IL1RAPL1 Proteins, Antibodies, cDNA Clones Research Reagents

IL1RAPL1 (Interleukin 1 Receptor Accessory Protein Like 1, also known as IL1R8; MRX10; MRX21; MRX34; OPHN4; IL1RAPL; TIGIRR-2; IL1RAPL-1; IL-1RAPL-1; IL-1-RAPL-1), located on Xp21.3-p21.2, is conserved in chimpanzee, Rhesus monkey, dog, cow, mouse, rat, chicken, zebrafish, and frog. The gene produces a 79969 Da protein composed of 696 amino acids. The protein encoded by this gene is a member of the interleukin 1 receptor family and is similar to the interleukin 1 accessory proteins. Diseases such as Mental Retardation, X-Linked 21, and Non-Syndromic X-Linked Intellectual Disability are associated with IL1RAPL1.

IL1RAPL1 Protein (3)

    IL1RAPL1 Antibody (1)

      IL1RAPL1 cDNA Clone (25)


      克隆载体 cDNA 产品

      In lentiviral vector

      IL1RAPL1 Lysate (3)

        IL1RAPL1 分子背景

        Interleukin-1 receptor accessory protein-like 1 (IL1RAPL1) is a member of the 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 signaling via the NFkB pathway. The means of signaling 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 the human cognitive ability to some extent, especially the memory and concentration capability.

        IL1RAPL1 参考文献

        • 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.

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