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  • AP-1  (8)
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  • 1
    Keywords: CELL ; Germany ; APOPTOSIS ; CELLS ; GROWTH ; PATHWAY ; PATHWAYS ; AP-1 ; ACTIVATION ; TIME ; MICE ; EFFICIENCY ; TOOL ; NEW-YORK ; INDUCTION ; T cells ; T-CELL ; T-CELLS ; T cell ; treatment ; SIGNAL ; c-Fos ; EAST ; c-Fos,apoptosis,early activation,induction,T cells ; GENOTYPES ; SIGNALING PATHWAY ; STIMULI ; WILD-TYPE ; SIGNALING PATHWAYS
    Abstract: We used c-Fos-deficient activated T cells from the spleen and c-Fos-deficient thymocytes to address the capacity of these cells to undergo apoptosis in response to various stimuli. To determine the role of c-Fos in apoptosis regulation in thymocytes, we challenged thymocytes from wild-type and c-Fos-deficient mice with either TPA or the glucocorticoid dexamethasone. After various time points cells were stained according to the Nicoletti method and analyzed by FACS. Thymocytes from both genotypes exhibited similar efficiency of apoptosis in response to treatment with TPA or dexamethasone. Our data provide clear evidence that c-Fos is not required for apoptosis regulation in activated T cells as well as in thymocytes
    Type of Publication: Book chapter
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  • 2
    Keywords: APOPTOSIS ; CELLS ; EXPRESSION ; Germany ; human ; SYSTEM ; DEATH ; SITE ; GENE ; GENE-EXPRESSION ; DRUG ; TISSUE ; NF-KAPPA-B ; LIGAND ; AP-1 ; primary ; INDUCTION ; T cells ; T-CELLS ; BINDING ; C-JUN ; SEQUENCE ; TRANSCRIPTION FACTORS ; ASSAY ; activation-induced cell death ; c-Fos ; CARCINOMA CELLS ; CD95 ligand ; CELL-DEATH ; CYCLOSPORINE-A ; FAS-LIGAND EXPRESSION ; INDUCED APOPTOSIS ; MOBILITY ; PROMOTER ; UP-REGULATION
    Abstract: The CD95 (APO-1/Fas) system plays a major role in induction of apoptosis in lymphoid and nonlymphoid tissues. The CD95 (APO- 1/Fas) ligand (CD95L) is induced in response to a variety of signals including TCR/CD3 stimulation or application of chemotherapeutic drugs. Here we report that an AP-1 site located in the 5' untranslated region of the CD95L gene is required for TCR/CD3-mediated induction of the human CD95L promoter. Electrophoretic mobility shift assays using nuclear extracts of Jurkat T cells as well as TCR/CD3-restimulated primary human T cells demonstrated specific binding of AP-1, predominantly composed of c-Jun and FosB, to this sequence. Ectopic expression of transdominant negative Jun mutants strongly reduced CD95L promoter activity and activation-induced cell death (AICD), confirming the functional significance of FosB/c-Jun binding. Thus, our results demonstrate an important novel function for FosB dimerized with c-Jun in TCR/CD3- mediated AICD in human T cells
    Type of Publication: Journal article published
    PubMed ID: 12618758
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  • 3
    Keywords: CANCER ; CELLS ; EXPRESSION ; GROWTH ; carcinoma ; GENE ; GENE-EXPRESSION ; GENES ; microarray ; PROTEIN ; SAMPLE ; SAMPLES ; murine ; AP-1 ; CARCINOGENESIS ; tumour ; SKIN ; MOUSE ; TRANSCRIPTION FACTORS ; IDENTIFICATION ; PROGRESSION ; gene expression ; PROMOTERS ; skin carcinogenesis ; METASTASIS ; SSH ; PCR ; TRANSFORMATION ; EPITHELIAL-CELLS ; squamous cell carcinoma ; FRAGMENTS ; MULTISTAGE CARCINOGENESIS ; real-time PCR ; expression profiling ; PHORBOL ESTER ; CDNA MICROARRAY ; NMRI MOUSE SKIN ; tumour promoter
    Abstract: Malignant transformation of mouse skin by chemical carcinogens and tumour promoters, such as the phorbol ester 12-O- tetradecanoylphorbol-13-acetate (TPA), is a multi-stage process that leads to squamous cell carcinoma (SCC) formation. In an effort to identify turnour-associated genes, we studied the influence of short-term TPA-treatment on the gene expression profile of murine skin. A comprehensive microarray with some 5,000 murine gene specific cDNA fragments was established and hybridised with pooled RNA derived from control and TPA-treated dorsal skin samples. Of these genes, 54 were up- and 35 were down-regulated upon TPA application. Additionally, we performed suppression subtractive hybridisation (SSH) with respective RNA pools to generate and analyse a cDNA library enriched for TPA- inducible genes. Expression data of selected genes were confirmed by quantitative real-time PCR and Northern blot analysis. Comparison of microarray and SSH data revealed that 26% of up-regulated genes identified by expression profiling matched with those present in the SSH library. Besides numerous known genes, we identified a large set of unknown cDNAs that represent previously unrecognised TPA-regulated genes in murine skin with potential function in tumour promotion. Additionally, some TPA-induced genes, such as SprrIA, Saa3, junB, II4ralpha, Gp38, RalGDS and Slpi exhibit high basal level in advanced stages of skin carcinogenesis, suggesting that at least a subgroup of the identified TPA-regulated genes may contribute to tumour progression and metastasis. (C) 2003 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 12640676
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  • 4
    Keywords: CANCER ; CELLS ; EXPRESSION ; GROWTH ; IN-VITRO ; INHIBITOR ; tumor ; carcinoma ; Germany ; IN-VIVO ; VITRO ; GENE ; PROTEIN ; TUMORS ; MICE ; PATIENT ; FAMILY ; AP-1 ; CARCINOGENESIS ; INDUCTION ; KERATINOCYTES ; SKIN ; BINDING ; fibroblasts ; MOUSE ; c-Fos ; PROMOTER ; MOUSE SKIN ; TRANSFORMATION ; BENIGN ; CARCINOMAS ; squamous cell carcinoma ; GLUCOCORTICOID-RECEPTOR ; SKIN-CANCER ; BINDING PROTEIN ; keratinocyte ; TRANSITION ; MALIGNANT PROGRESSION ; INTERSTITIAL COLLAGENASE ; CELL-CARCINOMA ; dexamethasone ; MOUSE KERATINOCYTES ; RECYCLING ENDOSOMES
    Abstract: Malignant transformation of mouse skin by tumor promoters and chemical carcinogens, such as the phorhol ester 12-O-tetradecanoylphorbol-13-acetate (TPA), is a multistage process leading to the formation of squamous cell carcinomas. it has been shown that mice lacking the AP-1 family member c-Fos exhibit an impaired transition from benign to malignant skin tumors. Here, we demonstrate enhanced expression of the small Ras-related GTPase Rab11a after short-term TPA treatment of mouse back skin. Expression of Rab11a in vivo and in vitro critically depended on c-Fos, because TPA application to the back skin of c-Fos-deficient mice and to mouse embryonic fibroblasts did not induce Rab11a mRNA or protein expression. Moreover, dexamethasone, which is a potent inhibitor of AP-1-mediated transactivation that exhibits anti-inflammatory and antitumor promoting activities, inhibited TPA-induced expression of Rab11a. Within the Rab11a gene promoter, we identified a functional AP-1 binding element that exhibited elevated c-Fos binding activity after TPA treatment of keratinocytes. Enhanced expression was not restricted to chemically induced mouse skin tumors but was also found in tumor specimens derived from patients with epithelial skin tumors. These data identify Rab11a as a novel, tumor-associated c-Fos/AP-1 target and may point to an as yet unrecognized function of Rab11a in the development of skin cancer
    Type of Publication: Journal article published
    PubMed ID: 15972968
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  • 5
    Keywords: CELLS ; EXPRESSION ; GROWTH ; IN-VITRO ; proliferation ; CELL ; Germany ; VITRO ; transcription ; TISSUE ; LINES ; MICE ; FAMILY ; TRANSCRIPTION FACTOR ; AP-1 ; TISSUES ; cell cycle ; CELL-CYCLE ; CYCLE ; MEMBER ; SIGNAL ; bone marrow ; BONE-MARROW ; TRANSGENIC MICE ; c-Fos ; NUMBER ; transgenic ; LINE ; MUTANT MICE ; ACTIVATING TRANSCRIPTION FACTOR-2 ; AP-1,bone,chondrocytes,cell cycle,osteoblasts,osteoporosis ; BONE-FORMATION ; EMBRYONIC LETHALITY ; GROWTH-PLATE CHONDROCYTES ; HERITABLE DISEASES ; LINEAGE DETERMINATION ; MOLECULAR INSIGHTS ; NATRIURETIC PEPTIDE ; OSTEOBLAST-LIKE CELLS ; OSTEOPOROSIS ; REGULATOR ; REGULATORS ; SKELETAL DEVELOPMENT
    Abstract: Functional analysis in mice has established an absolute requirement of JunB, a member of the AP-1 transcription factor family, during early embryonic development. To investigate the role of JunB during mid and late gestation and postnatally Ubi-junB transgenic mice were used to generate two junB(-/-) Ubi-junB mutant lines, in which embryonic lethality was rescued but strongly reduced JunB; expression in several adult tissues was observed. Mutant mice from both rescue lines were growth retarded and shared significantly reduced longitudinal bone growth. Mutant long bones were characterised by reduced numbers of growth plate chondrocytes and a severe osteoporosis. Decreased JunB levels in epiphysal growth plate chondrocytes and bone lining osteoblasts correlated with deregulated expression of Cyclin A, Cyclin D1 and p16(INK4a), key regulators of cell cycle control. Furthermore, junB(-/-) Ubi-junB bone marrow stromal cells were unable to differentiate into bone forming osteoblasts in vitro. Our data demonstrate that JunB plays a crucial role in endochondral ossification by regulating proliferation and function of chondrocytes and osteoblasts
    Type of Publication: Journal article published
    PubMed ID: 14576352
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  • 6
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    Journal of Cell Science 117 (25), 5965-5973 
    Keywords: AP-1 ; SUBUNIT ; SUBUNITS
    Type of Publication: Journal article published
    PubMed ID: 15564374
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  • 7
    Keywords: CANCER ; CELLS ; EXPRESSION ; tumor ; TUMOR-CELLS ; CELL ; Germany ; human ; GENE-EXPRESSION ; PROTEIN ; PROTEINS ; NF-KAPPA-B ; TUMOR-NECROSIS-FACTOR ; AP-1 ; CARCINOGENESIS ; COMPARATIVE GENOMIC HYBRIDIZATION ; SQUAMOUS-CELL CARCINOMA ; GLYCATION END-PRODUCTS ; RAGE ; NF-kappa B ; TUMOR CELLS ; inflammation ; CALCIUM-BINDING PROTEINS ; CALCIUM-BINDING PROTEIN ; HUMAN CANCER ; LEVEL ; TUMOR-CELL ; MICROVASCULAR ENDOTHELIAL-CELLS ; chronic inflammation ; CALCIUM-BINDING ; function ; S100 ; HUMAN CANCERS ; CANCERS ; MALIGNANCY-ASSOCIATED REGIONS ; TRANSENDOTHELIAL MIGRATION
    Abstract: Calprotectin (S100A8/A9), a heterodimer of the two calcium-binding proteins S100A8 and S100A9, was originally discovered as immunogenic protein expressed and secreted by neutrophils. Subsequently, it has emerged as important pro-inflammatory mediator in acute and chronic inflammation. More recently, increased S100A8 and S100A9 levels were also detected in various human cancers, presenting abundant expression in neoplastic tumor cells as well as infiltrating immune cells. Although, many possible functions have been proposed for S100A8/A9, its biological role still remains to be defined. Altogether, its expression and potential cytokine-like function in inflammation and in cancer suggests that S100A8/A9 may play a key role in inflammation-associated cancer. (c) 2006 Elsevier Inc. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 16846592
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  • 8
    Keywords: CANCER ; GENES ; transcription ; AP-1 ; PROGRESSION ; Jun ; PTEN ; GLIOMA ; FOS ; PROMOTER METHYLATION ; PODOPLANIN ; INTEGRATED GENOMIC ANALYSIS ; HUMAN GLIOBLASTOMA
    Abstract: Recently, we found strong overexpression of the mucin-type glycoprotein podoplanin (PDPN) in human astrocytic brain tumors, specifically in primary glioblastoma multiforme (GB). In the current study, we show an inverse correlation between PDPN expression and PTEN levels in primary human GB and glioma cell lines, and we report elevated PDPN protein levels in the subventricular zone of brain tissue sections of PTEN-deficient mice. In human glioma cells lacking functional PTEN, reintroduction of wild-type PTEN, inhibition of the PTEN downstream target protein kinase B/AKT, or interference with transcription factor AP-1 function resulted in efficient downregulation of PDPN expression. In addition, we observed hypoxia-dependent PDPN transcriptional control and demonstrated that PDPN expression is subject to negative transcriptional regulation by promoter methylation in human GB and in glioma cell lines. Treatment of PTEN-negative glioma cells with demethylating agents induced expression of PDPN. Together, our findings show that increased PDPN expression in human GB is caused by loss of PTEN function and activation of the PI3K-AKT-AP-1 signaling pathway, accompanied by epigenetic regulation of PDPN promoter activity. Silencing of PDPN expression leads to reduced proliferation and migration of glioma cells, suggesting a functional role of PDPN in glioma progression and malignancy. Thus, specific targeting of PDPN expression and/or function could be a promising strategy for the treatment of patients with primary GB
    Type of Publication: Journal article published
    PubMed ID: 22394497
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