NMDAR1 (GRIN1) (NM_007327) Human Recombinant Protein

CAT#: TP790146

Purified recombinant protein of Human glutamate receptor, ionotropic, N-methyl D-aspartate 1 (GRIN1), transcript variant NR1-3, with C-terminal DDK tag, secretory expressed in CHO cells, 50ug

Product Images

Specifications

Product Data

• Species: Human
• Expression Host: CHO
• Expression cDNA Clone or AA Sequence:
  Protein Sequence

  A DNA sequence from TrueORF clone, RC216458, encoding the region Arg19-Asp559 of GRIN1
• Tag: C-DDK
• Predicted MW: 61.2 kDa
• Concentration: >0.05 µg/µL as determined by microplate BCA method
• Purity: > 80% as determined by SDS-PAGE and Coomassie blue staining
• Buffer: PBS, pH 7.4, 10% glycerol
• Note: For testing in cell culture applications, please filter before use. Note that you may experience some loss of protein during the filtration process.
• Storage: Store at -80°C.
• Stability: Stable for 12 months from the date of receipt of the product under proper storage and handling conditions. Avoid repeated freeze-thaw cycles.

Reference Data

• RefSeq: NP_015566
• Locus ID: 2902
• UniProt ID: Q05586
• Cytogenetics: 9q34.3
• Refseq Size: 5137
• Refseq ORF: 2814
• Synonyms: GluN1; MRD8; NDHMSD; NDHMSR; NMD-R1; NMDA1; NMDAR1; NR1
• Summary: The protein encoded by this gene is a critical subunit of N-methyl-D-aspartate receptors, members of the glutamate receptor channel superfamily which are heteromeric protein complexes with multiple subunits arranged to form a ligand-gated ion channel. These subunits play a key role in the plasticity of synapses, which is believed to underlie memory and learning. Cell-specific factors are thought to control expression of different isoforms, possibly contributing to the functional diversity of the subunits. Alternatively spliced transcript variants have been described. [provided by RefSeq, Jul 2008]
• Protein Families: Druggable Genome, Ion Channels: Glutamate Receptors, Transmembrane
• Protein Pathways: Alzheimer's disease, Amyotrophic lateral sclerosis (ALS), Calcium signaling pathway, Huntington's disease, Long-term potentiation, Neuroactive ligand-receptor interaction