Render Target: STATIC
Render Timestamp: 2024-10-15T10:05:27.990Z
Commit: 56767fe525c928647c8401233a175d0d607d385d
XML generation date: 2024-08-01 15:23:54.288
Product last modified at: 2024-06-27T13:36:20.573Z
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PDP - Template Name: Polyclonal Antibody
PDP - Template ID: *******59c6464

CNPase Antibody #2986

Filter:
  • WB

    Supporting Data

    REACTIVITY H M R
    SENSITIVITY Endogenous
    MW (kDa) 47
    SOURCE Rabbit
    Application Key:
    • WB-Western Blotting 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 
    • R-Rat 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000

    Storage

    Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA and 50% glycerol. Store at –20°C. Do not aliquot the antibody.

    Protocol

    Specificity / Sensitivity

    CNPase Antibody detects endogenous levels of total CNPase protein.

    Species Reactivity:

    Human, Mouse, Rat

    Source / Purification

    Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to human CNPase. Antibodies are purified by protein A and peptide affinity chromatography.

    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).
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