Render Target: SSR
Render Timestamp: 2024-11-14T22:43:46.823Z
Commit: 3c1f305a63297e594ac8d7bb5424007d592d68be
XML generation date: 2024-09-30 01:59:53.790
Product last modified at: 2024-11-11T15:15:12.502Z
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PDP - Template Name: Monoclonal Antibody
PDP - Template ID: *******c5e4b77
R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.

Doublecortin (F6K9E) Rabbit mAb #56130

Filter:
  • WB
  • IP
  • IF

    Supporting Data

    REACTIVITY H M R
    SENSITIVITY Endogenous
    MW (kDa) 35, 45
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    • IF-Immunofluorescence 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 
    • R-Rat 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Simple Western™ 1:50 - 1:250
    Immunoprecipitation 1:100
    Immunofluorescence (Frozen) 1:200 - 1:800
    Immunofluorescence (Immunocytochemistry) 1:50

    Storage

    Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/mL BSA, 50% glycerol, and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.

    For a carrier free (BSA and azide free) version of this product see product #48679.

    Protocol

    Specificity / Sensitivity

    Doublecortin (F6K9E) Rabbit mAb recognizes endogenous levels of total doublecortin protein. This antibody can detect an additional 35 kDa amino terminus specific isoform expressed in human and rat, but not mouse.

    Species Reactivity:

    Human, Mouse, Rat

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues near the amino terminus of human doublecortin protein.

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