Transcriptional interference between c-Jun and the glucocorticoid receptor: Mutual inhibition of DNA binding due to direct protein-protein interaction

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

[2]  P. Eriksson,et al.  Protein-protein contacts in the glucocorticoid receptor homodimer influence its DNA binding properties. , 1990, The Journal of biological chemistry.

[3]  M. Karin,et al.  Jun-B differs in its biological properties from, and is a negative regulator of, c-Jun , 1989, Cell.

[4]  M. Karin,et al.  Dissection of functional domains of the pituitary-specific transcription factor GHF-1 , 1989, Nature.

[5]  J. Drouin,et al.  Glucocorticoid receptor binding to a specific DNA sequence is required for hormone-dependent repression of pro-opiomelanocortin gene transcription , 1989, Molecular and cellular biology.

[6]  M. Karin,et al.  Different requirements for formation of Jun: Jun and Jun: Fos complexes. , 1989, Genes & development.

[7]  K. Yamamoto,et al.  Mutations in the glucocorticoid receptor zinc finger region that distinguish interdigitated DNA binding and transcriptional enhancement activities. , 1989, Genes & development.

[8]  I. Screpanti,et al.  Tumor-promoting phorbol ester and ras oncogene expression inhibit the glucocorticoid-dependent transcription from the mouse mammary tumor virus long terminal repeat. , 1989, Molecular endocrinology.

[9]  M. Karin,et al.  The CUP2 gene product, regulator of yeast metallothionein expression, is a copper-activated DNA-binding protein , 1989, Molecular and cellular biology.

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

[11]  P. Chambon,et al.  Steroid hormone receptors compete for factors that mediate their enhancer function , 1989, Cell.

[12]  S. Krane,et al.  Increases in levels of procollagenase messenger RNA in cultured fibroblasts induced by human recombinant interleukin 1 beta or serum follow c-jun expression and are dependent on new protein synthesis. , 1989, The Journal of clinical investigation.

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

[14]  R. Evans,et al.  Transcriptional inhibition by a glucocorticoid receptor-β-galactosidase fusion protein , 1988, Cell.

[15]  R. Offringa,et al.  Similar effects of adenovirus E1A and glucocorticoid hormones on the expression of the metalloprotease stromelysin. , 1988, Nucleic acids research.

[16]  L. Matrisian,et al.  Growth factors regulate transin gene expression by c-fos-dependent and c-fos-independent pathways. , 1988, Science.

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

[18]  R. Evans,et al.  Multiple and cooperative trans-activation domains of the human glucocorticoid receptor , 1988, Cell.

[19]  K. Yamamoto,et al.  Hormone-mediated repression: a negative glucocorticoid response element from the bovine prolactin gene. , 1988, Genes & development.

[20]  T. Hunter,et al.  The c-fos protein interacts with c-Jun AP-1 to stimulate transcription of AP-1 responsive genes , 1988, Cell.

[21]  Mark Ptashne,et al.  Negative effect of the transcriptional activator GAL4 , 1988, Nature.

[22]  J D Baxter,et al.  Negative regulation by glucocorticoids through interference with a cAMP responsive enhancer. , 1988, Science.

[23]  J. Abecassis,et al.  The collagenase gene family in humans consists of at least four members. , 1988, The Biochemical journal.

[24]  S. McKnight,et al.  The leucine zipper: a hypothetical structure common to a new class of DNA binding proteins. , 1988, Science.

[25]  R. Tjian,et al.  Fos-associated protein p39 is the product of the jun proto-oncogene. , 1988, Science.

[26]  T. Hunter,et al.  Oncogene jun encodes a sequence-specific trans- activator similar to AP-1 , 1988, Nature.

[27]  H. Ruley,et al.  Transcription from the stromelysin promoter is induced by interleukin-1 and repressed by dexamethasone. , 1987, The Journal of biological chemistry.

[28]  R. Tjian,et al.  Human proto-oncogene c-jun encodes a DNA binding protein with structural and functional properties of transcription factor AP-1. , 1987, Science.

[29]  M. Karin,et al.  A pituitary-specific trans-acting factor can stimulate transcription from the growth hormone promoter in extracts of nonexpressing cells , 1987, Cell.

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

[31]  P. Herrlich,et al.  12-O-tetradecanoyl-phorbol-13-acetate induction of the human collagenase gene is mediated by an inducible enhancer element located in the 5'-flanking region , 1987, Molecular and cellular biology.

[32]  R. Doolittle,et al.  Homology between the DNA-binding domain of the GCN4 regulatory protein of yeast and the carboxyl-terminal region of a protein coded for by the oncogene jun. , 1987, Proceedings of the National Academy of Sciences of the United States of America.

[33]  K. Wood,et al.  Firefly luciferase gene: structure and expression in mammalian cells , 1987, Molecular and cellular biology.

[34]  R. Tjian,et al.  Activation of transcription by two factors that bind promoter and enhancer sequences of the human metallothionein gene and SV40 , 1987, Nature.

[35]  P. Herrlich,et al.  Comparison of human stromelysin and collagenase by cloning and sequence analysis. , 1986, The Biochemical journal.

[36]  J. Drouin,et al.  Glucocorticoid inhibition of transcription from episomal proopiomelanocortin gene promoter. , 1986, Proceedings of the National Academy of Sciences of the United States of America.

[37]  G. O'Connor,et al.  Half-life of synovial cell collagenase mRNA is modulated by phorbol myristate acetate but not by all-trans-retinoic acid or dexamethasone. , 1986, Biochemistry.

[38]  B. Groner,et al.  The v‐mos and H‐ras oncogene expression represses glucocorticoid hormone‐dependent transcription from the mouse mammary tumor virus LTR. , 1986, The EMBO journal.

[39]  R. Richards,et al.  Suppression of urokinase‐type plasminogen activator mRNA levels in human fibrosarcoma cells and synovial fibroblasts by anti‐inflammatory glucocorticoids. , 1986, The EMBO journal.

[40]  W. Stigelman,et al.  Goodman and Gilman's the Pharmacological Basis of Therapeutics , 1986 .

[41]  G. Litwack,et al.  Thermal activation of the purified rat hepatic glucocorticoid receptor. Evidence for a two-step mechanism. , 1985, The Journal of biological chemistry.

[42]  M. Karin,et al.  Characterization of DNA sequences through which cadmium and glucocorticoid hormones induce human metallothionein-IIA gene , 1984, Nature.

[43]  D. Steiner,et al.  Expression of a preproinsulin-beta-galactosidase gene fusion in mammalian cells. , 1983, Proceedings of the National Academy of Sciences of the United States of America.

[44]  M. Beato,et al.  The glucocorticoid receptor binds to defined nucleotide sequences near the promoter of mouse mammary tumour virus , 1983, Nature.

[45]  B. Howard,et al.  Recombinant genomes which express chloramphenicol acetyltransferase in mammalian cells , 1982, Molecular and cellular biology.

[46]  W. Pratt,et al.  Specific glucocorticoid-binding macromolecules from mouse fibroblasts growing in vitro. A possible steroid receptor for growth inhibition. , 1970, Molecular pharmacology.

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

[48]  J. Noel,et al.  A novel expression vector for high-level synthesis and secretion of foreign proteins in Escherichia coli: overproduction of bovine pancreatic phospholipase A2. , 1990, Gene.

[49]  F. Studier,et al.  Use of T7 RNA polymerase to direct expression of cloned genes. , 1990, Methods in enzymology.

[50]  M. Karin,et al.  Jun and v-jun contain multiple regions that participate in transcriptional activation in an interdependent manner. , 1989, The New biologist.

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

[52]  K. Yamamoto,et al.  Glucocorticoid receptor mutants that are constitutive activators of transcriptional enhancement , 1987, Nature.

[53]  William N. Kelley,et al.  Textbook of rheumatology , 1985 .

[54]  P. Cohen,et al.  Molecular aspects of cellular regulation , 1980 .

[55]  A. Fauci,et al.  Mechanisms of glucocorticoid action on immune processes. , 1979, Annual review of pharmacology and toxicology.