Signal transduction and gene control.

[1]  M. Karin,et al.  Ha-Ras augments c-Jun activity and stimulates phosphorylation of its activation domain , 1991, Nature.

[2]  Tony Hunter,et al.  Activation of protein kinase C decreases phosphorylation of c-Jun at sites that negatively regulate its DNA-binding activity , 1991, Cell.

[3]  L. Cantley,et al.  Oncogenes and signal transduction , 1991, Cell.

[4]  I. Verma,et al.  Phosphorylation of the C terminus of Fos protein is required for transcriptional transrepression of the c-fos promoter , 1990, Nature.

[5]  Vincent Bours,et al.  Cloning of a mitogen-inducible gene encoding a κB DNA-binding protein with homology to the rel oncogene and to cell-cycle motifs , 1990, Nature.

[6]  T. Taniguchi,et al.  Absence of the type I IFN system in EC cells: Transcriptional activator (IRF-1) and repressor (IRF-2) genes are developmentally regulated , 1990, Cell.

[7]  M. Karin,et al.  Transcriptional interference between c-Jun and the glucocorticoid receptor: Mutual inhibition of DNA binding due to direct protein-protein interaction , 1990, Cell.

[8]  Stephan Gebel,et al.  Antitumor promotion and antiinflammation: Down-modulation of AP-1 (Fos/Jun) activity by glucocorticoid hormone , 1990, Cell.

[9]  S. Kliewer,et al.  Functional antagonism between oncoprotein c-Jun and the glucocorticoid receptor , 1990, Cell.

[10]  K. Yamamoto,et al.  Transcription factor interactions: selectors of positive or negative regulation from a single DNA element. , 1990, Science.

[11]  G. Nolan,et al.  Cloning of the p50 DNA binding subunit of NF-κB: Homology to rel and dorsal , 1990, Cell.

[12]  A. Israël,et al.  The DNA binding subunit of NF-κB is identical to factor KBF1 and homologous to the rel oncogene product , 1990, Cell.

[13]  F. C. Lucibello,et al.  Mutual transrepression of Fos and the glucocorticoid receptor: involvement of a functional domain in Fos which is absent in FosB. , 1990, The EMBO journal.

[14]  M. Sporn,et al.  Interleukin-1 stimulates and all-trans-retinoic acid inhibits collagenase gene expression through its 5' activator protein-1-binding site. , 1990, Molecular endocrinology.

[15]  M. Karin,et al.  Regulation of the pituitary-specific homeobox gene GHF1 by cell-autonomous and environmental cues , 1990, Nature.

[16]  U. Zabel,et al.  Purified human IκB can rapidly dissociate the complex of the NF-κB transcription factor with its cognate DNA , 1990, Cell.

[17]  D. Baltimore,et al.  Activation in vitro of NF-κB" by phosphorylation of its inhibitor IκB" , 1990, Nature.

[18]  M. Greenberg,et al.  Membrane depolarization and calcium induce c-fos transcription via phosphorylation of transcription factor CREB , 1990, Neuron.

[19]  M. Karin,et al.  Elevation of AP1 activity during F9 cell differentiation is due to increased c-jun transcription. , 1990, The New biologist.

[20]  M. Sporn,et al.  Autoinduction of transforming growth factor beta 1 is mediated by the AP-1 complex , 1990, Molecular and cellular biology.

[21]  M. Montminy,et al.  Characterization of a bipartite activator domain in transcription factor CREB , 1990, Cell.

[22]  M. Montminy,et al.  Cyclic AMP stimulates somatostatin gene transcription by phosphorylation of CREB at serine 133 , 1989, Cell.

[23]  T. Hunter,et al.  Transcriptional induction of the murine c-rel gene with serum and phorbol-12-myristate-13-acetate in fibroblasts , 1989, Molecular and cellular biology.

[24]  D. Baltimore,et al.  A 65-kappaD subunit of active NF-kappaB is required for inhibition of NF-kappaB by I kappaB. , 1989, Genes & development.

[25]  Takashi Miyata,et al.  Structurally similar but functionally distinct factors, IRF-1 and IRF-2, bind to the same regulatory elements of IFN and IFN-inducible genes , 1989, Cell.

[26]  D. Baltimore,et al.  NF-κB: A pleiotropic mediator of inducible and tissue-specific gene control , 1989, Cell.

[27]  S. Mizel,et al.  In vitro activation and nuclear translocation of NF-kappa B catalyzed by cyclic AMP-dependent protein kinase and protein kinase C , 1989, Molecular and cellular biology.

[28]  D. Linzer,et al.  Co-localization of elements required for phorbol ester stimulation and glucocorticoid repression of proliferin gene expression. , 1989, Genes & development.

[29]  M. Karin,et al.  Induction of human growth hormone promoter activity by the adenosine 3',5'-monophosphate pathway involves a novel responsive element. , 1989, Molecular endocrinology.

[30]  J. Minna,et al.  Deregulated expression of human c-jun transforms primary rat embryo cells in cooperation with an activated c-Ha-ras gene and transforms rat-1a cells as a single gene. , 1989, Proceedings of the National Academy of Sciences of the United States of America.

[31]  W. Biggs,et al.  A cluster of phosphorylation sites on the cyclic AMP-regulated nuclear factor CREB predicted by its sequence , 1989, Nature.

[32]  D. Brenner,et al.  Prolonged activation of jun and collagenase genes by tumour necrosis factor-α , 1989, Nature.

[33]  Richard Treisman,et al.  Isolation and properties of cDNA clones encoding SRF, a transcription factor that binds to the c-fos serum response element , 1988, Cell.

[34]  T. Meyer,et al.  Cyclic AMP-responsive DNA-binding protein: structure based on a cloned placental cDNA. , 1988, Science.

[35]  Peter Angel,et al.  The jun proto-oncogene is positively autoregulated by its product, Jun/AP-1 , 1988, Cell.

[36]  T. Deerinck,et al.  The pituitary-specific transcription factor GHF-1 is a homeobox-containing protein , 1988, Cell.

[37]  D. Baltimore,et al.  I kappa B: a specific inhibitor of the NF-kappa B transcription factor. , 1988, Science.

[38]  T. Taniguchi,et al.  Regulated expression of a gene encoding a nuclear factor, IRF-1, that specifically binds to IFN-β gene regulatory elements , 1988, Cell.

[39]  M. Montminy,et al.  Phosphorylation-induced binding and transcriptional efficacy of nuclear factor CREB , 1988, Nature.

[40]  B. Wasylyk,et al.  Transforming but not immortalizing oncogenes activate the transcription factor PEA1. , 1988, The EMBO journal.

[41]  I. Verma,et al.  Transcriptional autoregulation of the proto-oncogene fos , 1988, Nature.

[42]  R. Evans,et al.  The steroid and thyroid hormone receptor superfamily. , 1988, Science.

[43]  M. Karin,et al.  Phorbol ester-inducible genes contain a common cis element recognized by a TPA-modulated trans-acting factor , 1987, Cell.

[44]  I. Verma,et al.  Modification of fos proteins: phosphorylation of c-fos, but not v-fos, is stimulated by 12-tetradecanoyl-phorbol-13-acetate and serum , 1987, Molecular and cellular biology.

[45]  E. Nigg,et al.  Rapid and reversible translocation of the catalytic subunit of cAMP‐dependent protein kinase type II from the Golgi complex to the nucleus. , 1985, The EMBO journal.

[46]  Michael E. Greenberg,et al.  Stimulation of 3T3 cells induces transcription of the c-fos proto-oncogene , 1984, Nature.

[47]  M. Karin The AP-1 complex and its role in transcriptional control by protein kinase C , 1991 .

[48]  M. Yaniv,et al.  Both Jun and Fos contribute to transcription activation by the heterodimer. , 1990, Oncogene.

[49]  P. Herrlich,et al.  'Nuclear' oncogenes convert extracellular stimuli into changes in the genetic program. , 1989, Trends in genetics : TIG.

[50]  L. M. Albright,et al.  Prokaryotic signal transduction mediated by sensor and regulator protein pairs. , 1989, Annual review of genetics.

[51]  Jonathan A. Cooper,et al.  Platelet-derived growth factor induces rapid but transient expression of the c-fos gene and protein , 1984, Nature.