Ha-Ras augments c-Jun activity and stimulates phosphorylation of its activation domain

[1]  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.

[2]  T. Hunter.  Cooperation between oncogenes , 1991, Cell.

[3]  R. Tjian,et al.  Control of c-Jun activity by interaction of a cell-specific inhibitor with regulatory domain δ: Differences between v- and c-Jun , 1990, 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]  I. Verma,et al.  Revertants of v-fos-transformed rat fibroblasts: suppression of transformation is dominant , 1990, Molecular and cellular biology.

[6]  C. Chang,et al.  Efficient transformation of chicken embryo fibroblasts by c-Jun requires structural modification in coding and noncoding sequences. , 1990, Genes & development.

[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]  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.

[10]  H. Ruley.  Transforming collaborations between ras and nuclear oncogenes. , 1990, Cancer cells.

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

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

[13]  J. Minna,et al.  jun-B inhibits and c-fos stimulates the transforming and trans-activating activities of c-jun , 1989, Cell.

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

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

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

[17]  R. Weinberg,et al.  Oncogenes, antioncogenes, and the molecular bases of multistep carcinogenesis. , 1989, Cancer research.

[18]  M. Yaniv,et al.  Characterization of junD: a new member of the jun proto‐oncogene family. , 1989, The EMBO journal.

[19]  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.

[20]  K. Alitalo,et al.  The cellular response to induction of the p21 c‐Ha‐ras oncoprotein includes stimulation of jun gene expression. , 1989, The EMBO journal.

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

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

[23]  I. Verma,et al.  Induction of proto-oncogene JUN/AP-1 by serum and TPA , 1988, Nature.

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

[25]  M. Yaniv,et al.  Transcriptional activation of c-jun during the G0/G1 transition in mouse fibroblasts , 1988, Nature.

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

[27]  R. Breathnach,et al.  Epidermal growth factor stimulates transcription of the c-jun proto-oncogene in rat fibroblasts , 1988, Nature.

[28]  A. Schönthal,et al.  Requirement for fos gene expression in the transcriptional activation of collagenase by other oncogenes and phorbol esters , 1988, Cell.

[29]  J. Piette,et al.  Constitutive synthesis of activator protein 1 transcription factor after viral transformation of mouse fibroblasts. , 1988, Proceedings of the National Academy of Sciences of the United States of America.

[30]  B. Wasylyk,et al.  v-jun is a transcriptional activator, but not in all cell-lines. , 1988, Nucleic acids research.

[31]  B. Wasylyk,et al.  A Harvey-ras responsive transcription element is also responsive to a tumour-promoter and to serum , 1988, Nature.

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

[33]  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.

[34]  H. Zarbl,et al.  Revertants of v-fos-transformed fibroblasts have mutations in cellular genes essential for transformation by other oncogenes , 1987, Cell.

[35]  T. Fleming,et al.  Involvement of functional protein kinase C in the mitogenic response to the H-ras oncogene product , 1987, Molecular and cellular biology.

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

[37]  R. Tjian,et al.  Purified transcription factor AP-1 interacts with TPA-inducible enhancer elements , 1987, Cell.

[38]  T. Curran,et al.  Microinjection of transforming ras protein induces c-fos expression , 1987, Molecular and cellular biology.

[39]  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.

[40]  R. Weinberg,et al.  Behavior of myc and ras oncogenes in transformation of rat embryo fibroblasts , 1986, Molecular and cellular biology.

[41]  R. Weinberg,et al.  Specific growth response of ras-transformed embryo fibroblasts to tumour promoters , 1985, Nature.

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

[43]  P. Vogt,et al.  jun: oncogene and transcription factor. , 1990, Advances in cancer research.

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

[45]  R. Weinberg.  Oncogenes and the molecular origins of cancer , 1989 .

[46]  M. Ashburner.  A Laboratory manual , 1989 .

[47]  E. Harlow,et al.  Antibodies: A Laboratory Manual , 1988 .

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