Cell Signaling Technology

Product Pathways - MAPK Signaling

Phospho-ATF-2 (Thr71) (11G2) Rabbit mAb #5112

Applications Reactivity MW (kDa) Source Isotype
W F H M R Mk 70 Rabbit IgG

Applications Key:  W=Western Blotting  F=Flow Cytometry
Reactivity Key:  H=Human  M=Mouse  R=Rat  Mk=Monkey
Species enclosed in parentheses are predicted to react based on 100% sequence homology. Species cross-reactivity is determined by Western blot.

Specificity / Sensitivity

Phospho-ATF-2 (Thr71) (11G2) Rabbit mAb 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

Monoclonal antibodies are produced by immunizing rabbits with a synthetic phospho-peptide (KLH-coupled) corresponding to residues surrounding Thr71 of human ATF2.

Western Blotting

Western Blotting

Western blot analysis of extracts from untreated or UV-treated COS cells, NIH/3T3 cells and C6 cells, using Phospho-ATF-2 (Thr71) (11G2) Rabbit mAb (upper), or ATF-2 (20F1) Rabbit mAb #9226 (lower).

Flow Cytometry

Flow Cytometry

Flow cytometric analysis of THP-1 cells, untreated (blue) or Anisomycin treated (green), using Phospho-ATF-2 (Thr71) (11G2) Rabbit mAb compared to a nonspecific negative control antibody (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

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Companion Products

Rabbit Monoclonals Produced Using Epitomics® Technology, U.S. Patent No. 5,675,063.

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