Publications

Non-ionotropic signaling through the NMDA receptor GluN2B carboxy-terminal domain drives dendritic spine plasticity and reverses fragile X phenotypes

 95
Non-ionotropic signaling through the NMDA receptor GluN2B carboxy-terminal domain drives dendritic spine plasticity and reverses fragile X phenotypes

Tags:

Previous Article

A nucleosome switch primes hepatitis B virus infection

Next Article

Reversing fragile X syndrome symptoms by modifying NMDA receptor signaling

Related Posts

Glycocalyx dysregulation impairs blood– brain barrier in ageing and disease

Glycocalyx dysregulation impairs blood– brain barrier i...

 176

Heterogeneity in the coordination of delta cells with beta cells is driven by both paracrine signals and low-density Cx36 gap junctions

Heterogeneity in the coordination of delta cells with b...

 35

Signaling pathways and therapeutic approaches in glioblastoma multiforme

Signaling pathways and therapeutic approaches in gliobl...

 73