Render Target: STATIC
Render Timestamp: 2024-11-27T11:12:15.307Z
Commit: d79925545b26f8827f92d145dadc6f0527debdb1
XML generation date: 2024-09-20 06:21:58.709
Product last modified at: 2024-06-04T11:30:11.889Z
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PDP - Template Name: Polyclonal Antibody
PDP - Template ID: *******59c6464

Phospho-ATF-2 (Thr69/71)/ATF-7 (Thr51/53) Antibody #40749

Filter:
  • WB
  • IHC

    Supporting Data

    REACTIVITY H M R Mk
    SENSITIVITY Endogenous
    MW (kDa) 65-75
    SOURCE Rabbit
    Application Key:
    • WB-Western Blotting 
    • IHC-Immunohistochemistry 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 
    • R-Rat 
    • Mk-Monkey 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunohistochemistry (Paraffin) 1:100

    Storage

    Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA and 50% glycerol. Store at –20°C. Do not aliquot the antibody.

    Protocol

    Specificity / Sensitivity

    Phospho-ATF-2 (Thr69/71)/ATF-7 (Thr51/53) Antibody detects endogenous levels of ATF-2 only when dually phosphorylated at both Thr69 and Thr71, and ATF-7 only when dually phosphorylated at both Thr51 and Thr53. It does not recognize ATF-2 singly phosphorylated at either Thr69 or Thr71, and it does not recognize ATF-7 singly phosphorylated at either Thr51 or Thr53.

    Species Reactivity:

    Human, Mouse, Rat, Monkey

    Source / Purification

    Polyclonal antibodies are produced by immunizing animals with a synthetic phosphopeptide corresponding to residues surrounding Thr69 and Thr71 of human ATF-2. Antibodies are purified by protein A and peptide affinity chromatography.

    Background

    The transcription factor ATF-2 (also called CRE-BP1) binds to both AP-1 and CRE DNA response elements and is a member of the ATF/CREB family of leucine zipper proteins (1). ATF-2 interacts with a variety of viral oncoproteins and cellular tumor suppressors and is a target of the SAPK/JNK and p38 MAP kinase signaling pathways (2-4). Various forms of cellular stress, including genotoxic agents, inflammatory cytokines, and UV irradiation, stimulate the transcriptional activity of ATF-2. Cellular stress activates ATF-2 by phosphorylation of Thr69 and Thr71 (2-4). Both SAPK and p38 MAPK have been shown to phosphorylate ATF-2 at these sites in vitro and in cells transfected with ATF-2. Mutations of these sites result in the loss of stress-induced transcription by ATF-2 (2-4). In addition, mutations at these sites reduce the ability of E1A and Rb to stimulate gene expression via ATF-2 (2).

    ATF-7 is another member of the ATF/CREB family of leucine zipper proteins (5). Similarly, Thr51 and Thr53 (corresponding to Thr69 and Thr71 of ATF-2, respectively) can be phosphorylated under different conditions (6,7).
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