12‐O‐tetradecanoylphorbol‐13‐acetate—induced levels of ap‐1 proteins: a 46‐kda protein immunoprecipitated by anti‐fra‐1 and induced in promotion‐resistant but not promotion‐sensitive JB6 cells

No abstract is available for this paper.

• Publication year

  1992

• Venue

  Molecular Carcinogenesis

• Publication date

  Unknown publication date

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1002/mc.2940060308PMID 1445622
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• Differential c‐jun expression in response to tumor promoters in JB6 cells sensitive or resistant to neoplastic transformation

  1992cited by this paper
• Both products of the fosB gene, FosB and its short form, FosB/SF, are transcriptional activators in fibroblasts.

  1991cited by this paper
• c-JUN, JUN B, and JUN D differ in their binding affinities to AP-1 and CRE consensus sequences: effect of FOS proteins.

  1991cited by this paper
• Defective induction of Jun and Fos-related proteins in phorbol ester-resistant EL4 mouse thymoma cells.

  1991cited by this paper
• fosB is a transforming gene encoding a transcriptional activator.

  1991cited by this paper
• The jun and fos protein families are both required for cell cycle progression in fibroblasts

  1991cited by this paper
• Constitutive expression of FosB and its short form, FosB/SF, induces malignant cell transformation in rat-1A cells.

  1991cited by this paper
• Alternative splicing of fosB transcripts results in differentially expressed mRNAs encoding functionally antagonistic proteins.

  1991cited by this paper
• The transactivating domain of the c-Jun proto-oncoprotein is required for cotransformation of rat embryo cells

  1991cited by this paper
• Gene regulation and genetic susceptibility to neoplastic transformation: AP-1 and p80 expression in JB6 cells.

  1991cited by this paper
• Expression of different Jun and Fos proteins during the G0-to-G1 transition in mouse fibroblasts: in vitro and in vivo associations

  1991cited by this paper
• High‐level Expression of Human c‐jun Gene Causes Cellular Transformation of Chicken Embryo Fibroblasts

  1991cited by this paper
• An alternative spliced form of FosB is a negative regulator of transcriptional activation and transformation by Fos proteins.

  1991cited by this paper
• Overexpression of c-jun, junB, or junD affects cell growth differently.

  1991cited by this paper
• Defective induction of Jun and Fos-related proteins in phorbol ester-resistant EL4 mouse thymoma cells.

  1991cited by this paper
• Retinoic acid is a negative regulator of AP-1-responsive genes.

  1991cited by this paper
• A naturally occurring truncated form of FosB that inhibits Fos/Jun transcriptional activity.

  1991cited by this paper
• Jun-Fos and receptors for vitamins A and D recognize a common response element in the human osteocalcin gene.

  1990cited by this paper
• Efficient transformation of chicken embryo fibroblasts by c-Jun requires structural modification in coding and noncoding sequences.

  1990cited by this paper
• Transcription factor interactions: selectors of positive or negative regulation from a single DNA element.

  1990cited by this paper
• Isolation of human fos-related genes and their expression during monocyte-macrophage differentiation.

  1990cited by this paper
• Negative regulation of the rat stromelysin gene promoter by retinoic acid is mediated by an AP1 binding site.

  1990cited by this paper
• Functional antagonism between oncoprotein c-Jun and the glucocorticoid receptor.

  1990cited by this paper
• jun: oncogene and transcription factor.

  1990cited by this paper
• Transcriptional interference between c-Jun and the glucocorticoid receptor: mutual inhibition of DNA binding due to direct protein-protein interaction.

  1990cited by this paper
• Overexpression of avian or mouse c-jun in primary chick embryo fibroblasts confers a partially transformed phenotype.

  1990cited by this paper
• Isolation and characterization of fra-2, an additional member of the fos gene family.

  1990cited by this paper
• Antitumor promotion and antiinflammation: down-modulation of AP-1 (Fos/Jun) activity by glucocorticoid hormone.

  1990cited by this paper
• Growth factor-responsive genes in fibroblasts.

  1990cited by this paper
• Interleukin-1 stimulates and all-trans-retinoic acid inhibits collagenase gene expression through its 5' activator protein-1-binding site.

  1990cited by this paper
• Activation of the ovalbumin gene by the estrogen receptor involves the fos-jun complex.

  1990cited by this paper
• The product of a fos-related gene, fra-1, binds cooperatively to the AP-1 site with Jun: transcription factor AP-1 is comprised of multiple protein complexes.

  1989cited by this paper
• jun-B inhibits and c-fos stimulates the transforming and trans-activating activities of c-jun.

  1989cited by this paper
• jun-D: a third member of the jun gene family.

  1989cited by this paper
• AP1/jun function is differentially induced in promotion-sensitive and resistant JB6 cells.

  1989cited by this paper
• 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.

  1989cited by this paper
• The product of a novel growth factor activated gene, fos B, interacts with JUN proteins enhancing their DNA binding activity.

  1989cited by this paper
• Characterization of junD: a new member of the jun proto‐oncogene family.

  1989cited by this paper
• fra-1: a serum-inducible, cellular immediate-early gene that encodes a fos-related antigen

  1988cited by this paper
• c-Jun dimerizes with itself and with c-Fos, forming complexes of different DNA binding affinities.

  1988cited by this paper
• Fos-associated protein p39 is the product of the jun proto-oncogene.

  1988cited by this paper
• Oncogene jun encodes a sequence-specific trans- activator similar to AP-1

  1988cited by this paper
• A gene activated by growth factors is related to the oncogene v-jun.

  1988cited by this paper
• The role of the leucine zipper in the fos–jun interaction

  1988cited by this paper
• DNA binding activities of three murine Jun proteins: stimulation by Fos.

  1988cited by this paper
• Fos and Jun bind cooperatively to the AP-1 site: reconstitution in vitro.

  1988cited by this paper
• The c-Ha-ras oncogene and a tumor promoter activate the polyoma virus enhancer.

  1987cited by this paper
• Purified transcription factor AP-1 interacts with TPA-inducible enhancer elements.

  1987cited by this paper
• Avian sarcoma virus 17 carries the jun oncogene.

  1987cited by this paper
• Human proto-oncogene c-jun encodes a DNA binding protein with structural and functional properties of transcription factor AP-1.

  1987cited by this paper
• 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

  1987cited by this paper
• Phorbol ester-inducible genes contain a common cis element recognized by a TPA-modulated trans-acting factor.

  1987cited by this paper
• Phorbol ester induces the transcriptional stimulatory activity of the SV40 enhancer

  1986cited by this paper
• Isolation of the oncogene and epidermal growth factor-induced transin gene: complex control in rat fibroblasts

  1986cited by this paper
• Comparison of human stromelysin and collagenase by cloning and sequence analysis.

  1986cited by this paper
• Genes and membrane signals involved in neoplastic transformation.

  1985cited by this paper
• c-fos protein can induce cellular transformation: a novel mechanism of activation of a cellular oncogene.

  1984cited by this paper
• Viral and cellular fos proteins: a comparative analysis.

  1984cited by this paper
• Candidate product of the FBJ murine osteosarcoma virus oncogene: characterization of a 55,000-dalton phosphoprotein

  1982cited by this paper
• FBJ murine osteosarcoma virus: identification and molecular cloning of biologically active proviral DNA

  1982cited by this paper
• A cell culture assay for tumor-promoter-dependent progression toward neoplastic phenotype: detection of tumor promoters and promotion inhibitors.

  1980cited by this paper
• Tumour promoter induces anchorage independence irreversibly

  1979cited by this paper
• Cleavage of Structural Proteins during the Assembly of the Head of Bacteriophage T4

  1970cited by this paper

• Involvement of PTEN in TPA‐mediated p53‐activation in mouse skin epidermal JB6 cells

  2012cites this paper
• Elevated Phosphate Activates N-ras and Promotes Cell Transformation and Skin Tumorigenesis

  2010cites this paper
• SAG/ROC2/Rbx2 is a novel activator protein-1 target that promotes c-Jun degradation and inhibits 12-O-tetradecanoylphorbol-13-acetate-induced neoplastic transformation.

  2007cites this paper
• No Point Mutation of H a m s or p53 Genes Preneoplastic-to-Neoplastic Progression as Mouse JB6 Cell Variants' Expressed in Modeled in

  2006cites this paper
• Metalloproteinases-3 Cells : One Is Homologous to Human Tissue Inhibitor of EpidermalExpressed in Preneoplastic or Neoplastic JB 6 Mouse Molecular Cloning of Five Messenger RNAs Differentially

  2006cites this paper
• Dominant-negative c-Jun (TAM67) target genes: HMGA1 is required for tumor promoter-induced transformation

  2004cites this paper
• The role of AP-1, NF-κB and ROS/NOS in skin carcinogenesis: The JB6 model is predictive

  2004cites this paper
• Nitric oxide does not mediate but inhibits transformation and tumor phenotype.

  2003cites this paper
• The role of AP-1, NF-кB and ROS/ NOS in skin carcinogenesis: The JB6 model is predictive

  2002cites this paper
• AP-1 transrepressing retinoic acid does not deplete coactivators or AP-1 monomers but may target specific Jun or Fos containing dimers

  2002cites this paper
• Transactivation of Fra-1 and Consequent Activation of AP-1 Occur Extracellular Signal-Regulated Kinase Dependently

  2002cites this paper
• cDNA cloning and mapping of mouse pleckstrin (Plek), a gene upregulated in transformation-resistant cells.

  2000cites this paper
• Activator protein 1 (AP-1)– and nuclear factor κB (NF-κB)–dependent transcriptional events in carcinogenesis

  2000cites this paper
• Nitric oxide synthase is induced in tumor promoter-sensitive, but not tumor promoter-resistant, JB6 mouse epidermal cells cocultured with interferon-gamma-stimulated RAW 264.7 cells: the role of tumor necrosis factor-alpha.

  2000cites this paper
• Activator protein 1 (AP-1)- and nuclear factor kappaB (NF-kappaB)-dependent transcriptional events in carcinogenesis.

  2000cites this paper
• Tumor promotion resistant cells are deficient in AP-1 DNA binding, JunD DNA binding and JunD expression and form different AP-1-DNA complexes than promotion sensitive cells.

  1999cites this paper
• Differentially expressed protein Pdcd4 inhibits tumor promoter-induced neoplastic transformation.

  1999cites this paper
• Molecular mechanisms of ultraviolet-B induced activator protein 1 activation in human keratinocytes

  1999cites this paper
• Extracellular Signal-regulated Kinase 1/2-mediated Phosphorylation of JunD and FosB Is Required for Okadaic Acid-induced Activator Protein 1 Activation*

  1999cites this paper
• Freshly Fractured Crystalline Silica Induces Activator Protein-1 Activation through ERKs and p38 MAPK*

  1999cites this paper
• Tumor promoter induces high mobility group HMG-Y protein expression in transformation-sensitive but not -resistant cells

  1998cites this paper
• Promotion‐sensitive epidermal and mammary epithelial cells maintained in suspension over agarose

  1998cites this paper
• Inhibitors of both nuclear factor-kappaB and activator protein-1 activation block the neoplastic transformation response.

  1997cites this paper
• Inhibition of Ultraviolet B-induced Activator Protein-1 (AP-1) Activity by Aspirin in AP-1-Luciferase Transgenic Mice*

  1997cites this paper
• Use of Mouse JB6 Cells to Identify Molecular Targets and Novel Agents for Prevention of Carcinogenesis

  1997cites this paper
• Okadaic acid stimulated TRE binding activity in a papilloma producing mouse keratinocyte cell line involves increased AP-1 expression.

  1996cites this paper
• Progressive elevation of ap-1 activity during preneoplastic-to-neoplastic progression as modeled in mouse jb6 cell variants.

  1995cites this paper
• c‐jun and multistage carcinogenesis: Association of overexpression of introduced c‐jun with progression toward a neoplastic endpoint in mouse JB6 cells sensitive to tumor promoter‐induced transformation

  1995cites this paper
• C-JUN/AP-1 as possible mediators of tumor necrosis factor-alpha-induced apoptotic response in mouse JB6 tumor cells.

  1995cites this paper
• Intermittent 50 Hz magnetic field and skin tumor promotion in SENCAR mice.

  1994cites this paper
• Differential transformation efficiency but not AP-1 induction under anchorage-dependent and -independent conditions.

  1994cites this paper
• Molecular cloning of five messenger RNAs differentially expressed in preneoplastic or neoplastic JB6 mouse epidermal cells: one is homologous to human tissue inhibitor of metalloproteinases-3.

  1994cites this paper
• Preferential primary‐response gene expression in promotion‐resistant versus promotion‐sensitive JB6 cells

  1994cites this paper
• A family of mitogen-activated protein kinase-related proteins interacts in vivo with activator protein-1 transcription factor.

  1994cites this paper
• No point mutation of ha‐ras or p53 genes expressed in preneoplastic‐to‐neoplastic progression as modeled in mouse JB6 cell variants

  1993cites this paper