Render Target: STATIC
Render Timestamp: 2024-11-22T11:49:00.661Z
Commit: 5c4accf06eb7154018ba3f54329c7590f97f534a
XML generation date: 2024-09-30 01:55:07.062
Product last modified at: 2024-10-15T11:15:46.649Z
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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.

CRMP-2 (D8L6V) Rabbit mAb #35672

Filter:
  • WB
  • IP
  • IHC
  • IF

    Supporting Data

    REACTIVITY H M R
    SENSITIVITY Endogenous
    MW (kDa) 60-80
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    • IHC-Immunohistochemistry 
    • IF-Immunofluorescence 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 
    • R-Rat 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunoprecipitation 1:50
    Immunohistochemistry (Paraffin) 1:50 - 1:200
    Immunofluorescence (Immunocytochemistry) 1:800

    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.

    Protocol

    Specificity / Sensitivity

    CRMP-2 (D8L6V) Rabbit mAb recognizes endogenous levels of total CRMP-2 protein.

    Species Reactivity:

    Human, Mouse, Rat

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding lle546 of human CRMP-2 protein.

    Background

    Collapsin Response Mediator Protein-2 (CRMP-2) is expressed at high levels in the developing nervous system and plays a critical role in axonal outgrowth by specifying axon/dendrite fate and establishing neuronal polarity (1,2). CRMP-2 enhances axon elongation and branching by binding to tubulin heterodimers to promote microtubule assembly (3). GSK-3β inactivates CRMP-2 by phosphorylating it at Thr514. CRMP-2 is primed following phosphorylation at Ser522 by CDK5 and at Thr518 by GSK-3β (2). Phosphorylation of CRMP-2, which decreases tubulin binding ability, can be inhibited by NT-3 and BDNF through the PI3 kinase/Akt pathway (2). CRMP-2 also mediates semaphorin-induced growth cone collapse (4). Hyperphosphorylation of CRMP-2 is found in Alzheimer disease plaques with concurrent elevated GSK-3β activity in these patients (5).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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