Mouse CHL-1/L1CAM-2 Biotinylated Antibody Summary
Applications
Please Note: Optimal dilutions should be determined by each laboratory for each application. General Protocols are available in the Technical Information section on our website.
Reconstitution Calculator
Preparation and Storage
- 12 months from date of receipt, -20 to -70 °C as supplied.
- 1 month, 2 to 8 °C under sterile conditions after reconstitution.
- 6 months, -20 to -70 °C under sterile conditions after reconstitution.
Background: CHL-1/L1CAM-2
Close homolog of L1 (CHL-1), also known as cell adhesion L1-like (CALL) and L1 cell adhesion molecule 2 (L1CAM-2), belongs to the L1 subfamily of immunoglobulin (Ig) superfamily cell adhesion molecules, which also includes L1, neurofascin and NgCAM-related cell adhesion molecule (NrCAM) (1‑3). These molecules are type I transmembrane proteins that have 6 Ig-like domains and 4‑5 fibronectin type III-like (FNIII) domains in their extracellular regions. They also share a highly conserved cytoplasmic region of approximately 110 amino acid (aa) residues containing an ankyrin-binding site. CHL-1 is expressed as a highly glycosylated 185 kDa transmembrane protein by subpopulations of neurons and glia of the central and peripheral nervous system (4, 5). Ectodomain shedding via the metalloprotease-disintegrin ADAM8 releases 165 kDa and 125 kDa soluble CHL-1 fragments, which can diffuse away to function at distant sites (6). CHL-1 is not capable of homotypic interactions, but an extracellular binding partner of CHL-1 has not been identified (4). Human CHL1 has been mapped to chromosome 3p26 and is a candidate gene for 3p- syndrome characterized by mental impairment (7). A missense CHL1 polymorphism associated increased risk of schizophrenia, has also been reported (8). The functional importance of CHL-1 in the nervous system is also evident in CHL-1 deficient mice, which display behavioral abnormalities and show misguided axons within the hippocampus and olfactory tract (9). Enhanced ectodomain-shedding of CHL-1 is also observed in Wobbler mice, the neurodegenerative mutant mice (6). In vitro, soluble or substrate-coated CHL-1 promotes neurite outgrowth and neuronal survival of both cerebellar and hippocampal neurons. Cell surface CHL-1 interacts with integrins in cis to potentiate integrin-dependent cell migration toward extracellular matrix proteins (10). For this enhanced cell motility, CHL-1 linkage to the actin cytoskeleton via interaction between ankyrin and the CHL-1 cytoplasmic region is required.
- Moos, M. et al. (1988) Nature 334:701.
- Holm, J. et al. (1996) Eur. J. Neusci. 8:1613.
- Wei, M. et al. (1998) Hum. Genet. 103:355.
- Hillenbrand, R. et al. (1999) Eur. J. Neurosci. 11:813.
- Liu, Q. et al. (2000) J. Neurosci. 20:7682.
- Naus, S. et al. (2004) J. Biol. Chem. 279:16083.
- Angeloni, D. et al. (1999) Am. J. Med. Genet. 86:482.
- Sakurai, K. et al. (2002) Mol. Psychiatry 7:412.
- Montag-Sallaz, M. et al. (2002) Mol. Cell. Biol. 22:7967.
- Buhusi, M. et al. (2003) J. Biol. Chem. 278(27):25024.
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