Prostate cancer cells maintain heterogeneous androgen receptor transcriptional activity through upregulation of AR-regulated coactivator GREB1, and cells with high activity rapidly develop resistance to antiandrogen therapy in a GREB1-dependent manner.

Coregulators mediate selective interactions between DNA-bound androgen receptor and other transcription factors, which control distinct prostate cancer biology, suggesting disruption of critical interactions in these complexes as a novel therapeutic strategy.

A novel first-in-class small molecule (ERX-11) that interacts with and disrupts the interactome of the estrogen receptor (ER), blocks the growth of ER-positive breast cancers, including those that are resistant to currently approved hormonal agents.

Mutagenesis studies identified an androgen receptor mutation that converts enzalutamide-a drug recently approved for the treatment of advanced prostate cancer-into an androgen receptor agonist, and modeling studies informed the design of novel drugs that are effective against the mutant receptor.

CBP/EP300 bromodomain inhibitors have a therapeutic application in oncology via targeting the IRF4 transcriptional program, a clinically validated network critical for multiple myeloma cell viability.

Effective antiestrogens engage a new structural interaction to improve therapeutic antagonism in hormone-resistant breast cancer cells expressing Y537S estrogen receptor alpha.

β₃-AR signalling via cGMP in cardiomyocytes is regulated via phosphodiesterase 2 and 5 degradation, it is potentially cardioprotective, but dysregulated in heart failure through signal redistribution and higher phosphodiesterase activity.

The α₁-adrenergic receptor augments the activity of the L-type Ca²⁺ channel Ca_V1.2 through PKC and the tyrosine kinases Pyk2 and Src and thereby synaptic plasticity.

The transcription factor ERG recruits the PRMT5 enzyme to methylate the androgen receptor, presenting a post-translational regulatory mechanism that could be therapeutically exploited to control cell proliferation.

Nemo-like kinase is a key protein promoting the pathogenesis of spinal and bulbar muscular atrophy.