REFERENCES
- Abate, C., D. Luk, and T. Curran 1991. Transcriptional regulation by Fos and Jun in vitro: interaction among multiple activator and regulatory domains. Mol. Cell. Biol. 11: 3624–3632.
- Abate, C., D. R. Marshak, and T. Curran 1991. Fos is phosphorylated by p34cdc2, cAMP-dependent protein kinase and protein kinase C at multiple sites clustered within regulatory regions. Oncogene 6: 2179–2185.
- Angel, P., and M. Karin 1991. The role of jun, fos and the AP-1 complex in cell proliferation and transformation. Biochim. Biophys. Acta 107: 129–157.
- Angel, P., T. Smeal, J. Meek, and M. Karin 1989. Jun and v-jun contain multiple regions that participate in transcriptional activation in an interdependent manner. New Biol. 1: 35–43.
- Argentin, S., Y.-L. Sun, I. Lihrmann, T. J. Schmidt, J. Drouin, and M. Nemer 1991. Distal cis-acting promoter sequences mediate glucocorticoid stimulation of cardiac atrial natriuretic factor gene transcription. J. Biol. Chem. 266: 23315–23322.
- Bannister, A. J., and T. Kouzarides 1995. CBP-induced stimulation of c-Fos activity is abrogated by E1A. EMBO J. 14: 4758–4762.
- Bartel, D. P., M. Sheng, L. F. Lau, and M. E. Greenberg 1989. Growth factors and membrane depolarization activate distinct programs of early response gene expression: dissociation of fos and jun induction. Genes Dev. 3: 304–313.
- Bernstein, L. R., D. K. Ferris, N. H. Colburn, and M. E. Sobel 1994. A family of mitogen-activated protein kinase-related proteins interacts in vivo with activator protein-1 transcription factor. J. Biol. Chem. 269: 9401–9404.
- Blenis, J. 1993. Signal transduction via the MAP kinases: proceed at your own RSK. Proc. Natl. Acad. Sci. USA 90: 5889–5892 (Review.)
- Bogoyevitch, M. A., M. B. Andersson, J. Gillespie-Brown, A. Clerk, P. E. Glennon, S. J. Fuller, and P. H. Sugden 1996. Adrenergic receptor stimulation of the mitogen-activated protein kinase cascade and cardiac hypertrophy. Biochem. J. 314: 115–121.
- Bohmann, D., and R. Tjian 1989. Biochemical analysis of transcriptional activation by Jun: differential activity of c- and v-Jun. Cell 59: 709–717.
- Brusselbach, S., U. Mohle-Steinlein, Z. Q. Wang, M. Schreiber, F. C. Lucibello, R. Muller, and E. F. Wagner 1995. Cell proliferation and cell cycle progression are not impaired in fibroblasts and ES cells lacking c-Fos. Oncogene 10: 79–86.
- Carrasco, D., and R. Bravo 1995. Tissue-specific expression of the fos-related transcription factor fra-2 during mouse development. Oncogene 10: 1069–1079.
- Chen, R. H., C. Abate, and J. Blenis 1993. Phosphorylation of the c-Fos transrepression domain by mitogen-activated protein kinase and 90-kDa ribosomal S6 kinase. Proc. Natl. Acad. Sci. USA 90: 10952–10956.
- Chen, R. H., P. C. Juo, T. Curran, and J. Blenis 1996. Phosphorylation of c-Fos at the C-terminus enhances its transforming activity. Oncogene 12: 1493–1502.
- Deng, T., and M. Karin 1993. JunB differs from c-Jun in its DNA-binding and dimerization domains, and represses c-Jun by formation of inactive heterodimers. Genes Dev. 7: 479–490.
- Deng, T., and M. Karin 1994. c-Fos transcriptional activity stimulated by H-Ras-activated protein kinase distinct from JNK and ERK. Nature 371: 171–175.
- Fisher, F., D. H. Crouch, P. S. Jayaraman, W. Clark, D. A. Gillespie, and C. R. Goding 1993. Transcription activation by Myc and Max: flanking sequences target activation to a subset of CACGTG motifs in vivo. EMBO J. 12: 5075–5082.
- Frost, J. A., T. D. Geppert, M. H. Cobb, and J. R. Feramisco 1994. A requirement for extracellular signal-regulated kinase (ERK) function in the activation of AP-1 by Ha-Ras, phorbol 12-myristate 13-acetate, and serum. Proc. Natl. Acad. Sci. USA 91: 3844–3848.
- Funk, M., B. Poensgen, W. Graulich, V. Jerome, and R. Muller 1997. A novel, transformation-relevant activation domain in Fos proteins. Mol. Cell. Biol. 17: 537–544.
- Gillespie-Brown, J., S. J. Fuller, M. A. Bogoyevitch, S. Cowley, and P. H. Sugden 1995. The mitogen-activated protein kinase kinase MEK1 stimulates a pattern of gene expression typical of the hypertrophic phenotype in rat ventricular cardiomyocytes. J. Biol. Chem. 270: 28092–28096.
- Gius, D., X. Cao, Rauscher F. J., III, D. R. Cohen, T. Curran, and V. P. Sukhatme 1990. Transcriptional activation and repression by Fos are independent functions: the C terminus represses immediate-early gene expression via CArG elements. Mol. Cell. Biol. 10: 4243–4255.
- Hirai, S., B. Bourachot, and M. Yaniv 1990. Both Jun and Fos contribute to transcription activation by the heterodimer. Oncogene 5: 39–46.
- Hu, E., E. Mueller, S. Oliviero, V. E. Papaioannou, R. Johnson, and B. M. Spiegelman 1994. Targeted disruption of the c-fos gene demonstrates c-fos-dependent and -independent pathways for gene expression stimulated by growth factors or oncogenes. EMBO J. 13: 3094–3103.
- Izumo, S., B. Nadal-Ginard, and V. Mahdavi 1988. Protooncogene induction and reprogramming of cardiac gene expression produced by pressure overload. Proc. Natl. Acad. Sci. USA 85: 339–343.
- Jooss, K. U., M. Funk, and R. Muller 1994. An autonomous N-terminal transactivation domain in Fos protein plays a crucial role in transformation. EMBO J. 13: 1467–1475.
- Karin, M. 1995. The regulation of AP-1 activity by mitogen-activated protein kinases. J. Biol. Chem. 270: 16483–16486 (Review.)
- Kerppola, T. K., and T. Curran 1991. Fos-jun heterodimers and jun homodimers bend DNA in opposite orientations: implications for transcription factor cooperativity. Cell 66: 317–326.
- Kerppola, T. K., and T. Curran 1993. Selective DNA bending by a variety of bZIP proteins. Mol. Cell. Biol. 13: 5479–5489.
- Komuro, I., T. Kaida, Y. Shibazaki, M. Kurabayashi, Y. Katoh, E. Hoh, F. Takaku, and Y. Yazaki 1990. Stretching cardiac myocytes stimulates protooncogene expression. J. Biol. Chem. 265: 3595–3598.
- Kovary, K., and R. Bravo 1991. Expression of different Jun and Fos proteins during the G0-to-G1 transition in mouse fibroblasts: in vitro and in vivo associations. Mol. Cell. Biol. 11: 2451–2459.
- Kryszke, M. H., J. Piette, and M. Yaniv 1987. Induction of a factor that binds to the polyoma virus A enhancer on differentiation of embryonal carcinoma cells. Nature 328: 254–256.
- Lucibello, F. C., E. P. Slater, K. U. Jooss, M. Beato, and R. Müller 1990. Mutual transrepression of fos and the glucocorticoid receptor: involvement of a functional domain in fos which is absent in fosB. EMBO J. 9: 2827–2834.
- McBride, K., L. Robitaille, S. Tremblay, S. Argentin, and M. Nemer 1993. Fos/Jun repression of cardiac-specific transcription in quiescent and growth-stimulated myocytes is targeted at a tissue-specific cis element. Mol. Cell. Biol. 13: 600–612.
- Meloche, S., G. Pages, and J. Pouyssegur 1992. Functional expression and growth factor activation of an epitope-tagged p44 mitogen-activated protein kinase, p44mapk. Mol. Biol. Cell 3: 63–71.
- Metz, R., A. J. Bannister, J. A. Sutherland, C. Hagemeier, E. C. O’Rourke, A. Cook, R. Bravo, and T. Kouzarides 1994. c-Fos-induced activation of a TATA-box-containing promoter involves direct contact with TATA-box-binding protein. Mol. Cell. Biol. 14: 6021–6029.
- Nakabeppu, Y., K. Ryder, and D. Nathans 1988. DNA binding activities of three murine Jun proteins: stimulation by Fos. Cell 55: 907–915.
- Naranjo, J. R., B. Mellstrom, J. Auwerx, F. Mollinedo, and P. Sassone-Corsi 1990. Unusual c-fos induction upon chromaffin PC12 differentiation by sodium butyrate: loss of fos autoregulatory function. Nucleic Acids Res. 18: 3605–3610.
- Ofir, R., V. J. Dwarki, D. Rashid, and I. M. Verma 1990. Phosphorylation of the C terminus of fos protein is required for transcriptional transrepression of the c-fos promoter. Nature 348: 80–82.
- Okazaki, K., and N. Sagata 1995. The Mos/MAP kinase pathway stabilizes c-Fos by phosphorylation and augments its transforming activity in NIH 3T3 cells. EMBO J. 14: 5048–5059.
- Ryseck, R. P., and R. Bravo 1991. c-JUN, JUN B, and JUN D differ in their binding affinities to AP-1 and CRE consensus sequences: effect of FOS proteins. Oncogene 6: 533–542.
- Sadoshima, J., and S. Izumo 1993. Mechanical stretch rapidly activates multiple signal transduction pathways in cardiac myocytes: potential involvement of an autocrine/paracrine mechanism. EMBO J. 12: 1681–1692.
- Sadoshima, J., Z. Qiu, J. P. Morgan, and S. Izumo 1995. Angiotensin II and other hypertrophic stimuli mediated by G protein-coupled receptors activate tyrosine kinase, mitogen-activated protein kinase, and 90-kD S6 kinase in cardiac myocytes. The critical role of Ca(2+)-dependent signaling. Circ. Res. 76: 1–15.
- Sassone-Corsi, P., J. C. Sisson, and I. M. Verma 1988. Transcriptional autoregulation of the proto-oncogene fos. Nature 334: 314–319.
- Schreiber, M., B. Baumann, M. Cotten, P. Angel, and E. F. Wagner 1995. Fos is an essential component of the mammalian UV response. EMBO J. 14: 5338–5349.
- Schunkert, H., L. Jahn, S. Izumo, C. S. Apstein, and B. H. Lorell 1991. Localization and regulation of c-fos and c-jun protooncogene induction by systolic wall stress in normal and hypertrophied rat hearts. Proc. Natl. Acad. Sci. USA 88: 11480–11484.
- Smeal, T., P. Angel, J. Meek, and M. Karin 1989. Different requirements for formation of jun:jun and jun:fos complexes. Genes Dev. 3: 2091–2100.
- Stein, B., Baldwin, A. S.Jr., D. W. Ballard, W. C. Greene, P. Angel, and P. Herrlich 1993. Cross-coupling of the NF-kappa B p65 and Fos/Jun transcription factors produces potentiated biological function. EMBO J. 12: 3879–3891.
- Sutherland, J. A., A. Cook, A. J. Bannister, and T. Kouzarides 1992. Conserved motifs in Fos and Jun define a new class of activation domain. Genes Dev. 6: 1810–1819.
- Suzuki, T., H. Okuno, T. Yoshida, T. Endo, H. Nishina, and H. Iba 1991. Difference in transcriptional regulatory function between c-Fos and Fra-2. Nucleic Acids Res. 19: 5537–5542.
- Taylor, L. K., D. R. Marshak, and G. E. Landreth 1993. Identification of a nerve growth factor- and epidermal growth factor-regulated protein kinase that phosphorylates the protooncogene product c-Fos. Proc. Natl. Acad. Sci. USA 90: 368–372.
- Vandel, L., C. M. Pfarr, S. Huguier, L. Loiseau, A. Sergeant, and M. Castellazzi 1995. Increased transforming activity of JunB and JunD by introduction of an heterologous homodimerization domain. Oncogene 10: 495–507.
- von Harsdorf, R., J. G. Edwards, Y. T. Shen, R. K. Kudej, R. Dietz, L. A. Leinwand, B. Nadal Ginard, and S. F. Vatner 1997. Identification of a cis-acting regulatory element conferring inducibility of the atrial natriuretic factor gene in acute pressure overload. J. Clin. Invest. 100: 1294–1304.
- Webster, K. A., D. J. Discher, and N. H. Bishopric 1993. Induction and nuclear accumulation of fos and jun proto-oncogenes in hypoxic cardiac myocytes. J. Biol. Chem. 268: 16852–16858.
- Wick, M., F. C. Lucibello, and R. Muller 1992. Inhibition of Fos- and Ras-induced transformation by mutant Fos proteins with structural alterations in functionally different domains. Oncogene 7: 859–867.
- Wilkinson, D. G., S. Bhatt, R. P. Ryseck, and R. Bravo 1989. Tissue-specific expression of c-jun and junB during organogenesis in the mouse. Development 106: 465–471.
- Wilson, T., and R. Treisman 1988. Fos C-terminal mutations block down-regulation of c-fos transcription following serum stimulation. EMBO J. 7: 4193–4202.
- Wisdom, R., and I. M. Verma 1993. Transformation by Fos proteins requires a C-terminal transactivation domain. Mol. Cell. Biol. 13: 7429–7438.
- Yamazaki, T., I. Komuro, S. Kudoh, Y. Zou, I. Shiojima, T. Mizuno, H. Takano, Y. Hiroi, K. Ueki, K. Tobe, et al. 1995. Mechanical stress activates protein kinase cascade of phosphorylation in neonatal rat cardiac myocytes. J. Clin. Invest. 96: 438–446.
- Yao, A., T. Takahashi, T. Aoyagi, K. Kinugawa, O. Kohmoto, S. Sugiura, and T. Serizawa 1995. Immediate-early gene induction and MAP kinase activation during recovery from metabolic inhibition in cultured cardiac myocytes. J. Clin. Invest. 96: 69–77.