Render Target: STATIC
Render Timestamp: 2024-11-22T11:25:05.098Z
Commit: 5c4accf06eb7154018ba3f54329c7590f97f534a
XML generation date: 2024-09-30 01:59:27.394
Product last modified at: 2024-09-30T08:02:32.014Z
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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.

p75NTR (E7I3M) Rabbit mAb #41680

Filter:
  • WB
  • IP
  • IHC

    Supporting Data

    REACTIVITY H M R
    SENSITIVITY Endogenous
    MW (kDa) 75
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    • IHC-Immunohistochemistry 
    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 1:50
    Immunohistochemistry (Paraffin) 1:50 - 1:200

    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 #59051.

    Protocol

    Specificity / Sensitivity

    p75NTR (E7I3M) Rabbit mAb recognizes endogenous levels of total p75NTR protein.

    Species Reactivity:

    Human, Mouse, Rat

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with recombinant protein specific to the cytoplasmic carboxy-terminal region of human p75NTR protein.

    Background

    The p75 neurotrophin receptor (p75NTR), a member of the TNF receptor superfamily, is distinguished by multiple cysteine-rich ligand-binding domains, a single transmembrane sequence, and a noncatalytic cytoplasmic domain (1). p75NTR displays paradoxical functions when acting alone or with other receptor proteins. Working in concert with Trk receptors, p75NTR recognizes neurotrophins and transmits trophic signals into the cell. Both p75NTR and TrkA are required to activate PI3K-Akt signaling, while TrkA can individually activate the MAP kinase pathway. In contrast, p75NTR, possibly through JNK, ensures appropriate apoptosis of injured neurons and improperly targeted neonatal neurons (2).

    The p75NTR protein undergoes sequential cleavage similar to APP and Notch. First, α-secretase removes the p75NTR ectodomain, eliminating ligand-mediated signaling. At this point, the membrane-tethered cleavage product can still fine-tune Trk-mediated trophic actions. γ-secretase cleaves within the transmembrane domain to liberate the cytoplasmic tail from its membrane anchor and allow the p75NTR intracellular domain to translocate to the nucleus (3,4).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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