Anti-GluN2D antibody [EPR28378-56] - BSA and Azide free

Supplementary info

This supplementary information is collated from multiple sources and compiled automatically.

Activity summary

GluN2D also known as GRIN2D or NR2D is a subunit of the NMDA (N-methyl-D-aspartate) receptor which plays an essential role in excitatory neurotransmission in the brain. It has a molecular mass of about 130 kDa. This protein is primarily expressed in the central nervous system including the neocortex hippocampus and thalamus. GluN2D's role within the NMDA receptor complex involves modulating synaptic plasticity learning and memory processes by binding with calcium ions.

Biological function summary

GluN2D contributes to the complexity of neuronal communication and signaling. It is an integral component of the NMDA receptor complex which is a heterotetramer consisting of GluN1 GluN2 and occasionally GluN3 subunits. The GluN2D subunit influences the receptor's biophysical and pharmacological properties affecting the duration and amplitude of the excitatory postsynaptic current. Through these functions GluN2D plays a role in synaptic transmission and neuroplasticity impacting how neurons adapt to various stimuli and experiences.

Pathways

GluN2D plays significant roles in synaptic signaling and neurodevelopmental pathways. In synaptic signaling GluN2D modulates calcium ion influx which is necessary for activating intracellular pathways involving proteins like CaMKII critical for long-term potentiation and memory formation. In development its involvement in neuronal differentiation and maturation interacts with proteins like PSD-95 which are essential for organizing synaptic architecture and function. These pathways highlight the functional importance of GluN2D in both synaptic and developmental contexts.

Associated diseases and disorders

GluN2D is associated with neurological and psychiatric conditions such as epilepsy and schizophrenia. Variations in GRIN2D gene expression or function can disrupt NMDA receptor activity leading to an imbalance in excitatory and inhibitory neurotransmission in the central nervous system. This imbalance can contribute to seizure generation in epilepsy or the symptoms observed in schizophrenia. Additionally GluN2D interactions with proteins like DLG4 associated with postsynaptic density further influence these disease mechanisms offering potential therapeutic targets for intervention.