Asset Details
Do you wish to reserve the book?
A non-canonical SWI/SNF complex is a synthetic lethal target in cancers driven by BAF complex perturbation
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
A non-canonical SWI/SNF complex is a synthetic lethal target in cancers driven by BAF complex perturbation
Do you wish to request the book?
A non-canonical SWI/SNF complex is a synthetic lethal target in cancers driven by BAF complex perturbation
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
A non-canonical SWI/SNF complex is a synthetic lethal target in cancers driven by BAF complex perturbation
2018
Overview
Mammalian SWI/SNF chromatin remodelling complexes exist in three distinct, final-form assemblies: canonical BAF (cBAF), PBAF and a newly characterized non-canonical complex (ncBAF). However, their complex-specific targeting on chromatin, functions and roles in disease remain largely undefined. Here, we comprehensively mapped complex assemblies on chromatin and found that ncBAF complexes uniquely localize to CTCF sites and promoters. We identified ncBAF subunits as synthetic lethal targets specific to synovial sarcoma and malignant rhabdoid tumours, which both exhibit cBAF complex (SMARCB1 subunit) perturbation. Chemical and biological depletion of the ncBAF subunit, BRD9, rapidly attenuates synovial sarcoma and malignant rhabdoid tumour cell proliferation. Importantly, in cBAF-perturbed cancers, ncBAF complexes maintain gene expression at retained CTCF-promoter sites and function in a manner distinct from fusion oncoprotein-bound complexes. Together, these findings unmask the unique targeting and functional roles of ncBAF complexes and present new cancer-specific therapeutic targets.
Michel et al. report unique localization of non-canonical BAF to CTCF sites and promoters, which confers synthetic lethality in canonical BAF-perturbed synovial sarcoma and malignant rhabdoid tumour cells.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ 38/91
/ 45/15
/ 45/41
/ 82/58
/ 82/83
/ Biomedical and Life Sciences
/ Cancer
/ Cell Proliferation - genetics
/ Chromatin Assembly and Disassembly - genetics
/ Chromosomal Proteins, Non-Histone - genetics
/ Chromosomal Proteins, Non-Histone - metabolism
/ Genes
/ Humans
/ Mutation
/ Nuclear Proteins - metabolism
/ Promoter Regions, Genetic - genetics
/ Sarcoma
/ Sarcoma, Synovial - genetics
/ Sarcoma, Synovial - metabolism
/ Transcription Factors - genetics
/ Transcription Factors - metabolism
/ Tumors
