The small molecule NMDA-receptor antagonist MK801 has been genetically targeted to specific cell types in brain tissue to examine the role of NMDA receptors in cocaine-induced synaptic plasticity.

Definition of leukemia gene expression mechanisms reveals general principles of cancer gene control and offers a pharmacologic strategy for its therapeutic reprogramming.

Project Rephetio combines data integration and systematic analysis to enable drug repurposing predictions on an unprecedented scale.

GDC-0810 is a novel, orally bioavailable SERD that exhibits robust pre-clinical activity in models of ER+ breast cancer, including models of tamoxifen resistance, and those that express the ERα mutations, ER.Y537S and ER.D538G.

Contrary to a generally accepted principle, the pore properties of KCNQ1 channels depend on the states of voltage-sensing domains activation; KCNE1 alters the voltage-sensing domains-pore coupling to modulate KCNQ1 channel properties.

GPR88 inhibits G-protein signaling of nearby GPCRs, and dampens b-arrestin recruitment by all GPCRs tested, likely by sequestration in intracellular compartments.

Optogenetic tools enable sophisticated measurements of a voltage-gated sodium channel implicated in pain, as well as high-throughput screening of candidate channel blockers.

The small molecule, 147, is a pro-drug that preferentially activates ATF6 signaling through a mechanism involving localized metabolic activation and selective covalent modification of ER resident proteins involved in regulating ATF6 activity.

The inhibitory or deletion effect of MELK does not impair the proliferation of basal-like breast cancer cell lines.

Molecular engineering can generate light-sensitive NMDA receptors with specific subunit combinations.