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Phospho-ATF-2 (Thr71) Antibody

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  • 询价
  • Cell Signaling Technology已认证
  • USA
  • 2026年01月01日
  • W, IP, IHC-P, IHC-F, IF-IC, F
  • Rabbit
  • H,M,R,Mk
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    • 技术资料
    • 抗体英文名

      Phospho-ATF-2 (Thr71) Antibody

    • 抗原

      synthetic phosphopeptide corresponding to residues surrounding Thr71 of human ATF2

    • 应用范围

      W, IP, IHC-P, IHC-F, IF-IC, F

    • 宿主

      Rabbit

    • 适应物种

      H,M,R,Mk

    • 级别

      详见MSDS文件

    • 库存

      大量

    • 保质期

      详见说明书

    • 供应商

      CST

    • 是否单克隆

      2

    • 保存条件

      -20°c

    • 规格

      100 ul (10 western blots)/300 ul (30 western blots)/carrier free & custom formulation / quantity

    规格:产品价格:¥请询价
    规格:100 ul (10 western blots)产品价格:¥请询价
    规格:300 ul (30 western blots)产品价格:¥请询价
    规格:carrier free & custom formulation / quantity产品价格:¥请询价

    pathway more info application references datasheet PDF MSDS PDF protocols

    Applications Key:  W=Western Blotting  IP=Immunoprecipitation  IHC-P=Immunohistochemistry (Paraffin)  IHC-F=Immunohistochemistry (Frozen)  IF-IC=Immunofluorescence (Immunocytochemistry)  F=Flow Cytometry
    Reactivity Key:  H=Human  M=Mouse  R=Rat  Mk=Monkey
    Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

    Applications Reactivity Sensitivity MW (kDa) Source
    W IP IHC-P IHC-F IF-IC F H M R Mk Endogenous 70 Rabbit
    Protocols
    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. It recognizes both Thr69/Thr71 dually phosphorylated ATF-2 and Thr71 singly phosphorylated ATF-2 equally well.

    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.

    Western Blotting

    Western Blotting

    Western blot analysis of extracts from HeLa, C6 and NIH/3T3 cells, untreated or anisomycin-treated, using Phospho-ATF-2 (Thr71) Antibody.

    IHC-P (paraffin)

    IHC-P (paraffin)

    Immunohistochemical analysis of paraffin-embedded human breast carcinoma showing nuclear localization, using Phospho-ATF-2 (Thr71) Antibody .

    IHC-P (paraffin)

    IHC-P (paraffin)

    Immunohistchemical analysis of paraffin-embedded human colon carcinoma using Phospho-ATF-2 (Thr71) Antibody.


    IHC-P (paraffin)

    IHC-P (paraffin)

    Immunohistochemical analysis of paraffin-embedded human lung carcinoma using Phospho-ATF-2 (Thr71) Antibody.

    IHC-F (frozen)

    IHC-F (frozen)

    Immunhistochemical analysis of frozen H1650 xenograft using Phospho-ATF-2 (Thr71) Antibody.

    Flow Cytometry

    Flow Cytometry

    Flow cytometric analysis of Jurkat cells, untreated (blue) or Anisomycin-treated (green), using Phospho-ATF-2 (Thr71) Antibody compared to a nonspecific negative control antibody (red).


    IF-IC

    IF-IC

    Confocal immunofluorescent analysis of HeLa cells, either untreated (left) or anisomycin-treated (right), using Phospho-ATF-2 (Thr71) Antibody (green). Actin filaments have been labeled with Alexa Fluor® 555 phalloidin (red).

    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).

    1. Abdel-Hafiz, H.A. et al. (1992) Mol. Endocrinol. 6, 2079-2089.
    2. Gupta, S. et al. (1995) Science 267, 389-393.
    3. van Dam, H. et al. (1995) EMBO J. 14, 1798-1811.
    4. Livingstone, C. et al. (1995) EMBO J. 14, 1785-1797.
    Application References

    Have you published research involving the use of our products? If so we'd love to hear about it. Please let us know !

    Companion Products

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

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