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Signal Ze’ev and cytosolic Lau* Eric and nuclear of crossroad functions the at – ATF2 Commentary ta. 08) lhuhtemcaim neligthese underlying mechanisms the Although 2008a). its Bhoumik with al., elicit 2003; functions al., et these et can (Berger associated localization has cytoplasmic ATF2 or work tissue nuclear earlier Intriguingly, the type; on cell depending 1997). activities or suppressor al., tumor al., or et et oncogenic Reimold 2005; Yamada al., et Pearson 1996; 2008; al., diseases et (Chen neurological cancer in including and implicated conditions, been pathological have activity several and/or expression ATF2 altered of 1). development Box organismal (see in models demonstrated genetic members been several activity transcriptional has predominantly the ATF2 of importance are of The al., family. which by et AP-1 the dictated Wang partners, of is 1998; ATF2 al., dimerization of et (Bhoumik osmotic output Merika ATF2 its transcriptional death 2009; or precise al., cell The stimuli, et hypoxic and 2011). its Choi to infection 2007; cytokine After al., viral responses et damage, active. cellular and DNA transcriptionally the stress, be stress to to contributes following order N-terminal in activation kinase Jun (ERK1) extracellular-signal-regulated by or 1 (MAPK14), p38 development, (JNK), 2010). requires embryonic al., et (Lopez-Bergami responses, ATF2 death cell cellular stress and diverse development as disease regulate that such or complexes functions, form homodimerize to Maf can or families factor Fos Jun, factor transcription the of CREB (AP1) members with 1 heterodimerize and 16 comprise ATF activator factors superfamily. the transcription of cAMP-response-element- of members families and (CREB) cAMP- factor) as binding known transcription also (ATF; dependent factor transcription activating The Introduction of mechanism This addiction’. compartments. ‘oncogene for subcellular paradigm both novel in a words: ATF2 represents Key it of the factor where function by transcription development, stress, and ATF2 modified cell genotoxic regulation non-genetically of severe to the a phosphorylation to (PKC of related of Notably, control exposure understanding C are death. following current kinase that cell primarily our activities protein mitochondrial-based global summarize cytosol, to transcriptional of promotes the contributes has specific and isoform to ATF2 has work potential to nucleus, translocate epsilon ATF-2) Recent the membrane also addition cancer. 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Agelopoulos, Hornung, D., James, S., Lyons, G., Ashton, J., Ackermann, 2822 20) I4b euao fatvtn rncito atr2rsos osrs and stress to response 2 factor transcription activating damage. of DNA regulator a TIP49b, (2001). hshrltdAF n TT nctnosagoacm n pyogenic and angiosarcoma cutaneous in al. et STAT3 granuloma. S. Shibata, and M., Takahara, phosphorylated-ATF2 T., Dainichi, H., Uchi, mammals. in phosphorylation 29 ATF2 triggering pathway P. response Fafournoux, acid and A. Bruhat, B., Derijard, inhibition. growth D. and B. Dynlacht, and acetylation. histone specific orchestrating Res. by P. transcription Fafournoux, and regulated C. Jousse, N., Jones, cells. liver embryonic of survival for essential is N. ATF2 Jones, via and V. Kouskoff, G., Lacaud, I6 yAF ouae T activation. ATM modulates ATF2 by TIP60 expression. D1 cyclin activating in P. 2 factor LuValle, transcription activating of target a as gene D1 chondrocytes. cyclin the of Identification ATF2 novel a of in properties. 1728. identification isoforms transactivation labor: potent (ATF2) and with 2 pregnancy species factor during transcription myometrium activating human the and protein modulator activating ATF2-small. element of N. isoform G. role spliced Finner, the novel pathway: a (JNK) and kinase (ATF2) Endocrinol. 2 NH2-terminal factor c-Jun transcription the of genes ATF4 both requires limitation acid phosphorylation. amino ATF2 by and expression expression CHOP of Induction (2004). ciaigtasrpinfco AF)i kncancer. skin al. in et (ATF2) N. 105 2 Jones, factor S., transcription Krajewski, activating P., Meltzer, A., Subtil, protein. response damage DNA 20 and factor transcription activating 20) T-eedn hshrlto fAF srqie o h N damage DNA the for required is ATF2 response. of phosphorylation ATM-dependent (2005). survival. patient predicts specimens L. 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PC12 for in transcription needed 10188-10195. gene ATF-2 hydroxylase tyrosine and of elevation protein element-binding cAMP-response lsioe ciao eeidcinb nelui- n erdcny phorbol tetradecanoyl and interleukin-1 family by Jun induction acetate. gene cooperation and and activator pathways ATF-2, plasminogen kinase Ets-2, protein mitogen-activated between distinct of Role (1999). T2rglto yteJKsga rndcinpathway. transduction signal JNK the by regulation ATF2 arsenite. by gene oxygenase-1 heme mouse Biophys. the Biochem. of Arch. induction regulate proteins zipper dependent. dimerization atr2icesstasciainadpoensaiiyo yoi-nuil factor hypoxia-inducible of stability protein hepatocytes. and in transactivation 1alpha increases 2 factor sfrso h R-PDAbnigpoenmdaeatvt faT-cell-specific a of activity mediate protein DNA-binding transcription enhancer. CRE-BP associated the of their isoforms of ubiquitination the target factors. kinases NH2-terminal pathway. hepatocellular signaling of c-JUN-mediated deprivation novel acid 286 a amino reveals by cells gene carcinoma c-JUN of Auto-activation (2011). element. CCAAT a via regulated is 792-798. stress genotoxic by rhoB factor-2. activator transcription the activating through 6789. osteoblasts and in complex transcription protein-1 interleukin-6 induces factor growth rtaoeptwyi euaino T2i cells. T ubiquitin/ in ATF2 the of of regulation Implication in hUBC9. pathway enzyme proteasome ubiquitin-conjugating the with (ATF2) ATF-2-c-jun on dependent is enhanceosome orientation. interferon heterodimer beta functional a of Assembly HMG protein architectural the and factors transcription by I(Y). enhancer gene beta IFN the E1A. 12S and p300 by promoter c-jun 2311-2321. the of activation co-operative the A. 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