Render Target: STATIC
Render Timestamp: 2024-11-20T11:50:01.927Z
Commit: 5c4accf06eb7154018ba3f54329c7590f97f534a
XML generation date: 2024-09-30 01:54:16.302
Product last modified at: 2024-09-30T08:02:41.456Z
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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.

TIGAR (D3F4A) Rabbit mAb #14751

Filter:
  • WB
  • IP

    Supporting Data

    REACTIVITY H
    SENSITIVITY Endogenous
    MW (kDa) 29
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    Species Cross-Reactivity Key:
    • H-Human 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunoprecipitation 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.

    Protocol

    Specificity / Sensitivity

    TIGAR (D3F4A) Rabbit mAb recognizes endogenous levels of total TIGAR protein.

    Species Reactivity:

    Human

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Pro171 of human TIGAR protein.

    Background

    The p53 tumor suppressor protein regulates the cellular response to multiple stresses, including DNA damage and oxidative stress. Activation of p53 can lead to cell cycle arrest and DNA repair, or apoptosis (1). Activated p53 transcription factor regulates the expression of multiple genes that regulate cell metabolism and the cell cycle. One p53-inducible gene is C12orf5, which encodes for a fructose-2,6-bisphosphatase known as TIGAR. TP53-inducible glycolysis and apoptosis regulator (TIGAR) protects cells from oxidative stress as it negatively regulates glycolysis and reduces the production of reactive oxygen species (ROS) in cells (2,3). Research studies demonstrate that knockdown of TIGAR expression induces autophagy and apoptosis (4,5), and its expression protects cells from ROS-related cell death (6,7). Additional studies show that TIGAR promotes cell cycle arrest and supports dephosphorylation of the retinoblastoma (Rb) protein (8).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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