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Phospho-ATF-2 (Thr71) Antibody

Phospho-ATF-2 (Thr71) Antibody #9221

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24329 Phospho-ATF-2 (Thr71)/ATF-7 (Thr53) Antibody

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Inquiry Info. # 9221

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Supporting Data

REACTIVITY	H M R Mk
SENSITIVITY	Endogenous
MW (kDa)	70
SOURCE	Rabbit

Application Key:

WB-Western Blotting
IP-Immunoprecipitation
IHC-Immunohistochemistry
IF-Immunofluorescence
F-Flow Cytometry

Species Cross-Reactivity Key:

H-Human
M-Mouse
R-Rat
Mk-Monkey

Product Information

Product Usage Information

Application	Dilution
Western Blotting	1:1000
Immunoprecipitation	1:250
Immunohistochemistry (Paraffin)	1:50
Immunohistochemistry (Frozen)	1:50
Immunofluorescence (Immunocytochemistry)	1:50
Flow Cytometry (Fixed/Permeabilized)	1:50

Storage

Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA and 50% glycerol. Store at –20°C. Do not aliquot the antibody.

Protocol

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.

Species Reactivity:

Human, Mouse, Rat, Monkey

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.

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).

Database Links

UniProt ID: P15336

Entrez-Gene Id: 1386

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