AP-1 as a regulator of cell life and death

WAF1, a potential mediator of p53 tumor suppression

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The role of Jun, Fos and the AP-1 complex in cell-proliferation and transformation

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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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AP-1 function and regulation

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The Regulation of AP-1 Activity by Mitogen-activated Protein Kinases

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Dissection of TNF Receptor 1 Effector Functions: JNK Activation Is Not Linked to Apoptosis While NF-κB Activation Prevents Cell Death

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Identification of an oncoprotein- and UV-responsive protein kinase that binds and potentiates the c-Jun activation domain.

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Requirement for ceramide-initiated SAPK/JNK signalling in stress-induced apoptosis

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AP-1 in cell proliferation and survival

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Requirement of JNK for Stress- Induced Activation of the Cytochrome c-Mediated Death Pathway

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Transcription Factor ATF2 Regulation by the JNK Signal Transduction Pathway

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Absence of excitotoxicity-induced apoptosis in the hippocampus of mice lacking the Jnk3 gene

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The Jnk1 and Jnk2 Protein Kinases Are Required for Regional Specific Apoptosis during Early Brain Development

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Altered gene expression in neurons during programmed cell death: identification of c-jun as necessary for neuronal apoptosis.

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A c-jun dominant negative mutant protects sympathetic neurons against programmed cell death

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Continuous c-fos expression precedes programmed cell death in vivo

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Activation of the transcription factor MEF2C by the MAP kinase p38 in inflammation

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AP-1 in mouse development and tumorigenesis

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Induction of gadd45β by NF-κB downregulates pro-apoptotic JNK signalling

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Wild-Type Human p53 and a Temperature-Sensitive Mutant Induce Fas/APO-1 Expression

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Inhibition of JNK activation through NF-κB target genes

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Tumor surveillance via the ARF–p53 pathwayPreprint

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Close encounters of many kinds: Fos-Jun interactions that mediate transcription regulatory specificity

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Jun-B differs in its biological properties from, and is a negative regulator of, c-Jun

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

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Amino-terminal phosphorylation of c-Jun regulates stress-induced apoptosis and cellular proliferation

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Rapid and Preferential Activation of the c- jun Gene during the Mammalian UV Response

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Menin Interacts with the AP1 Transcription Factor JunD and Represses JunD-Activated Transcription

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c-fos protein can induce cellular transformation: A novel mechanism of activation of a cellular oncogene

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BMK1/ERK5 regulates serum‐induced early gene expression through transcription factor MEF2C

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Requirement for fos gene expression in the transcriptional activation of collagenase by other oncogenes and phorbol esters

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

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Dominant-Negative c-Jun Promotes Neuronal Survival by Reducing BIM Expression and Inhibiting Mitochondrial Cytochrome c Release

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c-Jun is essential for normal mouse development and hepatogenesis

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

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Induction of c‐fos expression through JNK‐mediated TCF/Elk‐1 phosphorylation.

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Pin1 is overexpressed in breast cancer and cooperates with Ras signaling in increasing the transcriptional activity of c‐Jun towards cyclin D1

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jun-B inhibits and c-fos stimulates the transforming and trans-activating activities of c-jun

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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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Activation of SAPK/JNK by TNF Receptor 1 Through a Noncytotoxic TRAF2-Dependent Pathway

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Avian sarcoma virus 17 carries the jun oncogene.

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The jun and fos protein families are both required for cell cycle progression in fibroblasts.

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Complete nucleotide sequence of a human c-onc gene: deduced amino acid sequence of the human c-fos protein.

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Induction of apoptosis by the transcription factor c‐Jun

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c-Jun and JunB Antagonistically Control Cytokine-Regulated Mesenchymal–Epidermal Interaction in Skin

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Cell cycle‐dependent variations in c‐Jun and JunB phosphorylation: a role in the control of cyclin D1 expression

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Expression and involvement of c-fos and c-jun protooncogenes in programmed cell death induced by growth factor deprivation in lymphoid cell lines.

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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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Transgenic mice demonstrate AP-1 (activator protein-1) transactivation is required for tumor promotion

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The absence of c-fos prevents light-induced apoptotic cell death of photoreceptors in retinal degeneration in vivo

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Cascade Induction of c-fos, c-myc, and Heat Shock 70K Transcripts during Regression of the Rat Ventral Prostate Gland

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c-fos is required for malignant progression of skin tumors

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JunB suppresses cell proliferation by transcriptional activation of p16INK4a expression

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Deregulated c-fos expression interferes with normal bone development in transgenic mice

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Lasting N-Terminal Phosphorylation of c-Jun and Activation of c-Jun N-Terminal Kinases after Neuronal Injury

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Mitogen-Activated Protein Kinase Cascades as Regulators of Stress Responses

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Stress-signalling kinase Sek1 protects thymocytes from apoptosis mediated by CD95 and CD3

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Mouse JunD negatively regulates fibroblast growth and antagonizes transformation by ras

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The Mammalian UV Response

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Cellular Transformation and Malignancy Induced by ras Require c-jun

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Functions of c-Jun in Liver and Heart Development

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JunD Protects Cells from p53-Dependent Senescence and Apoptosis

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JunB is essential for mammalian placentation

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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.

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Fos Family Members Induce Cell Cycle Entry by Activating Cyclin D1

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Cooperation between STAT3 and c-Jun Suppresses Fas Transcription

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Role of DNA 5-Methylcytosine Transferase in Cell Transformation by fos

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Chronic Myeloid Leukemia with Increased Granulocyte Progenitors in Mice Lacking JunB Expression in the Myeloid Lineage

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Peripheral Axotomy Induces Long-Term c-Jun Amino-Terminal Kinase-1 Activation and Activator Protein-1 Binding Activity by c-Jun and junD in Adult Rat Dorsal Root GangliaIn Vivo

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Induction of Apoptosis by c-Fos Protein

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Transformation by ras modifies AP1 composition and activity

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Oncogenic transformation by ras and fos is mediated by c-Jun N-terminal phosphorylation

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Protein kinase A and AP-1 (c-Fos/JunD) are induced during apoptosis of mouse mammary epithelial cells.

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c-fos expression induces bone tumors in transgenic mice.

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Serum‐regulated transcription by serum response factor (SRF): a novel role for the DNA binding domain.

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JunB can substitute for Jun in mouse development and cell proliferation

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c-Jun-Dependent CD95-L Expression Is a Rate-Limiting Step in the Induction of Apoptosis by Alkylating Agents

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Targeted disruption of the murine junD gene results in multiple defects in male reproductive function

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p21-induced cycle arrest in G1 protects cells from apoptosis induced by UV-irradiation or RNA polymerase II blockage

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Regulation of Fra-1 and Fra-2 phosphorylation differs during the cell cycle of fibroblasts and phosphorylation in vitro by MAP kinase affects DNA binding activity.

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Autocrine growth and anchorage independence: two complementing Jun-controlled genetic programs of cellular transformationPreprint

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Dynamic regulation of c-Jun N-terminal kinase activity in mouse brain by environmental stimuli

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p53-mediated protective responses to UV irradiation

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Bcl-3 Expression Promotes Cell Survival following Interleukin-4 Deprivation and Is Controlled by AP1 and AP1-Like Transcription Factors

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c-Jun interacts with the corepressor TG-interacting factor (TGIF) to suppress Smad2 transcriptional activity

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Heparin-binding epidermal growth factor-like growth factor, a v-Jun target gene, induces oncogenic transformation

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Reactivation of proliferin gene expression is associated with increased angiogenesis in a cell culture model of fibrosarcoma tumor progression

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Cell proliferation and cell cycle progression are not impaired in fibroblasts and ES cells lacking c-Fos.

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