, and alter pre-mRNA splicing.
John, Schmitz   +4 more
core   +1 more source

Rare SF3B1 R625 mutations in cutaneous melanoma [PDF]

open access: yesMelanoma Research, 2014
RNA splicing is the cellular process that has only recently been found to be an important target for various cancers. Among the spliceosome genes that are involved in cancers, SF3B1 is most frequently mutated. Recurrent mutation in codon 625 has been found in uveal melanoma, but this mutation has not been identified in cutaneous melanoma. We used whole-
Yong, Kong   +2 more
openaire   +2 more sources

Copy-number and gene dependency analysis reveals partial copy loss of wild-type SF3B1 as a novel cancer vulnerability

open access: yeseLife, 2017
Genomic instability is a hallmark of human cancer, and results in widespread somatic copy number alterations. We used a genome-scale shRNA viability screen in human cancer cell lines to systematically identify genes that are essential in the context of ...
Brenton R Paolella   +26 more
doaj   +1 more source

Expression of circular RNAs in myelodysplastic neoplasms and their association with mutations in the splicing factor gene SF3B1

open access: yesMolecular Oncology, 2023
Mutations in the splicing factor 3b subunit 1 (SF3B1) gene are frequent in myelodysplastic neoplasms (MDS). Because the splicing process is involved in the production of circular RNAs (circRNAs), we investigated the impact of SF3B1 mutations on circRNA ...
Iva Trsova   +19 more
doaj   +1 more source

SPHINX31 acts as a SRPK1 inhibitor targeting the ATR/DNA‐PKcs/CHK1 replicative checkpoint to inhibit cell growth in non‐small cell lung cancer

open access: yesMolecular Oncology, EarlyView.
The kinase SRPK1 directly interacts with the protein TOPBP1 and regulates the pre‐mRNA splicing of WIZ thereby contributing to the activation of the ATR/CHK1 replicative checkpoint in response to replicative stress. This allows cancer cells' genomic stability and survival.
Amani Shreim   +17 more
wiley   +1 more source

deboever-sf3b1-2014

open access: yes, 2014
Files for replicating SF3B1 study.
Christopher DeBoever (541416)
core   +1 more source

SF3B1 mutations constitute a novel therapeutic target in breast cancer [PDF]

open access: yes, 2015
Mutations in genes encoding proteins involved in RNA splicing have been found to occur at relatively high frequencies in several tumour types including myelodysplastic syndromes, chronic lymphocytic leukaemia, uveal melanoma, and pancreatic cancer, and ...
Wai, P   +19 more
core   +1 more source

CRISPR editing of sftb-1/SF3B1 in Caenorhabditis elegans allows the identification of synthetic interactions with cancer-related mutations and the chemical inhibition of splicing.

open access: yesPLoS Genetics, 2019
SF3B1 is the most frequently mutated splicing factor in cancer. Mutations in SF3B1 likely confer clonal advantages to cancer cells but they may also confer vulnerabilities that can be therapeutically targeted.
Xènia Serrat   +6 more
doaj   +1 more source

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