Contactin-1 (human, recombinant)

Contactin-1 is a neural cell adhesion molecule and member of the immunoglobulin (Ig) superfamily.¹ It is composed of six Ig-like repeats, four fibronectin type III-like domains, and a hydrophobic C-terminal sequence that contains a glycosylphosphatidylinositol (GPI) anchor site.^1,2 Contactin-1 is primarily expressed in the brain and to a lesser extent in lung, pancreas, skeletal muscle, and kidney.² It is involved in many neuronal developmental processes, including axonal and neurite growth, glial cell differentiation, myelination, and synaptogenesis.^1,3 Contactin-1 has several interaction partners, such as Notch, protein tyrosine phosphatase α (PTPα), and tenascin-R, and binds to them in either cis or trans.³ Increased expression of CNTN1, the gene encoding contactin-1, is associated with decreased overall survival in patients with bladder urothelial carcinoma or stomach adenocarcinoma.¹ Mutations in CNTN1 are associated with familial lethal congenital myopathy.⁴ Cerebrospinal fluid (CSF) levels of contactin-1 are decreased in patients with Parkinson’s disease.⁵ Cayman’s Contactin-1 (human, recombinant) protein consists of 984 amino acids, has a calculated molecular weight of 110 kDa, and a predicted N-terminus of Glu21 after signal peptide cleavage. By SDS-PAGE, under reducing conditions, the apparent molecular mass of the protein is 125 kDa due to glycosylation.

WARNING This product is not for human or veterinary use.

1. Gu, Y., Li, T., Kapoor, A., et al. Contactin 1: An important and emerging oncogenic protein promoting cancer progression and metastasis. Genes (Basel) 11(8), 874 (2020).

2. Reid, R.A., Bronson, D.D., Young, K.M., et al. Identification and characterization of the human cell adhesion molecule contactin. Brain Res. Mol. Brain Res. 21(1-2), 1-8 (1994).

3. Shimoda, Y., and Watanabe, K. Contactins: Emerging key roles in the development and function of the nervous system. Cell Adh. Migr. 3(1), 64-70 (2009).

4. Compton, A.G., Albrecht, D.E., Seto, J.T., et al. Mutations in contactin-1, a neural adhesion and neuromuscular junction protein, cause a familial form of lethal congenital myopathy. Am. J. Hum. Genet. 83(6), 714-724 (2008).

5. Chatterjee, M., van Steenoven, I., Huisman, E., et al. Contactin-1 is reduced in cerebrospinal fluid of Parkinson’s disease patients and is present within Lewy bodies. Comparative Study 10(8), 1177 (2020).