NCAM-L1 (D5D3K) Rabbit mAb (BSA and Azide Free) #97986
- WB
- IHC
Supporting Data
| REACTIVITY | H Mk |
| SENSITIVITY | Endogenous |
| MW (kDa) | 220 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IHC-Immunohistochemistry
Species Cross-Reactivity Key:
- H-Human
- Mk-Monkey
Product Information
Product Usage Information
This product is the carrier-free version of product #90269. All data were generated using the same antibody clone in the standard formulation which contains BSA and glycerol.
This formulation is ideal for use with technologies requiring specialized or custom antibody labeling, including fluorophores, metals, lanthanides, and oligonucleotides. It is not recommended for ChIP, ChIP-seq, CUT&RUN, or CUT&Tag assays. If you require a carrier-free formulation for chromatin profiling, please contact us. Optimal dilutions/concentrations should be determined by the end user.
Formulation
Supplied in 1X PBS, BSA, and Azide Free.
For standard formulation of this product see product #90269.
Storage
Specificity / Sensitivity
NCAM-L1 (D5D3K) Rabbit mAb (BSA and Azide Free) recognizes endogenous levels of total NCAM-L1/L1CAM protein.
Species Reactivity:
Human, Monkey
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues near the carboxy terminus of human NCAM-L1/L1CAM protein.
Background
Neural cell adhesion molecule L1 (NCAM-L1/L1CAM) is a single pass transmembrane glycoprotein member of the immunoglobulin superfamily, containing six amino-terminal extracellular Ig-like domains followed by five fibronectin type-III domains (1). NCAM-L1 is mainly expressed in the brain, and plays an important role in the developing nervous system, with involvement in neurite fasciculation and outgrowth, myelination, neuronal migration, and neuronal cell adhesion (2). Mutations in the NCAM-L1 gene cause varying degrees of neurological disease including X-linked hydrocephalus, MASA syndrome, spastic paraplegia type 1, and X-linked corpus callosum agenesis, together known as L1 syndrome (3). Apart from the nervous system, NCAM-L1 is overexpressed in many cancers and supports a poor prognosis by facilitating aggressive tumor growth, metastasis, and chemoresistance (4,5).
Limited Uses
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