|Application ||WB, IHC|
|Calculated MW||54537 Da|
|Other Names||Cyclic AMP-dependent transcription factor ATF-2, cAMP-dependent transcription factor ATF-2, Activating transcription factor 2, Cyclic AMP-responsive element-binding protein 2, CREB-2, cAMP-responsive element-binding protein 2, HB16, Histone acetyltransferase ATF2, cAMP response element-binding protein CRE-BP1, ATF2, CREB2, CREBP1|
|Target/Specificity||A synthetic peptide corresponding to residues N-terminus of human ATF-2 was used as immunogen. The antibody does not cross-react with other ATF family members.|
|Format||50 mM Tris-Glycine (pH 7.4), 0.15 M NaCl, 40% Glycerol, 0.01% sodium azide and 0.05% BSA.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||ATF-2 Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Transcriptional activator which regulates the transcription of various genes, including those involved in anti- apoptosis, cell growth, and DNA damage response. Dependent on its binding partner, binds to CRE (cAMP response element) consensus sequences (5'-TGACGTCA-3') or to AP-1 (activator protein 1) consensus sequences (5'-TGACTCA-3'). In the nucleus, contributes to global transcription and the DNA damage response, in addition to specific transcriptional activities that are related to cell development, proliferation and death. In the cytoplasm, interacts with and perturbs HK1- and VDAC1-containing complexes at the mitochondrial outer membrane, thereby impairing mitochondrial membrane potential, inducing mitochondrial leakage and promoting cell death. The phosphorylated form (mediated by ATM) plays a role in the DNA damage response and is involved in the ionizing radiation (IR)-induced S phase checkpoint control and in the recruitment of the MRN complex into the IR-induced foci (IRIF). Exhibits histone acetyltransferase (HAT) activity which specifically acetylates histones H2B and H4 in vitro. In concert with CUL3 and RBX1, promotes the degradation of KAT5 thereby attenuating its ability to acetylate and activate ATM. Can elicit oncogenic or tumor suppressor activities depending on the tissue or cell type.|
|Cellular Location||Nucleus. Cytoplasm. Mitochondrion outer membrane. Note=Shuttles between the cytoplasm and the nucleus and heterodimerization with JUN is essential for the nuclear localization. Localization to the cytoplasm is observed under conditions of cellular stress and in disease states. Localizes at the mitochondrial outer membrane in response to genotoxic stress Phosphorylation at Thr-52 is required for its nuclear localization and negatively regulates its mitochondrial localization. Co- localizes with the MRN complex in the IR-induced foci (IRIF)|
|Tissue Location||Ubiquitously expressed, with more abundant expression in the brain|
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Provided below are standard protocols that you may find useful for product applications.
ATF-2 (activating transcription factor-2, CRE-BP1) is a transcription factor that binds the cAMP response element (CRE) and AP-1 response element and is abundantly expressed in the brain. Various forms of cellular stress, including genotoxic agents, inflammatory cytokines, and UV irradiation, stimulate the transcriptional activity of ATF-2 (2). SAPK and p38 MAPK can activate, in response to cellular stress, ATF-2 by phosphorylating this protein at Thr69 and Thr71. Mutations of these sites result in the loss of stress-induced transcription by ATF-2 (2-4).
1. Maekawa, T., et al. Leucine zipper structure of the protein CRE-BP1 binding to the cyclic AMP response element in brain. EMBO J. 8: 2023
2. Gupta, S., et al. Transcription factor ATF2 regulation by the JNK signal transduction pathway. Science 267: 389
3. van Dam, H., et al. ATF-2 is preferentially activated by stress-activated protein kinases to mediate c-jun induction in response to genotoxic agents. EMBO J. 14: 1798
4. Livingstone, C., et al. ATF-2 contains a phosphorylation-dependent transcriptional activation domain. EMBO J. 14: 1785
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