Cell Signaling Technology

Product Pathways - MAPK Signaling

Phospho-ATF-2 (Thr71) (11G2) Rabbit mAb (PE Conjugate) #13850

Applications Dilution Species-Reactivity Sensitivity MW (kDa) Isotype
F 1:50 Human,Mouse,Rat,Monkey, Endogenous Rabbit IgG

Species cross-reactivity is determined by western blot.

Applications Key: F=Flow Cytometry,

Specificity / Sensitivity

Phospho-ATF-2 (Thr71) (11G2) Rabbit mAb (PE Conjugate) detects endogenous levels of ATF-2 only when phosphorylated at Thr71. The unconjugated antibody does not cross-react with phosphorylated c-Jun, CREB, or other transcription factors, but it does recognize ATF-2 dually phosphorylated at Thr69/Thr71 and singly phosphorylated at Thr71 equally well.

Source / Purification

Monoclonal antibody is produced by immunizing animals with a synthetic phosphopeptide corresponding to residues surrounding Thr71 of human ATF-2 protein.

Description

This Cell Signaling Technology antibody is conjugated to phycoerythrin (PE) and tested in-house for direct flow cytometry analysis in human cells. The antibody is expected to exhibit the same species cross-reactivity as the unconjugated Phospho-ATF-2 (Thr71) (11G2) Rabbit mAb #5112.

Flow Cytometry

Flow Cytometry

Flow cytometric analysis of Jurkat cells, untreated (blue) or treated with Anisomycin #2222 (green), using Phospho-ATF-2 (Thr71) (11G2) Rabbit mAb (PE Conjugate).

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, 2079-89.
  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.

Application References

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Protocols

Companion Products


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

U.S. Patent No. 5,675,063.

Cell Signaling Technology is a trademark of Cell Signaling Technology, Inc.

Cell Signaling Technology® is a trademark of Cell Signaling Technology, Inc.

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