Human Contactin-4 Isoform a Alexa Fluor® 647-conjugated Antibody
R&D Systems, part of Bio-Techne | Catalog # AF2205R

Key Product Details
Species Reactivity
Applications
Label
Antibody Source
Product Specifications
Immunogen
Asp19-Gly1001
Accession # Q8IWV2
Specificity
Clonality
Host
Isotype
Applications
Western Blot
Neutralization
Formulation, Preparation, and Storage
Purification
Formulation
Shipping
Stability & Storage
Background: Contactin-4
Contactin-4 (CNTN4), also known as BIG-2 (Brain-derived Immunoglobulin Superfamily molecule 2), is an axonal cell adhesion molecule that belongs to the contactin family, a subfamily of the Ig superfamily (1‑3). The contactin family comprises six members (CNTN1/F3, CNTN2/TAG-1, CNTN3/BIG-1, CNTN4/BIG-2, CNTN5/NB-2 and CNTN6/NB-3) and are characterized by the presence of six Ig-like domains, four fibronectin type III-like repeats, and a glycosylphosphatidylinositol (GPI)‑anchoring domain. Contactin family proteins exist as membrane-bound proteins, but can also be released as soluble proteins by GPI‑specific phospholipase D. Soluble Contactins are functionsl proteins that are able to promote neurite outgrowth. Human CNTN4 has been mapped to chromosome 3p26‑p25. Three alternative transcripts of CNTN4, encoding isoforms a, b, and c precursor proteins containing 1026, 282, and 698 amino acid (aa) residues, respectively, have been described. Human CNTN4 isoform a shares 94% aa sequence identity with its rat homolog. It also shares from 44‑66% aa sequence identity with other CNTN family members. CNTN family members display overlapping but distinct expression patterns. CNTN4 expression is detected in multiple organs including brains, pancreas, kidney, aorta, small intestine, thyroid, uterus and testis. However, expression of the 282 aa isoform b is primarily restricted to the brain. CNTN4 has been suggested to play important roles in the formation of neuronal networks during nervous sytems development. Disruption of CNTN4 has been implicated in the 3p deletion syndrome characterized by growth failure, developmental delay, and mental retardation. CNTN-4 expression is induced in human neuroblastoma tumor cells treated with retinoic acid and may be responsible for the the neuritogenic response of tumor cells to retinoids. R&D Systems' recombinant CNTN4 shows in vitro neurite outgrowth promoting activity when used as an immobilized substrate for hippocampal neuron outgrowth.
Alternate Names
Gene Symbol
UniProt
Additional Contactin-4 Products
Product Specific Notices
This product is provided under an agreement between Life Technologies Corporation and R&D Systems, Inc, and the manufacture, use, sale or import of this product is subject to one or more US patents and corresponding non-US equivalents, owned by Life Technologies Corporation and its affiliates. The purchase of this product conveys to the buyer the non-transferable right to use the purchased amount of the product and components of the product only in research conducted by the buyer (whether the buyer is an academic or for-profit entity). The sale of this product is expressly conditioned on the buyer not using the product or its components (1) in manufacturing; (2) to provide a service, information, or data to an unaffiliated third party for payment; (3) for therapeutic, diagnostic or prophylactic purposes; (4) to resell, sell, or otherwise transfer this product or its components to any third party, or for any other commercial purpose. Life Technologies Corporation will not assert a claim against the buyer of the infringement of the above patents based on the manufacture, use or sale of a commercial product developed in research by the buyer in which this product or its components was employed, provided that neither this product nor any of its components was used in the manufacture of such product. For information on purchasing a license to this product for purposes other than research, contact Life Technologies Corporation, Cell Analysis Business Unit, Business Development, 29851 Willow Creek Road, Eugene, OR 97402, Tel: (541) 465-8300. Fax: (541) 335-0354.
For research use only