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Human IL-1R8 / IL1RAPL1 Protein (His Tag)

IL1R8,IL1RAPL,MRX10,MRX21,MRX34,OPHN4,TIGIRR-2

Catalog Number P10177-H08H
Organism Species Human
Host Human Cells
Synonyms IL1R8,IL1RAPL,MRX10,MRX21,MRX34,OPHN4,TIGIRR-2
Molecular Weight The recombinant human IL1R8 consists of 347 amino acids and has a predicted molecular mass of 40 kDa. As a result of glycosylation, the apparent molecular mass of rh IL1R8 is approximately 50-55 kDa in SDS-PAGE under reducing conditions.
predicted N Leu 19
SDS-PAGE
Purity > 95 % as determined by SDS-PAGE
Protein Construction A DNA sequence encoding the human IL1R8 (NP_055086.1) extracellular domain (Met 1-Leu 354) was expressed with a C-terminal polyhistidine tag.
Bio-activity
Research Area Neuroscience |Neurotransmission |Calcium Signaling |Calcium Channel |N-type
Formulation Lyophilized from sterile PBS, pH 7.4
1. Normally 5 % - 8 % trehalose, mannitol and 0.01% Tween80 are added as protectants before lyophilization. Specific concentrations are included in the hardcopy of COA.
Background Interleukin-1 receptor accessory protein-like 1 (IL1RAPL1) is a member of interleukin-1 receptor family. The protein structurally comprises three extracellular immunoglobulin domains, which presumably mediate binding of an as yet unidentified ligand, a transmembrane region, and an intracellular domain, which is likely to enable signalling via the NFkB pathway. The means of signalling is almost certain to be identical to that used by the IL1R family and the more distally related Toll protein. L1RAPL1 protein physically interacts via its 150 aa C-terminal domain with neuronal calcium sensor-1 (NCS-1), a protein widely expressed in neurons and the related chromaffin and PC12 cells. IL1RAPL1 is an integral membrane protein responsible for a nonsyndromic form of mental retardation (MR). It is suggested to affect human cognitive ability to some extent, especially the memory and concentration capability.
Reference
  • Frdric Gambino, et al. (2007) IL1-receptor accessory protein-like 1 (IL1RAPL1), a protein involved in cognitive functions, regulates N-type Ca2+-channel and neurite elongation. Proc Natl Acad Sci. 104 (21): 9063-8.
  • Wheway JM, et al. (2003) A complex deletion-inversion-deletion event results in a chimeric IL1RAPL1-dystrophin transcript and a contiguous gene deletion syndrome. J Med Genet. 40: 127-131.