Cigall Kadoch

This study shows that inhibiting mSWI/SNF complexes enhances the effectiveness of KRAS inhibitors in lung cancers by reversing epithelial-mesenchymal transition resistance.

The paper identifies SWIFT, a SWI/SNF subunit domain that mediates transcription factor interactions, showing its role in chromatin targeting and cancer cell proliferation.

This study identifies shifted mSWI/SNF subcomplex stoichiometry in DDEC/UEC cancers and shows that SMARCA4/2 inhibitors reduce tumor growth and synergize with chemotherapy.

The paper identifies a small molecule, BRD1732, that is ubiquitinated in cells, leading to proteasome inhibition through accumulation of ubiquitin chains.

The paper identifies chr22q as a regulatory hub where genetic risk for neuropsychiatric conditions is associated with coordinated gene expression downregulation in brain tissue.

The paper introduces GIN, a resource that decodes molecular grammars of human intrinsically disordered regions (IDRs) and identifies their functional roles in biological processes and disease.

This study identifies mSWI/SNF complex activity as a targetable dependency in POU2F3-positive small cell lung cancer, showing that inhibiting mSWI/SNF or BRD9 reduces tumor growth and improves survival.

This study shows that Arid1a loss enhances pancreatic β-cell regeneration by activating EGF signaling, protecting against diabetes.