Render Target: STATIC
Render Timestamp: 2024-12-20T11:16:44.709Z
Commit: f2d32940205a64f990b886d724ccee2c9935daff
XML generation date: 2024-10-16 17:30:09.266
Product last modified at: 2024-12-17T18:55:21.192Z
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PDP - Template Name: Polyclonal Antibody
PDP - Template ID: *******59c6464

Doublecortin Antibody #4604

Filter:
  • IF

    Supporting Data

    REACTIVITY M R
    SENSITIVITY Endogenous
    MW (kDa)
    SOURCE Rabbit
    Application Key:
    • IF-Immunofluorescence 
    Species Cross-Reactivity Key:
    • M-Mouse 
    • R-Rat 

    Product Information

    Product Usage Information

    Application Dilution
    Immunofluorescence (Frozen) 1:800

    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

    Doublecortin Antibody detects endogenous levels of total doublecortin protein. Nonspecific labeling of fixed frozen mouse pancreas, colon, small intestine, retina, and cell bodies in adult brain are observed by immunofluorescence.


    For superior performance in tissue, Doublecortin (F6K9E) Rabbit mAb #56130 is recommended.


    Species Reactivity:

    Mouse, Rat

    Source / Purification

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

    Background

    Mutations in doublecortin (DCX) cause Lissencephaly (smooth brain), a neuronal migration disorder characterized by epilepsy and mental retardation (1). Doublecortin is a microtubule-associated protein that stabilizes and bundles microtubules. A conserved doublecortin domain mediates the interaction with microtubules, and interestingly most missense mutations cluster in this domain (2). Kinases JNK, CDK5, and PKA phosphorylate doublecortin. JNK phosphorylates Thr321, Thr331, and Ser334 while PKA phosphorylates Ser47 and CDK5 phosphorylates Ser297 (3-5). Phosphorylation of Ser297 lowers the affinity of doublecortin to microtubules. Furthermore, mutations of Ser297 result in migration defects (5).
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