K562 SF3B1 Mutants and Splicing
Ontology highlight
ABSTRACT:
INSTRUMENT(S): Orbitrap Fusion Lumos, Orbitrap Fusion
ORGANISM(S): Homo Sapiens (human)
TISSUE(S): Cell Culture
SUBMITTER: 
James Wright
LAB HEAD: Jyoti Choudhary
PROVIDER: PXD030127 | Pride | 2024-11-20
REPOSITORIES: Pride
Dataset's files
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| 13MAR17_Suruchi_14.raw | Raw | |||
| 13MAR17_Suruchi_15.raw | Raw | |||
| 13MAR17_Suruchi_16.raw | Raw | |||
| 13MAR17_Suruchi_17.raw | Raw | |||
| 13MAR17_Suruchi_18.raw | Raw |
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Publications
SF3B1 hotspot mutations confer sensitivity to PARP inhibition by eliciting a defective replication stress response.
Bland Philip P Saville Harry H Wai Patty T PT Curnow Lucinda L Muirhead Gareth G Nieminuszczy Jadwiga J Ravindran Nivedita N John Marie Beatrix MB Hedayat Somaieh S Barker Holly E HE Wright James J Yu Lu L Mavrommati Ioanna I Read Abigail A Peck Barrie B Allen Mark M Gazinska Patrycja P Pemberton Helen N HN Gulati Aditi A Nash Sarah S Noor Farzana F Guppy Naomi N Roxanis Ioannis I Pratt Guy G Oldreive Ceri C Stankovic Tatjana T Barlow Samantha S Kalirai Helen H Coupland Sarah E SE Broderick Ronan R Alsafadi Samar S Houy Alexandre A Stern Marc-Henri MH Pettit Stephen S Choudhary Jyoti S JS Haider Syed S Niedzwiedz Wojciech W Lord Christopher J CJ Natrajan Rachael R
Nature genetics 20230731 8
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<sup>MUT</sup>) cells are selectively sensitive to poly (ADP-ribose) polymerase inhibitors (PARPi), independent of hotspot mutation and tumor site. SF3B1<sup>MUT</sup> cells display a defective response to PARPi-induced replication stress that occurs via downregulation of the cyclin-depe ...[more]
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