Reactivity | HuSpecies Glossary |
Applications | Bioactivity |
Format | Carrier-Free |
Details of Functionality | Measured by the ability of the immobilized protein to support the adhesion of U‑118‑MG human glioblastoma/astrocytoma cells. The ED50 for this effect is 0.7-2.8 μg/mL. |
Source | Mouse myeloma cell line, NS0-derived human Neuronal Pentraxin R/NPTXR protein Ala24-Ala500, with an N-terminal 6-His tag |
Accession # | |
N-terminal Sequence | His |
Protein/Peptide Type | Recombinant Proteins |
Gene | NPTXR |
Purity | >95%, by SDS-PAGE under reducing conditions and visualized by silver stain |
Endotoxin Note | <0.10 EU per 1 μg of the protein by the LAL method. |
Dilutions |
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Theoretical MW | 51.3 kDa. Disclaimer note: The observed molecular weight of the protein may vary from the listed predicted molecular weight due to post translational modifications, post translation cleavages, relative charges, and other experimental factors. |
SDS-PAGE | 55-65 kDa, reducing conditions |
Storage | Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
|
Buffer | Lyophilized from a 0.2 μm filtered solution in PBS. |
Purity | >95%, by SDS-PAGE under reducing conditions and visualized by silver stain |
Reconstitution Instructions | Reconstitute at 300 μg/mL in PBS. |
The Neuronal Pentraxin Receptor (NPTXR; also called NPR) is a 55‑65 kDa, type II transmembrane glycoprotein within the Pentraxin family. NPTXR is co‑expressed and forms heteromultimers with the related, secreted proteins NPTX1 and NPTX2/NARP (1, 2). Human NPTXR is a 500 amino acid (aa) protein that includes a 477 aa extracellular domain (ECD) with one calcium-binding Pentraxin domain. The human NPTXR ECD shares 88% and 89% aa sequence identity with mouse and rat NPTXR, respectively. A 62 kDa soluble form is generated by TACE/ADAM17 proteolytic cleavage C-terminal to the transmembrane segment (3). Soluble forms of 55 kDa and 45 kDa have also been reported (2, 3). NPTXR is expressed on cerebellar Purkinje and granule cells, and hippocampal neurons of the CA1, CA3 and dentate gyrus regions (1). It is enriched on axonal membranes at excitatory synapses where, with NPTX1, it recruits the GluR4 subunit of AMPA-type glutamate receptors (AMPAR) to promote synaptogenesis (3, 4). Synaptic activity stimulates mGluR1 or mGluR5 receptors, which then activate TACE, causing release of the NPTXR heteromultimer complex from the membrane (3). NPTX1/2 within the complex mediate binding AMPAR, while the soluble (but not transmembrane) form of NPTXR within the complex mediates AMPAR endocytosis and mGluR1/5‑mediated long-term depression (3). NPTXR is reported to be increased in cerebrospinal fluid or serum of Alzheimer’s disease patients as compared to controls (5). Aberrant expression of transmembrane NPTXR has also been reported in small-cell lung cancers (SCLC; 6).
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