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  • 1
    Keywords: RECEPTOR ; CELLS ; EXPRESSION ; IN-VITRO ; IRRADIATION ; proliferation ; SURVIVAL ; CELL ; COMBINATION ; IN-VIVO ; VIVO ; GENERATION ; PROTEIN ; PROTEINS ; transcription ; MICE ; ACTIVATION ; DNA ; TRANSCRIPTION FACTOR ; ANTIGEN ; T cell ; T cells ; T-CELL ; T-CELLS ; BINDING ; PHOSPHORYLATION ; CELL-SURVIVAL ; ELEMENT ; ELEMENT-BINDING PROTEIN ; knockout ; MUTANT ; NO ; TRANSCRIPTION FACTORS ; TRANSGENIC MICE ; PROMOTER ; transgenic ; RESPONSIVE ELEMENT ; T lymphocyte ; OVEREXPRESSION ; rodent ; T lymphocytes ; BINDING PROTEIN ; thymus ; BINDING-PROTEIN ; IL-2 PRODUCTION ; MOLECULAR-BASIS
    Abstract: Recent generation of genetically modified Creb1 mutant mice has revealed an important role for CREB (CAMP responsive element binding protein) and the related proteins CREM (CAMP responsive element modulator) and ATF1 (activating transcription factor 1) in cell survival, in agreement with previous studies using overexpression of dominant-negative CREB (dnCREB). CREB and ATF1 are abundantly expressed in T cells and are rapidly activated by phosphorylation when T cells are stimulated through the T cell antigen receptor. We show that T cell-specific loss of CREB in mice, in combination with the loss of ATF1, results in reduced thymic cellularity and delayed thymic recovery following sublethal irradiation but no changes in T cell development or activation. These data show that loss of CREB function has specific effects on thymic T lymphocyte proliferation and homeostasis in vivo
    Type of Publication: Journal article published
    PubMed ID: 15214044
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  • 2
    Keywords: RECEPTOR ; CELLS ; CELL ; Germany ; GENE ; PROTEIN ; PROTEINS ; TISSUE ; MICE ; TUMOR-NECROSIS-FACTOR ; DNA ; MACROPHAGES ; MECHANISM ; CONTRAST ; DENDRITIC CELLS ; KERATINOCYTES ; mechanisms ; SKIN ; T cell ; T cells ; T-CELL ; T-CELLS ; SUPPRESSION ; treatment ; cytokines ; TARGET ; MUTANT ; inactivation ; DNA-BINDING ; BETA ; MOUSE MODEL ; TARGETS ; side effects ; REPRESSION ; DIMERIZATION ; chemokine ; TNF-ALPHA ; NEUTROPHILS ; CYTOKINE ; molecular ; PERSISTENT ; RECOMBINANT ; INFILTRATION ; MOLECULAR-MECHANISM ; RE ; keratinocyte ; allergy ; IMMUNE SUPPRESSION ; chemokines ; INFLAMMATORY CYTOKINES ; MOLECULAR-MECHANISMS ; PHASE ; USA ; corticosteroids ; GLUCOCORTICOIDS ; RESISTANT ; SKIN INFLAMMATION ; CONTACT ; MEDICINE ; INFLAMMATORY RESPONSE ; EPIDERMAL LANGERHANS CELLS ; HYPERSENSITIVITY REACTIONS ; INFLAMMATORY PROTEIN-2
    Abstract: Glucocorticoids (GCs) are widely used in the treatment of allergic skin conditions despite having numerous side effects. Here we use Cre/loxP-engineered tissue- and cell-specific and function-selective GC receptor (GR) mutant mice to identify responsive cell types and molecular mechanisms underlying the and inflammatory activity of GCs in contact hypersensitivity (CHS). CHS was repressed by GCs only at the challenge phase, i.e., during reexposure to the hapten. Inactivation of the GR gene in keratinocytes or T cells of mutant mice did not attenuate the effects of GCs, but its ablation in macrophages and neutrophils abolished downregulation of the inflammatory response. Moreover, mice expressing a DNA binding-defective GR were also resistant to GC treatment. The persistent infiltration of macrophages and neutrophils in these mice is explained by an impaired repression of inflammatory cytokines and chemokines such as IL-1 beta, monocyte chemoattractant protein-1, macrophage inflammatory protein-2, and IFN-gamma-inducible protein 10. In contrast TNF-alpha repression remained intact. Consequently, injection of recombinant proteins of these cytokines and chemokines partially reversed suppression of CHS by GCs. These studies provide evidence that in contact allergy, therapeutic action of corticosteroids is in macrophages and neutrophils and that dimerization GR is required
    Type of Publication: Journal article published
    PubMed ID: 17446934
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  • 3
    Keywords: CELLS ; EXPRESSION ; CELL ; Germany ; human ; PROSTATE ; INFORMATION ; GENE ; HYBRIDIZATION ; microarray ; RNA ; SAMPLE ; SAMPLES ; transcription ; TISSUE ; MESSENGER-RNA ; QUALITY ; TISSUES ; CYCLE ; AMPLIFICATION ; NUMBER ; REPRODUCIBILITY ; PCR ; STRATEGIES ; REVERSE TRANSCRIPTION ; CDNA SYNTHESIS ; linear RNA amplification-,laser-assisted microdissection,small-amount RNA,reverse transcription,olig ; SINGLE-CELL
    Abstract: Microarray-based gene profiling of laser-assisted microdissected tissues or clinical biopsies is still a challenge since the amount of total RNA in such samples is limited and amplification of RNA is mandatory. Representative amplification of mRNA is highly dependent on the reverse transcription reaction, which is error prone, and on the number of amplification cycles. To improve the accuracy of RNA amplification, we optimized, combined, and tested different amplification strategies for Affymetrix oligonucleotide array hybridization. We demonstrate that different protocols differ significantly in quality of mRNA amplification. To demonstrate the accuracy and reproducibility of our optimized protocol in a clinical setting, we analyzed total RNAs from laser-assisted, microdissected cells of human prostate tissues. On the basis of these results, we recommend a standard reverse transcription reaction for small-sample-transcriptome profiling experiments as part of the Minimal Information about a Microarray Experiment (MIAME) set of standards. (C) 2003 Elsevier Inc. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 15028277
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  • 4
    Keywords: RECEPTOR ; APOPTOSIS ; CELLS ; EXPRESSION ; IN-VITRO ; SURVIVAL ; tumor ; Germany ; IN-VIVO ; INHIBITION ; PATHWAY ; PATHWAYS ; VITRO ; DEATH ; GENE ; MICE ; TRANSDUCTION ; COMPLEX ; COMPLEXES ; MECHANISM ; T-CELL ; T-CELLS ; BINDING ; signal transduction ; CD95 ligand ; CELL-DEATH ; PROMOTER ; MUTATION ; SIGNAL-TRANSDUCTION ; inactivation ; FACTOR-KAPPA-B ; glucocorticoid receptor ; GLUCOCORTICOID-RECEPTOR ; REPRESSION ; CROSS-TALK ; CD95 ; signaling ; molecular ; PROGRAM ; RE ; PH ; regulation ; RHEUMATOID-ARTHRITIS ; INFLAMMATORY RESPONSES ; cell death ; ABILITY ; APOPTOTIC CELLS ; FAS LIGAND ; NEGATIVE REGULATION ; THYMOCYTE DEVELOPMENT
    Abstract: Glucocorticoids (GCs) play an important role in the regulation of peripheral T-cell survival. Their molecular mechanism of action and the question of whether they have the ability to inhibit apoptosis in vivo, however, are not fully elucidated. Signal transduction through the glucocorticoid receptor (GR) is complex and involves different pathways. Therefore, we used mice with T-cell-specific inactivation of the GR as well as mice with a function-selective mutation in the GR to determine the signaling mechanism. Evidence is presented for a functional role of direct binding of the GR to 2 negative glucocorticoid regulatory elements (nGREs) in the CD95 (APO-1/Fas) ligand (L) promoter. Binding of GRs to these nGREs reduces activation-induced CD95L expression in T cells. These in vitro results are fully supported by data obtained in vivo. Administration of GCs to mice leads to inhibition of activation-induced cell death (AICD). Thus, GC-mediated inhibition of CD95L expression of activated T cells might contribute to the anti-inflammatory function of steroid drugs
    Type of Publication: Journal article published
    PubMed ID: 15802531
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