Anti-Neuroligin 1 antibody [N97A/31]

Supplementary info

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

Activity summary

Neuroligin 1 also known as NLGN1 is a member of the neuroligin family of cell adhesion molecules. It plays a significant mechanical role at synaptic junctions where it mediates synapse formation and maintenance. Neuroligin 1 weighs approximately 97 kDa and is mainly expressed in the brain particularly in postsynaptic densities of excitatory glutamatergic synapses. Neuroligin 1 interacts with neurexins on the presynaptic side facilitating trans-synaptic connections important for proper neuronal communication.

Biological function summary

Neuroligin 1 contributes to synaptic organization and signaling by being part of a larger protein complex. This complex involves postsynaptic scaffolding proteins such as PSD-95 which anchor neuroligin to the cytoskeleton and receptors like NMDA and AMPA receptors. Neuroligin 1 regulates synaptic stabilization and plasticity which are essential for learning and memory processes. Through these interactions it impacts synaptic strength and efficiency playing an integral role in the modulation of synaptic activity.

Pathways

Neuroligin 1 is a critical component of synaptic development and function pathways. It operates within the synaptic signaling and plasticity pathways affecting neurotransmitter function and reception. Neuroligin 1 functions in coordination with proteins such as neurexins and SHANK proteins to regulate the assembly and maturation of synapses. These interactions influence calcium signaling and involve the recruitment of other synaptic proteins that further contribute to synaptic modulation.

Associated diseases and disorders

Neuroligin 1 is linked to neurological conditions like autism spectrum disorders (ASD) and schizophrenia. Mutations or dysregulations of neuroligin 1 impact synaptic connectivity leading to altered neuronal networks and communication deficits involved in these conditions. The balance of excitatory and inhibitory synaptic function that neuroligin and its binding partners including neurexins and SHANK3 control is directly implicated in the pathophysiology of these disorders. Disruptions in neuroligin-neurexin signaling pathways may therefore contribute to the synaptic dysfunctions observed in ASD and schizophrenia.