A drug used in hormone replacement therapy can target estrogen receptors that have become resistant to breast cancer treatments.

A compound can change the activity of NMDA receptors in some regions of a synapse without affecting those in other regions.

Self-reactive B cells downregulate the IgM but not the IgD B cell receptor, and this serves as a critical tolerance mechanism because IgD is less sensitive to bona fide endogenous antigens than IgM.

Biochemical and genetic experiments show that Ebf and Lhx2 cooperate to specify olfactory receptor enhancers, which cooperate to drive olfactory receptor expression.

The activation of beige adipocyte thermogenesis by cold temperatures and β3-adrenergic receptor agonists induce beige adipocyte formation, function and perdurance.

A family of engineered immune receptors trigger internalization of cancer cells and antigen-coated targets.

Glutamate receptor auxiliary proteins exert their effects on receptor gating through two divergent extracellular loops, explaining subunit specificity and allowing the construction of null versions that form complexes normally but do not modify receptor gating.

Excitotoxicity driven by NMDA receptor hyper-activation does not involve DAPK1-dependent events in vitro or in vivo, and previously described DAPK1-NMDAR disrupting peptides act by blocking the NMDA receptor.

Neurons in the hypothalamus that promote satiety manifest plasticity of their response to the excitatory transmitter, glutamate, by re-organizing the composition of a specific glutamare receptor.

A novel form of hippocampal synaptic plasticity is expressed by a change in channel function of GluA3-containing AMPA-receptors.