Unconjugated Rabbit anti-Human Phospho-ATF2(T71) Monoclonal Antibody [IgG]

Activating transcription factor 2 antibody, Activating transcription factor 2 splice variant ATF2 var2 antibody, ATF 2 antibody, Atf-2 antibody, Atf2 antibody, ATF2 protein antibody, ATF2_HUMAN antibody, cAMP Response Element Binding Protein 2 antibody, cAMP response element binding protein CRE BP1 antibody, cAMP response element-binding protein CRE-BP1 antibody, cAMP responsive element binding protein 2, formerly antibody, cAMP-dependent transcription factor ATF-2 antibody, cAMP-responsive element-binding protein 2 antibody, CRE BP1 antibody, CRE-BP antibody, CREB 2 antibody, CREB-2 antibody, CREB2 antibody, CREBP1 antibody, Cyclic AMP dependent transcription factor ATF 2 antibody, Cyclic AMP-dependent transcription factor ATF-2 antibody, Cyclic AMP-responsive element-binding protein 2 antibody, D130078H02Rik antibody, D18875 antibody, HB 16 antibody, HB16 antibody, Histone acetyltransferase ATF2 antibody, MGC105211 antibody, MGC105222 antibody, MGC111558 antibody, MGC142504 antibody, mXBP antibody, MXBP protein antibody, Tg(Gzma-Klra1)7Wum antibody, TREB 7 antibody, TREB7 antibody

ATF2 is a member of the ATF/CREB family of basic region leucine zipper DNA binding proteins that regulates transcription by binding to a consensus cAMP response element (CRE) in the promoter of various viral and cellular genes. Many of these genes are important in cell growth and differentiation, and in stress and immune responses. ATF2 is a nuclear protein that binds DNA as a dimer and can form dimers with members of the ATF/CREB and Jun/Fos families. It is a stronger activator as a heterodimer with cJun than as a homodimer. Several isoforms of ATF2 arise by differential splicing. The stable native full length ATF2 is transcriptionally inactive as a result of an inhibitory direct intramolecular interaction of its carboxy terminal DNA binding domain with the amino terminal transactivation domain. Following dimerization ATF2 becomes a short lived protein that undergoes ubiquitination and proteolysis, seemingly in a protein phosphatase-dependent mechanism. Stimulation of the transcriptional activity of ATF2 occurs following cellular stress induced by several genotoxic agents, inflammatory cytokines, and UV irradiation. This activation requires phosphorylation of two threonine residues in ATF2 by both JNK/SAP kinase and p38 MAP kinase. ATF2 is abundantly expressed in brain.