Cell Signaling Technology
XP Monoclonal Antibody

Product Pathways - Neuroscience

CNPase (D83E10) XP® Rabbit mAb #5664

Applications Reactivity Sensitivity MW (kDa) Isotype
W IP IF-F H M R Endogenous 47 Rabbit IgG

Applications Key:  W=Western Blotting  IP=Immunoprecipitation  IF-F=Immunofluorescence (Frozen)
Reactivity Key:  H=Human  M=Mouse  R=Rat
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

Protocols

* Product-specific protocol.

Specificity / Sensitivity

CNPase (D83E10) XP® Rabbit mAb recognizes endogenous levels of total CNPase protein.

Source / Purification

Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Val81 of human CNPase protein.

Western Blotting

Western Blotting

Western blot analysis of extracts from various brain tissues using CNPase (D83E10) XP® Rabbit mAb.

IF-F

IF-F

Confocal immunofluorescent analysis of rat cerebellum using CNPase (D83E10) XP® Rabbit mAb (green) and α/β-Synuclein (Syn205) Mouse mAb #2644 (red). Blue pseudocolor = DRAQ5® #4084 (fluorescent DNA dye).

Background

CNPase (2', 3’-cyclic nucleotide 3'-phosphodiesterase) catalyzes the in vitro hydrolysis of 2’, 3’-cyclic nucleotides to produce 2’-nucleotides. The in vivo molecular function and native substrate of this nucleotide phosphodiesterase remains under investigation (1). High CNPase expression is seen in oligodendrocytes and Schwann cells as CNPase accounts for roughly 4% of the total myelin protein in the central nervous system (2). CNPase binds to tubulin heterodimers and plays a role in tubulin polymerization, and oligodendrocyte process outgrowth (3). Typical myelination is seen in CNPase knock-out mice, but they suffer severe neurodegeneration from axonal loss and oligodendrocytes display abnormal paranodal loop structure prior to axonal degeneration. Paranodal loops typically contact the axolemma in axon-glial signaling; neurodegeneration in CNPase knock-out mice is a secondary consequence of impaired cell-cell communication (4).

  1. Esposito, C. et al. (2008) Biochemistry 47, 308-19.
  2. Kozlov, G. et al. (2003) J Biol Chem 278, 46021-8.
  3. Lee, J. et al. (2005) J Cell Biol 170, 661-73.
  4. Lappe-Siefke, C. et al. (2003) Nat Genet 33, 366-74.

Application References

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For Research Use Only. Not For Use In Diagnostic Procedures.

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