DSCAM in A172 Human Cell Line. DSCAM was detected in immersion fixed A172 human glioblastoma cell line using Mouse Anti-Human DSCAM Long Isoform Monoclonal Antibody (Catalog # MAB36661) at 10 µg/mL for 3 hours at room temperature. Cells were stained using the NorthernLights™ 557-conjugated Anti-Mouse IgG Secondary Antibody (orange; Catalog # NL007) and counterstained with DAPI (blue). View our protocol for Fluorescent ICC Staining of Cells on Coverslips.
Preparation and Storage
Reconstitute at 0.5 mg/mL in sterile PBS.
The product is shipped at ambient temperature. Upon receipt, store it immediately at the temperature recommended below. *Small pack size (SP) is shipped with polar packs. Upon receipt, store it immediately at -20 to -70 °C
Stability & Storage
Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
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.
Down syndrome cell adhesion molecule (DSCAM) is a 220 kDa type I transmembrane glycoprotein and member of the immunoglobulin superfamily (1). Human DSCAM, which maps to a Down syndrome region of chromosome 21q22.2‑22.3, is synthesized as a 2012 amino acid (aa) precursor that contains a 17 aa signal sequence, a 1578 aa extracellular domain (ECD), a 21 aa transmembrane segment, and a 396 aa cytoplasmic tail. The ECD contains ten Ig-like C2-type domains, six fibronectin type III domains, and 16 potential sites for N-linked glycosylation. Splicing variants lead to a second, shorter isoform, which has a ten aa substitution for aa 1562‑1571 in the longer isoform, and a deletion of residues corresponding to aa 1572‑2012 in the longer isoform. Human mature DSCAM is 98% aa identical to mature mouse and rat DSCAM. Studies on mice have shown that DSCAM is expressed widely in the developing nervous system (1, 2). More recent studies indicate that DSCAM plays an important role in neurite arborization, cell body spacing, and lamina-specific synaptic targeting in vertebrate retina (2‑4). DSCAM directly binds to cytoplasmic Pak1 and stimulates Pak1 phosphorylation and activity (5). In addition, DSCAM activates both JNK and p38 MAP kinases, and expression of the cytoplasmic domain of DSCAM induces a morphological change in cultured cells that is JNK-dependent (5). Thus, it appears that DSCAM signals through Pak1 and functions in axon guidance. Furthermore, DSCAM, in collaboration with DCC, interacts with Netrin-1 and is a receptor required for Netrin-dependent commissural axon outgrowth and pathfinding (2, 6).
Yamakawa, K. et al. (1998) Hum. Mol. Genet. 7:227.
Liu, G. et al. (2009) Proc. Natl. Acad. Sci. U.S.A. 106:2951.
Fuerst, P.G. et al. (2008) Nature 451:470.
Yamagata, M. and J.R. Sanes (2008) Nature 451:465.
Li, W. and K.-L. Guan (2004) J. Biol. Chem. 279:32824.
Ly, A. et al. (2008) Cell 133:11241.
Down Syndrome Cell Adhesion Molecule
Entrez Gene IDs:
1826 (Human); 13508 (Mouse)
CHD2-42; CHD2-52; Down syndrome cell adhesion molecule; human CHD2-52 down syndrome cell adhesion molecule, 10CHD2
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