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.
The orphan receptor GPR158 is highly regulated by stress exposure and acts on key neuronal signaling pathways in the prefrontal cortex to control depressive-like behaviors.
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.
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.
