Nada Mageed

Apr 29, 2024 | nature.com | Raymond Carter |Baranda S. Hansen |Katherine A. Donovan |Moritz Hunkeler |Wojciech Rosikiewicz |Meghan G. McReynolds | +8 more

Correction to: Nature https://doi.org/10.1038/s41586-024-07250-1 Published online 27 March 2024In the version of the article initially published, the far-right labels in Fig. 4h (now reading “Viable cells” and “Lethal in SMARCB1-deficient RT cells”) were swapped and have now been corrected in the HTML and PDF versions of the article. About this articleRadko-Juettner, S., Yue, H., Myers, J.A. et al. Author Correction: Targeting DCAF5 suppresses SMARCB1-mutant cancer by stabilizing SWI/SNF.

Mar 27, 2024 | nature.com | Raymond Carter |Baranda S. Hansen |Katherine A. Donovan |Moritz Hunkeler |Wojciech Rosikiewicz |Nada Mageed | +8 more

AbstractWhereas oncogenes can potentially be inhibited with small molecules, the loss of tumour suppressors is more common and is problematic because the tumour-suppressor proteins are no longer present to be targeted. Notable examples include SMARCB1-mutant cancers, which are highly lethal malignancies driven by the inactivation of a subunit of SWI/SNF (also known as BAF) chromatin-remodelling complexes.

Mar 20, 2024 | nature.com | Hai-Tsang Huang |Ryan Lumpkin |Yuan Xiong |James Chen |Katherine A. Donovan |Eric S. Fischer | +2 more

AbstractProtein ubiquitylation controls diverse processes within eukaryotic cells, including protein degradation, and is often dysregulated in disease. Moreover, small-molecule degraders that redirect ubiquitylation activities toward disease targets are an emerging and promising therapeutic class. Over 600 E3 ubiquitin ligases are expressed in humans, but their substrates remain largely elusive, necessitating the development of new methods for their discovery.