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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.

NeuroD1 (D90G12) Rabbit mAb #7019

Filter:
  • WB
  • IP
  • IF

    Supporting Data

    REACTIVITY H
    SENSITIVITY Endogenous
    MW (kDa) 49
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    • IF-Immunofluorescence 
    Species Cross-Reactivity Key:
    • H-Human 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunoprecipitation 1:50
    Immunofluorescence (Immunocytochemistry) 1:1600 - 1:3200

    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

    NeuroD1 (D90G12) Rabbit mAb detects endogenous levels of total NeuroD1 protein.


    Species Reactivity:

    Human

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Gly315 of human NeuroD1 protein.

    Background

    NeuroD1 is a member of the basic helix-loop-helix (bHLH) family of transcription factors. These proteins function by forming heterodimers with E-proteins and binding to the canonical E-box sequence CANNTG (1,2). Neuronal activity results in CaMKII-mediated phosphorylation of NeuroD1 at Ser336, which is necessary for formation and growth of dendrites (3,4). NeuroD1 is also phosphorylated at Ser274 though the results are context dependent as phosphorylation by Erk stimulates NeuroD1 activity in pancreatic β-cells while phosphorylation by GSK-3β inhibits NeuroD1 in neurons (3). NeuroD1 is crucially important in both the pancreas and developing nervous system, and plays a large role in the development of the inner ear and mammalian retina (3). Mice lacking NeuroD1 become severely diabetic and die shortly after birth due to defects in β-cell differentiation (2,3,5,6). The lack of NeuroD1 in the brain results in severe defects in development (5). Human mutations have been linked to a number of types of diabetes, including type I diabetes mellitus and maturity-onset diabetes of the young (1,3).

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