Anti-NPTXR antibody [EPR25684-238] - BSA and Azide free (Detector)

Supplementary info

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

Activity summary

NPTXR also known as Neuronal Pentraxin Receptor is a protein involved in the synaptic organization. It has a molecular mass of approximately 65 kDa. NPTXR expresses mainly in the central nervous system including the brain and spinal cord. As a synaptic protein it plays a role in modulating neuron-neuron interactions and signaling pathways critical for the central nervous system's proper function.

Biological function summary

Neuronal pentraxin receptor contributes to synaptic plasticity and maintenance. It forms a complex with other pentraxin proteins like NPTX1 and NPTX2 facilitating the clustering of AMPA receptors at synapses. This interaction enhances excitatory synaptic transmission which is important for processes like learning and memory. NPTXR therefore plays a significant role in maintaining synaptic strength and integrity.

Pathways

The neuronal pentraxin receptor influences the glutamatergic signaling pathway. This pathway involves neurotransmitter glutamate and its receptors which include AMPA-type glutamate receptors at postsynaptic sites. NPTXR's interaction with AMPA receptors via NPTX1 and NPTX2 promotes receptor clustering critical for NMDA receptor phosphorylation. As a result this protein contributes to synaptic plasticity influencing learning and memory pathways in neurons.

Associated diseases and disorders

NPTXR has implications in neurodegenerative diseases and schizophrenia. Altered synaptic plasticity and receptor clustering can lead to cognitive deficits frequently observed in Alzheimer's disease. Additionally studies suggest a potential link between NPTXR and schizophrenia where dysregulated synaptic organization impacts neurotransmission. NPTXR's association with AMPA receptors through other pentraxins implicates it in these disorders highlighting its significance as a therapeutic target.