Cellular Transformation and Malignancy Induced by ras Require c-jun

The small GTP-binding protein rac regulates growth factor-induced membrane ruffling

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JNK1: A protein kinase stimulated by UV light and Ha-Ras that binds and phosphorylates the c-Jun activation domain

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Activation of MAP kinase kinase is necessary and sufficient for PC12 differentiation and for transformation of NIH 3T3 cells

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Mammalian Ras interacts directly with the serine/threonine kinase Raf.

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Phosphatidylinositol-3-OH kinase direct target of Ras

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Proteins regulating Ras and its relatives

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

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Antitumor promotion and antiinflammation: Down-modulation of AP-1 (Fos/Jun) activity by glucocorticoid hormone

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Phosphorylation of c-jun mediated by MAP kinases

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SV40 large tumor antigen forms a specific complex with the product of the retinoblastoma susceptibility gene

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Transformation of Mammalian Cells by Constitutively Active MAP Kinase Kinase

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The SRF accessory protein Elk-1 contains a growth factor-regulated transcriptional activation domain

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Transcription Factor Interactions: Selectors of Positive or Negative Regulation from a Single DNA Element

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Functional antagonism between oncoprotein c-Jun and the glucocorticoid receptor

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Differential Activation of ERK and JNK Mitogen-Activated Protein Kinases by Raf-1 and MEKK

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An essential role for Rac in Ras transformation

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Normal and oncogenic p21ras proteins bind to the amino-terminal regulatory domain of c-Raf-1

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Oncogenic and transcriptional cooperation with Ha-Ras requires phosphorylation of c-Jun on serines 63 and 73

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The small GTP-binding protein rac regulates growth factor-induced membrane ruffling

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Direct interaction of Ras and the amino-terminal region of Raf-1 in vitro

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Induction of proto-oncogene JUN/AP-1 by serum and TPA

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Multiple ras functions can contribute to mammalian cell transformation

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FBJ murine osteosarcoma virus: identification and molecular cloning of biologically active proviral DNA

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Complex formation between RAS and RAF and other protein kinases.

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

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Transcriptional activation of c-jun during the G0/G1 transition in mouse fibroblasts

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Ras-Dependent Induction of Cellular Responses by Constitutively Active Phosphatidylinositol-3 Kinase

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c-Jun is essential for normal mouse development and hepatogenesis

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Characterization of junD: a new member of the jun proto‐oncogene family.

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The collagenase gene promoter contains a TPA and oncogene‐responsive unit encompassing the PEA3 and AP‐1 binding sites.

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A null mutation at the c-jun locus causes embryonic lethality and retarded cell growth in culture.Preprint

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Functional antagonism between c-Jun and MyoD proteins: A direct physical association

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Functional analysis of a growth factor-responsive transcription factor complex

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c-fos is required for malignant progression of skin tumors

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Isolation of the Oncogene and Epidermal Growth Factor-Induced Transin Gene: Complex Control in Rat Fibroblasts

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Mouse JunD negatively regulates fibroblast growth and antagonizes transformation by ras

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Activated Ras interacts with the Ral guanine nucleotide dissociation stimulator.

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Identification of the guanine nucleotide dissociation stimulator for Ral as a putative effector molecule of R-ras, H-ras, K-ras, and Rap.

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ralGDS family members interact with the effector loop of ras p21.

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mXBP/CRE-BP2 and c-Jun form a complex which binds to the cyclic AMP, but not to the 12-O-tetradecanoylphorbol-13-acetate, response element.

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Direct cloning of leucine zipper proteins: Jun binds cooperatively to the CRE with CRE-BP1

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A yeast gene (BEM1) necessary for cell polarization whose product contains two SH3 domains

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Emerging concepts in the Ras superfamily of GTP‐binding proteins

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Transformation suppressor activity of a Jun transcription factor lacking its activation domain

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Recombinant Retroviruses Encoding Simian Virus 40 Large T Antigen and Polyomavirus Large and Middle T Antigens

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Targeted disruption of the c‐fos gene demonstrates c‐fos‐dependent and ‐independent pathways for gene expression stimulated by growth factors or oncogenes.

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Efficient transformation of chicken embryo fibroblasts by c-Jun requires structural modification in coding and noncoding sequences.Preprint

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The Transactivating Domain of the c-Jun Proto-Oncoprotein Is Required for Cotransformation of Rat Embryo Cells

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Jun family members are controlled by a calcium-regulated, cyclosporin A-sensitive signaling pathway in activated T lymphocytes.Preprint

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Immortalization of rodent embryo fibroblasts by SV40 Is maintained by the Å gene

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Drosophila Jun mediates Ras-dependent photoreceptor determination

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Isolation of the Oncogene and Epidermal Growth Factor-Induced Transin Gene: Complex Control in Rat Fibroblasts

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Transcription factors junB and c-jun are selectively up-regulated and functionally implicated in fibrosarcoma development.Preprint

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Embryonic stem (ES) cells lacking functional c-jun: consequences for growth and differentiation, AP-1 activity and tumorigenicity.

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Recombinant Retroviruses Encoding Simian Virus 40 Large T Antigen and Polyomavirus Large and Middle T Antigens

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Sequences from polyomavirus and simian virus 40 large T genes capable of immortalizing primary rat embryo fibroblasts

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mXBP/CRE-BP2 and c-Jun Form a Complex Which Binds to the Cyclic AMP, but Not to the 12- O -Tetradecanoylphorbol-13-Acetate, Response Element

Ivashkiv, L. B., Liou, H., Kara, C. J., Lamph, W. W., Verma, I. M., & Glimcher, L. H. (1990) · Molecular and Cellular Biology · doi:10.1128/mcb.10.4.1609-1621.1990 · Cited by 56 · see citing works

ralGDS Family Members Interact with the Effector Loop of ras p21

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Transformation by FosB requires a trans-activation domain missing in FosB2 that can be substituted by heterologous activation domains.Preprint

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The Transactivating Domain of the c-Jun Proto-Oncoprotein Is Required for Cotransformation of Rat Embryo Cells

Alani, R. M., Brown, P. H., Binétruy, B., et al. (1991) · Molecular and Cellular Biology · doi:10.1128/mcb.11.12.6286-6295.1991 · Cited by 39 · see citing works

Signal transduction by the JNK group of MAP kinases

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MAP kinase signalling pathways in cancer

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AP-1 as a regulator of cell life and death

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AP-1 function and regulation

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AP-1: a double-edged sword in tumorigenesis

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AP-1 in cell proliferation and survival

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Hypoxia-inducible factor-1alpha is a positive factor in solid tumor growth.

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AP-1 in mouse development and tumorigenesis

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c‐Jun regulates cell cycle progression and apoptosis by distinct mechanisms

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β-Catenin Regulates the Expression of the Matrix Metalloproteinase-7 in Human Colorectal Cancer

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Transcription Factor HIF-1 Is a Necessary Mediator of the Pasteur Effect in Mammalian Cells

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Targeting JNK for therapeutic benefit: from junk to gold?

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Control of cell cycle progression by c-Jun is p53 dependentPreprint

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Oncoprotein Networks

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Ras Protein Farnesyltransferase: A Strategic Target for Anticancer Therapeutic Development

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Requirement of NF-κB Activation to Suppress p53-Independent Apoptosis Induced by Oncogenic Ras

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Diverse functions of JNK signaling and c-Jun in stress response and apoptosis

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c-Jun Can Recruit JNK to Phosphorylate Dimerization Partners via Specific Docking Interactions

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Liver Tumor Development

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A new group of conserved coactivators that increase the specificity of AP-1 transcription factors

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Withdrawal of Survival Factors Results in Activation of the JNK Pathway in Neuronal Cells Leading to Fas Ligand Induction and Cell Death

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Distinct roles of Jun : Fos and Jun : ATF dimers in oncogenesis

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Selective activation of NF-κB subunits in human breast cancer: potential roles for NF-κB2/p52 and for Bcl-3

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5′-AMP-Activated Protein Kinase (AMPK) Is Induced by Low-Oxygen and Glucose Deprivation Conditions Found in Solid-Tumor Microenvironments

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Rac Regulation of Transformation, Gene Expression, and Actin Organization by Multiple, PAK-Independent Pathways

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eIF3 targets cell-proliferation messenger RNAs for translational activation or repression

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The H3K27me3 demethylase JMJD3 contributes to the activation of the<i>INK4A–ARF</i>locus in response to oncogene- and stress-induced senescence

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AP-1 — The Jun proteins: Oncogenes or tumor suppressors in disguise?

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