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PhosphoPlus® ATF-2 (Thr71) Antibody Duet
Primary Antibodies

PhosphoPlus® ATF-2 (Thr71) Antibody Duet #8220

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Western Blotting Image 1

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).

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Western Blotting Image 2

Western blot analysis of extracts from 293 and NIH/3T3 cells, untreated or UV-treated, using ATF-2 (20F1) Rabbit mAb.

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Flow Cytometry Image 3

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).

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IHC-P (paraffin) Image 4

Immunohistochemical analysis of paraffin-embedded human endometrial carcinoma using ATF-2 (20F1) Rabbit mAb.

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Product Includes Quantity Applications Reactivity MW(kDa) Isotype
Phospho-ATF-2 (Thr71) (11G2) Rabbit mAb 5112 100 µl
  • WB
  • F
H M R Mk 70 Rabbit IgG
ATF-2 (20F1) Rabbit mAb 9226 100 µl
  • WB
  • IP
  • IHC
H M R Mk 65 to 75 Rabbit IgG

PhosphoPlus® Duets from Cell Signaling Technology (CST) provide a means to assess protein activation status. Each Duet contains an activation-state and total protein antibody to your target of interest. These antibodies have been selected from CST's product offering based upon superior performance in specified applications.

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, 2079-89.
  2. Gupta, S. et al. (1995) Science 267, 389-93.
  3. van Dam, H. et al. (1995) EMBO J 14, 1798-811.
  4. Livingstone, C. et al. (1995) EMBO J 14, 1785-97.
For Research Use Only. Not For Use In Diagnostic Procedures.

Cell Signaling Technology is a trademark of Cell Signaling Technology, Inc.
PhosphoPlus is a trademark of Cell Signaling Technology, Inc.
U.S. Patent No. 7,429,487, foreign equivalents, and child patents deriving therefrom.

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