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Render Timestamp: 2024-07-26T10:40:35.159Z
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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.

VAPB (E7R3Z) Rabbit mAb #95339

Filter:
  • WB
  • IF

    Supporting Data

    REACTIVITY H M R
    SENSITIVITY Endogenous
    MW (kDa) 27
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IF-Immunofluorescence 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 
    • R-Rat 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunofluorescence (Frozen) 1:50 - 1:200
    Immunofluorescence (Immunocytochemistry) 1:400 - 1:1600

    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

    VAPB (E7R3Z) Rabbit mAb recognizes endogenous levels of total VAPB protein. This antibody non-specifically labels spermatids in fixed frozen mouse testis by immunofluorescence.


    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 VAPB protein.

    Background

    The human VAP family proteins, which include VAPA (also known as VAP33), VAPB, and VAPC, were initially identified as homologues of vesicle-associated membrane protein (VAMP)-associated protein (VAP) that is involved in exocytosis of neurotransmitters (1). VAPB is an integral endoplasmic reticulum (ER) protein whose amino terminus projects into the cytosol. A proline to serine substitution at position-56 (VAPBP56S) leads to an autosomal-dominant form of amyotrophic lateral sclerosis (ALS), classified as ALS-8. (2). VAPB has been implicated in a variety of processes, including ER stress and the unfolded protein response (UPR), ER to Golgi transport, and bouton formation at the neuromuscular junction (1,2). The P56S mutation causes almost complete loss of function of VAPB to mediate UPR by inducing its misfolding and localization shift to non-ER compartments (1). A possible role of VAPB as a pathologic marker in PBMCs from ALS patients has been published (3).

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