How does the cBAF complex use disordered protein to engage diverse transcriptional regulators like YAP1, SOX2, and CBP/p300? Our new Mol Cell paper reveals β-catenin’s role as a molecular adapter

Huge thank you to all @hodgeshc.bsky.social lab co-authors, as well as our helpful reviewers and editors at Nucleic Acids Research (6/6)

Why does it matter? Across all cancer types tested, SWI/SNF inhibition sensitizes addicted cells to retinoic acid, which also acts during G1. We argue that SWI/SNF inhibitors may have major value as part of combined maintenance therapies, not only for acute treatment (5/6)

Analysis of the cyclic patterns of DNA accessibility revealed that SWI/SNF-dependent CRC binding sites are found at G1-specific enhancers, where SMARCA4 and the CRC are essential for activating replication commitment genes (4/6)

SMARCA4 sustains both chromatin binding and expression of the adrenergic core regulatory circuitry (CRC). Despite the presence of pioneer TFs, SWI/SNF inhibition rapidly breaks CRC autoregulatory activity within 1 hour (3/6)

We use neuroblastoma to study the mechanisms of SWI/SNF addiction. We show that SMARCA4, the ATPase of SWI/SNF complexes, is a novel pharmacologically targetable vulnerability of adrenergic neuroblastoma cells (2/6)

For the first time, we find a common mechanism for SWI/SNF addiction in cancer! Our paper reveals that G1 phase is a critical junction for SWI/SNF activity in several addicted cancers, including neuroblastoma, AML, prostate cancer, and uveal melanoma academic.oup.com/nar/advance-... (1/6)