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Phospho-ATF-2 (Thr71) Antibody #9221

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Inquiry Info. # 9221

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    Product Specifications

    REACTIVITY H M R Mk
    SENSITIVITY Endogenous
    MW (kDa) 70
    SOURCE Rabbit
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    • IHC-Immunohistochemistry 
    • IF-Immunofluorescence 
    • F-Flow Cytometry 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 
    • R-Rat 
    • Mk-Monkey 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunoprecipitation 1:250
    Immunohistochemistry (Paraffin) 1:50
    Immunohistochemistry (Frozen) 1:50
    Immunofluorescence (Immunocytochemistry) 1:50
    Flow Cytometry (Fixed/Permeabilized) 1:50

    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 (Thr71) Antibody detects endogenous levels of ATF-2 only when phosphorylated at threonine 71. This antibody does not cross-react with phosphorylated c-Jun, CREB or other transcription factors. This antibody recognizes both Thr69/Thr71 dually phosphorylated ATF-2 and Thr71 singly phosphorylated ATF-2 equally well.

    Species Reactivity:

    Human, Mouse, Rat, Monkey

    Source / Purification

    Polyclonal antibodies are produced by immunizing animals with a synthetic phosphopeptide corresponding to residues surrounding Thr71 of human ATF2. 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).

    Alternate Names

    Activating transcription factor 2; activating transcription factor 2 splice variant ATF2-var2; ATF-2; ATF2; cAMP response element-binding protein CRE-BP1; cAMP responsive element binding protein 2, formerly; cAMP-dependent transcription factor ATF-2; cAMP-responsive element-binding protein 2; CRE-BP1; CREB-2; CREB2; CREBP1; Cyclic AMP-dependent transcription factor ATF-2; Cyclic AMP-responsive element-binding protein 2; HB16; histone acetyltransferase ATF2; MGC111558; TREB7

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