Cell Signaling Technology

Product Pathways - Neuroscience

Contactin-2 (D4M7G) Rabbit mAb #26372

No. Size Price
26372S 100 µl ( 10 western blots ) ¥3,100.00 现货查询 购买询价
26372 carrier free & custom formulation / quantityemail request
Applications Dilution Species-Reactivity Sensitivity MW (kDa) Isotype
W 1:1000 Mouse,Rat, Endogenous 130 Rabbit IgG

Species cross-reactivity is determined by western blot.

Applications Key: W=Western Blotting,


Species predicted to react based on 100% sequence homology: Human,

Specificity / Sensitivity

Contactin-2 (D4M7G) Rabbit mAb recognizes endogenous levels of total contactin-2 protein.

Source / Purification

Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Val375 of human contactin-2 protein.

Western Blotting

Western Blotting

Western blot analysis of extracts from various tissue using Contactin-2 (D4M7G) Rabbit mAb (upper) and β-Actin (D6A8) Rabbit mAb #8457 (lower).


Myelinated axons contain un-myelinated gaps called nodes of Ranvier. These regularly spaced gaps are critical for the proper propagation and rapid conduction of nerve impulses in the central and peripheral nervous system (1). The structure and organization of the nodes of Ranvier is dictated by interaction between the axon and glial cells (2). Voltage-gated sodium channels concentrated at the nodes and potassium channels clustered at the paranodes are responsible for propagation of the action potentials (3,4). Other proteins that contribute to the architecture and function of the nodes of Ranvier include βIV spectrin (5), ankyrin-G (6), and the L1 cell adhesion molecules, neurofascin and NrCAM (7,8).

Contactin-2 (CNTN2, TAG-1) is a glycosyl-phosphatidyl-inositol-anchored cell adhesion protein that is expressed at the juxtaparanodal region of the nodes of Ranvier by oligodendrocytes, Schwann cells, and axons (9,10). Contactin-2 plays an important role in the proper organization of the juxtaparanodes through interaction with Caspr2 and the recruitment of the Kv1.1 and Kv1.2 potassium channel subunits (11). Research studies indicate that contactin-2 is a substrate of β-secretase 1 (12,13). A deletion mutation in the corresponding CNTN2 gene results in familial adult myoclonic epilepsy-5, which is characterized by seizures, involuntary myoclonic muscle twitches, and mild intellectual disability (14).

  1. Black, J.A. et al. (1990) Trends Neurosci 13, 48-54.
  2. Salzer, J.L. (1997) Neuron 18, 843-6.
  3. Waxman, S.G. et al. (1989) Proc Natl Acad Sci U S A 86, 1406-10.
  4. Ritchie, J.M. (1992) Trends Neurosci 15, 345-51.
  5. Berghs, S. et al. (2000) J Cell Biol 151, 985-1002.
  6. Zhou, D. et al. (1998) J Cell Biol 143, 1295-304.
  7. Davis, J.Q. et al. (1996) J Cell Biol 135, 1355-67.
  8. Ratcliffe, C.F. et al. (2001) J Cell Biol 154, 427-34.
  9. Traka, M. et al. (2002) J Neurosci 22, 3016-24.
  10. Girault, J.A. and Peles, E. (2002) Curr Opin Neurobiol 12, 476-85.
  11. Traka, M. et al. (2003) J Cell Biol 162, 1161-72.
  12. Kuhn, P.H. et al. (2012) EMBO J 31, 3157-68.
  13. Gautam, V. et al. (2014) Mol Neurodegener 9, 4.
  14. Stogmann, E. et al. (2013) Brain 136, 1155-60.

Application References

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