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- Additional protein information
- Analytical tools
Phospho-ATF-2 (Thr69/71) Blocking Peptide #1040
This product is discontinued
Western blot analysis of whole cell lysates from NIH/3T3 cells treated and untreated with UV light, probed with Phospho-ATF-2 (Thr69/71) Antibody #9225 (left) and with the same antibody co-incubated with specific blocking peptide (right).Learn more about how we get our images
Gallery: Phospho-ATF-2 (Thr69/71) Blocking Peptide #1040
This peptide is used to block Phospho-ATF-2 (Thr69/71) Antibody #9225 reactivity.
The quality of the peptide was evaluated by reversed-phase HPLC and by mass spectrometry. The peptide blocks Phospho-ATF-2 (Thr69/71) Antibody #9225 by immunohistochemistry and Western Blotting.
For immunohistochemistry, add twice the volume of peptide as volume of antibody used in 100 µl total volume. Incubate for a minimum of 30 minutes prior to adding the entire volume to the slide. Recommended antibody dilutions can be found on the relevant product data sheet.
For Western immunoblotting, add 10 µl of antibody and 10 µl of blocking peptide to 10 ml of antibody dilution buffer, and incubate at room
temperature for 30 minutes before allowing to react with the blot.Storage: Supplied in 20 mM potassium phosphate (pH 7.0), 50 mM NaCl, 0.1 mM EDTA, 1 mg/ml BSA and 5% glycerol. Store at –20°C.
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).
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