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  • CELL  (25)
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  • 1
    Keywords: gene expression ; BIOLOGY ; EXPRESSION ; CELL ; GENE ; GENE-EXPRESSION ; representational difference analysis ; analysis
    Type of Publication: Book chapter
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  • 2
    Keywords: CELLS ; EXPRESSION ; CELL ; Germany ; PATHWAY ; PATHWAYS ; ACETATE-NONUTILIZING MUTANTS ; CDNA ; CDNA CLONES ; CLONES ; CLONING ; CRASSA ; DISTINCT ; DNA-microarray analysis,transcriptional profiling,correspondence analysis,acetate metabolism,Neurosp ; ENZYMES ; FILAMENTOUS FUNGUS ; GENE ; GENE-EXPRESSION ; GENES ; GENOME ; GENOME SEQUENCE ; HYBRIDIZATION ; microarray ; NMT1 ; PROTEIN ; PROTEINS ; RNA ; SACCHAROMYCES-CEREVISIAE ; SAMPLE ; SAMPLES ; transcription
    Abstract: Nutrient-dependent variations in transcript levels of the filamentous fungus Neurospora crassa were studied on a microarray containing some 4700 cDNAs. Cells were grown in minimal and acetate medium. The isolated RNA was analyzed in comparison to the results obtained upon the hybridization of samples prepared from the RNA of cells grown in full medium. Altogether, 160 cDNA clones exhibited significant variations, falling into five distinct subgroups of very similar transcription profiles. This is indicative of the occurrence of a high degree of co-regulation of genes in N. crassa. Especially the regulation of the expression of proteins involved in metabolic pathways was found to be strongly regulated at the RNA level. (C) 2003 Elsevier Inc. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 14599890
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  • 3
    Keywords: ANGIOGENESIS ; CELLS ; ENDOTHELIAL-CELLS ; EXPRESSION ; IN-VITRO ; proliferation ; CELL ; Germany ; human ; MODEL ; VITRO ; DISEASE ; SITE ; SITES ; DISTINCT ; GENE ; GENE-EXPRESSION ; GENES ; microarray ; PROTEINS ; transcription ; SURGERY ; NF-KAPPA-B ; ACTIVATION ; RESPONSES ; DNA ; TRANSCRIPTION FACTOR ; INDUCTION ; KERATINOCYTES ; BINDING ; cell cycle ; CELL-CYCLE ; CYCLE ; treatment ; cytokines ; IDENTIFICATION ; PATTERNS ; gene expression ; microarrays ; PROMOTER ; UP-REGULATION ; NUMBER ; PROMOTERS ; STRESS ; DNA-REPAIR ; REPAIR ; EXTRACELLULAR-MATRIX ; BETA ; ADHESION ; HUMAN-PAPILLOMAVIRUS TYPE-16 ; NF-kappa B ; DNA repair ; inflammation ; CDNA MICROARRAY ; CYTOKINE ; MATRIX ; RE ; extracellular matrix ; endothelial cell ; endothelial cells ; INTERLEUKIN-1 ; GENE-TRANSCRIPTION ; INTEGRINS ; analysis ; PROFILES ; BINDING-SITE ; INTERCELLULAR-ADHESION ; ONSET ; CANDIDATE ; UNIT ; BINDING-SITES ; ENDOTHELIAL-CELL ; PROINFLAMMATORY CYTOKINES ; cDNA arrays ; CERVICAL KERATINOCYTES ; mRNA gene transcription ; nuclear factor kappa-B ; PERIODONTAL-DISEASES
    Abstract: Proinflammatory cytokines such as interleukin-1 beta are known to be synthesized in oral gingivitis and periodontitis and lead to the activation of the transcription factor nuclear factor-kappa B (NF-kappa B). Although numerous effects of interleukin-1 beta on mesenchymal cells are known, e.g. up-regulation of intercellular adhesion moelcule-1 in endothelial cells, little is known of the effects of interleukin-1 beta on oral keratinocytes. The purpose of the present study was to seek interleukin-1 beta-mediated alterations in mRNA gene transcription and a putative activation of NF-kappa B in oral gingival keratinocytes. As an in vitro model for gingivitis and periodontitis, immortalized human gingival keratinocytes (IHGK) were stimulated with the proinflammatory cytokine interleukin-1 beta. An epithelia-specific cDNA microarray was used to analyze mRNA expression profiles from IHGK cells treated with 200 units interleukin-1 beta/ml for 3, 6, 9, 12, and 24 h. Indirect immunofluorescence was carried out to detect NF-kappa B in IHGK following interleukin-1 beta treatment. Detailed analysis revealed distinct patterns of time-dependent changes, including genes induced or repressed early (3-6 h) or late (12-24 h) after interleukin-1 beta treatment. Differentially expressed genes were involved in (i) cell stress, (ii) DNA repair, (iii) cell cycle and proliferation, (iv) anti-pathogen response, (v) extracellular matrix turnover, and (vi) angiogenesis. A large number of genes were responsive to NF-kappa B and induction was concomitant with nuclear translocation of the p65 RelA subunit of NF-kappa B. Interestingly, many of these genes contain multiple NF-kappa B binding sites in their promoters. Analysis of altered gene expression allows identification of gene networks associated with inflammatory responses. In addition to a number of well-known genes involved in gingivitis and periodontitis, we identified novel candidates that might be associated with the onset and maintenance of an inflammatory disease
    Type of Publication: Journal article published
    PubMed ID: 16953820
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  • 4
    Keywords: CELL ; Germany ; VOLUME ; HYBRIDIZATION ; DNA ; BIOLOGY ; SEQUENCE ; SEQUENCES ; polymorphism ; POLYMORPHISMS ; single nucleotide polymorphism ; SPECTROSCOPY ; TARGET ; IDENTIFICATION ; ASSAY ; SNP ; MUTATIONS ; specificity ; FLUORESCENCE ; PERIPHERAL-BLOOD ; real-time PCR ; IMMUNODEFICIENCY-VIRUS TYPE-1 ; SINGLE ; RESIDUES ; INCREASE ; LEADS ; SINGLE NUCLEOTIDE POLYMORPHISMS ; SNPs ; MYCOBACTERIUM-TUBERCULOSIS ; single-nucleotide ; fluorescence spectroscopy ; technique ; BREAST-CANCER PATIENTS ; ELECTRON-TRANSFER ; single-molecule spectroscopy ; RESISTANT ; CONTACT ; INCREASES ; DNA hairpin probes ; MONONUCLEOTIDE MOLECULES
    Abstract: This article presents a new, highly sensitive method for the identification of single nucleotide polymorphisms (SNPs) in homogeneous solutions using fluorescently labeled hairpin-structured oligonucleotides (smart probes) and fluorescence single-molecule spectroscopy. While the hairpin probe is closed, fluorescence intensity is quenched due to close contact between the chromophore and several guanosine residues. Upon hybridization to the respective target SNP sequence, contact is lost and the fluorescence intensity increases significantly. High specificity is achieved by blocking sequences containing mismatch with unlabeled oligonucleotides. Time-resolved single-molecule fluorescence spectroscopy enables the detection of individual smart probes passing a small detection volume. This method leads to a subnanomolar sensitivity for this single nucleotide specific DNA assay technique. (c) 2007 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 17399707
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  • 5
    Keywords: CANCER ; CELLS ; EXPRESSION ; tumor ; TUMOR-CELLS ; carcinoma ; CELL ; Germany ; neoplasms ; DIAGNOSIS ; NEW-YORK ; microarray ; transcription ; TISSUE ; DNA ; MICROARRAY DATA ; MUTATIONS ; Jun ; PHENOTYPE ; vimentin ; HEAD ; adenocarcinoma ; pathology ; BEHAVIOR ; MICROARRAY ANALYSIS ; expression profiling ; TUMOR CELLS ; DIFFERENTIAL-DIAGNOSIS ; CELL CARCINOMA ; OF-THE-LITERATURE ; pancreas ; review ; DUCTAL ADENOCARCINOMA ; AUTOPSY ; analysis ; pancreatic ; TUMOR-CELL ; GENOTYPE ; DNA-MICROARRAY ; USA ; pancreatic ductal adenocarcinoma ; MYOEPITHELIAL CARCINOMA ; pancreatic neoplasm ; PSEUDOPAPILLARY TUMORS
    Abstract: Pancreatic neoplasms have been reliably classified on the basis of their histopathology and immunophenotype. In this study, we report on a pancreatic tumor whose phenotype and genotype could not be assigned to any known tumor entity. The tumor was observed in the pancreatic head of a 54-year-old woman. It was found to be a solid infiltrating carcinoma with abundant clear cells. Apart from cytokeratin, the tumor cells expressed vimentin, S100, and MUC-1. DNA microarray analysis revealed a transcription profile clearly differing from that of normal pancreatic tissue and pancreatic ductal adenocarcinoma. Despite metastatic behavior, the tumor displayed a more favorable course than conventional pancreatic ductal adenocarcinoma. We suggest that this tumor be called solid type clear cell carcinoma of the pancreas
    Type of Publication: Journal article published
    PubMed ID: 17453235
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  • 6
    Keywords: CELLS ; EXPRESSION ; CELL ; GENE ; GENE-EXPRESSION ; SACCHAROMYCES-CEREVISIAE ; METABOLISM ; MECHANISM ; REDUCTION ; mechanisms ; BIOLOGY ; PHOSPHORYLATION ; SIGNAL ; ALPHA ; gene expression ; heat shock ; NUMBER ; STRESS ; MAMMALIAN-CELLS ; INCREASE ; mRNA ; LEVEL ; ENGLAND ; PROCESSING BODIES ; TRANSLATION INITIATION ; STRESS GRANULES ; P-BODIES ; TURNOVER ; AFRICAN TRYPANOSOME ; UNTRANSLATED REGION ; CYTOPLASMIC FOCI ; CELL BIOLOGY ; POSITION ; trypanosome ; Trypanosoma brucei ; BLOOD-STREAM ; eIF2 alpha ; LEISHMANIA-MAJOR ; MESSENGER-RNA DEGRADATION ; SPLICED-LEADER RNA ; stress granule
    Abstract: In trypanosomes there is an almost total reliance on post-transcriptional mechanisms to alter gene expression; here, heat shock was used to investigate the response to an environmental signal. Heat shock rapidly and reversibly induced a decrease in polysome abundance, and the consequent changes in mRNA metabolism were studied. Both heat shock and polysome dissociation were necessary for (1) a reduction in mRNA levels that was more rapid than normal turnover, (2) an increased number of P-body-like granules that contained DHH1, SCD6 and XRNA, (3) the formation of stress granules that remained largely separate from the P-body-like granules and localise to the periphery of the cell and, (4) an increase in the size of a novel focus located at the posterior pole of the cell that contain XRNA, but neither DHH1 nor SCD6. The response differed from mammalian cells in that neither the decrease in polysomes nor stress-granule formation required phosphorylation of eIF2 alpha at the position homologous to that of serine 51 in mammalian eIF2 alpha and in the occurrence of a novel XRNA-focus
    Type of Publication: Journal article published
    PubMed ID: 18713834
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  • 7
    Keywords: CANCER ; tumor ; CELL ; Germany ; human ; SYSTEM ; SYSTEMS ; DISEASE ; liver ; PROTEIN ; PROTEINS ; SAMPLE ; SAMPLES ; MOLECULES ; TISSUE ; TISSUES ; BIOLOGY ; MOLECULE ; IDENTIFICATION ; MEMBRANE ; INSTABILITY ; ELECTROPHORESIS ; pancreatic cancer ; SECTIONS ; molecular biology ; pancreas ; PANCREATIC-CANCER ; EXTRACTION ; SEPARATION ; USA ; protein fractionation ; CELL-CELL ; EFFECTOR MOLECULE ; ISLETS ; protein extraction
    Abstract: Proteins are the major class of effector molecules in cellular systems. For the identification of functional differences between normal and diseased tissues, a reliable analysis of their protein content is essential. Reproducible isolation and fractionation of intact proteins are important in this respect, but their complexity in structure and concentration, their close interaction, and their instability represent major challenges. For protein isolation in tissues, the breakdown of cell-cell and cell-matrix connections within a tissue without affecting protein quality is a critical factor. We compared different processes for a compartmental protein preparation from pancreatic tissue, one of the most challenging tissues for protein isolation because of its high protease content. Success of the different procedures varied greatly. Based on a scheme of tissue-slicing and subsequent cell isolation, we established a reliable workflow for the fractional extraction of cytosolic proteins, membrane and organelle proteins, nuclear proteins, and cytoskeletal filaments. The tissue slices also allow for a representative confirmation of individual samples' cellular status by histochemical processes, and a proper separation or mixing of cellular material from across a tumor if required
    Type of Publication: Journal article published
    PubMed ID: 19450236
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  • 8
    Keywords: CANCER ; EXPRESSION ; CELL ; Germany ; GENOME ; microarray ; PROTEIN ; PROTEINS ; PATIENT ; COMPLEX ; COMPLEXES ; QUALITY ; BIOLOGY ; antibodies ; antibody ; ASSAY ; microarrays ; DESIGN ; ARRAYS ; REPRODUCIBILITY ; CANCER-PATIENTS ; CANCER PATIENTS ; pancreatic cancer ; PROTEOMICS ; PROTEOMIC ANALYSIS ; SERUM ; FEATURES ; PANCREATIC-CANCER ; antibody microarray ; HEALTHY-SUBJECTS ; methods ; HUMAN PLASMA ; DEPLETION ; QUANTITATIVE PROTEOMICS ; proteomic ; ABUNDANCE PROTEINS ; BIOMARKER DISCOVERY
    Abstract: Antibody microarrays have the potential to enable comprehensive proteomic analysis of small amounts of sample material. Here, protocols are presented for the production, quality assessment, and reproducible application of antibody microarrays in a two-color mode with an array of 1,800 features, representing 810 antibodies that were directed at 741 cancer-related proteins. In addition to measures of array quality, we implemented indicators for the accuracy and significance of dual-color detection. Dual-color measurements outperform a single-color approach concerning assay reproducibility and discriminative power. In the analysis of serum samples, depletion of high-abundance proteins did not improve technical assay quality. On the contrary, depletion introduced a strong bias in protein representation. In an initial study, we demonstrated the applicability of the protocols to proteins derived from urine samples. We identified differences between urine samples from pancreatic cancer patients and healthy subjects and between sexes. This study demonstrates that biomedically relevant data can be produced. As demonstrated by the thorough quality analysis, the dual-color antibody array approach proved to be competitive with other proteomic techniques and comparable in performance to transcriptional microarray analyses.
    Type of Publication: Journal article published
    PubMed ID: 20164060
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  • 9
    Keywords: CANCER ; CELLS ; EXPRESSION ; tumor ; TUMOR-CELLS ; carcinoma ; CELL ; Germany ; MODEL ; INFORMATION ; SYSTEM ; SYSTEMS ; EXPOSURE ; SITE ; SITES ; GENE ; GENES ; GENOME ; transcription ; DRUG ; TUMORS ; LINES ; DNA ; BIOLOGY ; CELL-LINES ; BREAST ; PROGRESSION ; resistance ; CARCINOMA CELLS ; TUMOR PROGRESSION ; CELL-LINE ; chemotherapy ; LINE ; DNA methylation ; CANCER-CELLS ; BREAST-CARCINOMA ; FREQUENT ; drug resistance ; DRUG-RESISTANCE ; METHYLATION ; SCIENCE ; development ; PROGNOSTIC MARKER ; PROFILES ; breast carcinoma ; DRUGS ; TOPOISOMERASE-II-ALPHA ; CANCERS ; epigenetic regulation ; Type ; CONTRIBUTE ; ANTHRACYCLINES ; MCJ GENE ; MDR1 PROMOTER
    Abstract: Acquired drug resistance represents a frequent obstacle which hampers efficient chemotherapy of cancers. The contribution of aberrant DNA methylation to the development of drug resistant tumor cells has gained increasing attention over the past decades. Hence, the objective of the presented study was to characterize DNA methylation changes which arise from treatment of tumor cells with the chemotherapeutic drug doxorubicin. DNA methylation levels from CpG islands (CGIs) linked to twenty-eight genes, whose expression levels had previously been shown to contribute to resistance against DNA double strand break inducing drugs or tumor progression in different cancer types were analyzed. High-definition DNA methylation profiles which consisted of methylation levels from 800 CpG sites mapping to CGIs around the transcription start sites of the selected genes were determined. In order to investigate the influence of CGI methylation on the expression of associated genes, their mRNA levels were investigated via qRT-PCR. It was shown that the employed method is suitable for providing highly accurate methylation profiles, comparable to those obtained via clone sequencing, the gold standard for high-definition DNA methylation studies. In breast carcinoma cells with acquired resistance against the double strand break inducing drug doxorubicin, changes in methylation of specific cytosines from CGIs linked to thirteen genes were detected. Moreover, similarities between methylation profiles obtained from breast and ovarian carcinoma cell lines with acquired doxorubicin resistance were found. The expression levels of a subset of analyzed genes were shown to be linked to the methylation levels of the analyzed CGIs. Our results provide detailed DNA methylation information from two separate model systems for acquired doxorubicin resistance and suggest the occurrence of similar methylation changes in both systems upon exposure to the drug
    Type of Publication: Journal article published
    PubMed ID: 20544021
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  • 10
    Keywords: CANCER ; CELLS ; EXPRESSION ; proliferation ; CELL ; PROTEIN ; TUMORS ; DNA ; MECHANISM ; MESSENGER-RNA ; breast cancer ; BREAST-CANCER ; METASTASIS ; TARGETS ; METHYLATION ; TRANSCRIPTIONAL REPRESSOR ; SIGNATURE ; CTCF
    Abstract: Estrogen receptor alpha (ER alpha) upregulation causes abnormal cell proliferation in about two thirds of breast cancers, yet understanding of the underlying mechanisms remains incomplete. Here, we show that high expression of the microRNA miR-375 in ER alpha-positive breast cell lines is a key driver of their proliferation. miR-375 overexpression was caused by loss of epigenetic marks including H3K9me2 and local DNA hypo-methylation, dissociation of the transcriptional repressor CTCF from the miR-375 promoter, and interactions of ER alpha with regulatory regions of miR-375. Inhibiting miR-375 in ER alpha-positive MCF-7 cells resulted in reduced ERa activation and cell proliferation. A combination of expression profiling from tumor samples and miRNA target prediction identified RASD1 as a potential miR-375 target. Mechanistic investigations revealed that miR-375 regulates RASD1 by targeting the 3' untranslated region in RASD1 mRNA. Additionally, we found that RASD1 negatively regulates ER alpha expression. Our findings define a forward feedback pathway in control of ER alpha expression, highlighting new strategies to treat ER alpha-positive invasive breast tumors.
    Type of Publication: Journal article published
    PubMed ID: 20978187
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