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  • 1
    Keywords: antibodies, antibody, ARRAY, ARRAYS, AUTOANTIBODIES, autoantibody, AUTOIMMUNE-DISEASES, automation,
    Abstract: The mouse is the premier genetic model organism for the study of disease and development. We describe the establishment of a mouse T helper cell type 1 (T-H 1) protein expression library that provides direct access to thousands of recombinant mouse proteins, in particular those associated with immune responses. The advantage of a system based on the combination of large cDNA expression libraries with microarray technology is the direct connection of the DNA sequence information from a particular clone to its recombinant, expressed protein. We have generated a mouse T-H 1 expression cDNA library and used protein arrays of this library to characterize the specificity and cross-reactivity of antibodies. Additionally, we have profiled the autoantibody repertoire in serum of a mouse model for systemic lupus erythematosus on these protein arrays and validated the putative autoantigens on highly sensitive protein microarrays. (c) 2004 Elsevier Inc. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 15718096
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  • 2
    Keywords: APOPTOSIS ; CELLS ; EXPRESSION ; SITE ; SITES ; GENE ; transcription ; TISSUE ; COMPLEX ; COMPLEXES ; CARCINOGENESIS ; cell cycle ; CELL-CYCLE ; CYCLE ; SEQUENCE ; SEQUENCES ; MOUSE ; IDENTIFICATION ; PROMOTER ; COLORECTAL-CANCER ; TUMOR-SUPPRESSOR GENE ; MUTATIONS ; METHYLATION ; HYPERMETHYLATION ; TRANSCRIPTIONAL REGULATION ; TRANSCRIPTS ; TRANSFECTION ; regulation ; AID ; transcript ; 5 '-RACE ; adenomatous polyposis coli ; APC ; APC GENE ; CHROMOSOME-5Q21 ; TATA-LESS PROMOTERS ; totipotent stem cells ; untranslated exon
    Abstract: The product of the oncosuppressor adenomatous polyposis coli (APC) gene is involved in cell cycle arrest and apoptosis and its loss of function is associated with the development of colorectal carcinogenesis. Its transcriptional regulation seems rather complex and has not been completely elucidated up to now. In an attempt to identify the transcription start sites for the mouse Ape gene we have detected a novel transcript in mouse embryonic stem (ES) cells and colon tissue. This transcript contains an untranslated exon, whose flanking sequences exhibited strong promoter activity in transient transfection experiments. These results suggest that we have identified a novel promoter for the mouse Ape gene, localized about 40 kb upstream of the initiating methionine, which drives expression of the unique Ape transcript type detected in undifferentiated totipotent ES cells. Transcripts bearing the novel exon combined either with exon 1 or with exon 2 were detected in all mouse tissues tested. (C) 2004 Elsevier Inc. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 15676281
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  • 3
    Keywords: ALU REPEATS, chimeric gene, DISEASE, DISEASES, DISORDERS, DNA-SEQUENCES, DUPLICATION, EVOLUTION, EXP
    Abstract: Segmental duplications (SDs) play a key role in genome evolution by providing material for gene diversification and creation of variant or novel functions. They also mediate recombinations, resulting in microdeletions, which have occasionally been associated with human genetic diseases. Here, we present a detailed analysis of a large genomic region (about 240 kb), located on human chromosome 1q22, that contains a tandem SD, SD1q22. This duplication occurred about 37 million years ago in a lineage leading to anthropoid primates, after their separation from prosimians but before the Old and New World monkey split. We reconstructed the hypothetical unduplicated ancestral locus and compared it with the extant SDI q22 region. Our data demonstrate that, as a consequence of the duplication, new anthropoid-specific genetic material has evolved in the resulting paralogous segments. We describe the emergence of two new genes, whose new functions could contribute to the speciation of anthropoid primates. Moreover, we provide detailed information regarding structure and evolution of the SD1q22 region that is a prerequisite for future studies of its anthropoid-specific functions and possible linkage to human genetic disorders. (c) 2006 Elsevier Inc. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 16545939
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  • 4
    Keywords: Germany ; human ; PATHWAY ; DISEASE ; DISEASES ; POPULATION ; RISK ; GENE ; GENES ; microarray ; COMPLEX ; COMPLEXES ; MARKER ; IMPACT ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; VARIANTS ; FREQUENCIES ; HUMANS ; microarrays ; genetics ; SNP ; affymetrix ; LINKAGE DISEQUILIBRIUM ; POPULATIONS ; VARIANT ; SINGLE NUCLEOTIDE POLYMORPHISMS ; CANDIDATE GENES ; POWER ; USA ; EXTENT ; GENOME-WIDE ASSOCIATION ; biotechnology ; Genetic ; WELL ; Genome-wide association studies ; COVERAGE ; Whole genome ; Illumina
    Abstract: Most genetic variants associated with complex diseases in humans are believed to have a small impact of risk. With traditional candidate gene/pathway approaches several associations with disease risk could be identified. However, now that genome-wide association Studies are feasible, the question arises if there is still a need for these approaches. By using HapMap data, we evaluated to which extent commercially available microarrays cover, through linkage disequilibrium, all currently known genes and biological processes in different populations. Furthermore, we estimated the power to detect all association with any specific SNP. Our study shows that coverage of individual genes and pathways by current commercial genotyping platforms is satisfactory for the vast majority of RefSeq gene regions. However, depending oil the gene or the population, there may still be a need for candidate gene approaches, especially when looking at polymorphisms with low allele frequencies. (C) 2009 Elsevier Inc. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 19162167
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  • 5
    Abstract: The albino-deletion complex in the mouse defines a genetically well-characterized region of chromosome 7 in which a number of loci essential for normal development and viability reside. One locus, designated alf or hsdr-1, is necessary for neonatal survival. Its absence results in hypoglycemia associated with biochemical and ultrastructural abnormalities in hepatocytes and proximal tubule cells of the kidney. We constructed a long-range physical map of the region defined by the proximal segment of the albino-deletion complex as a step toward localizing alf/hsdr-1. Sixteen markers, including 11 whose isolation is described here and in the accompanying paper (A. Schedl et al., 1992, Genomics 14, 288-297), were ordered on a panel of albino-deletion DNAs and their distribution was examined by pulsed-field gel electrophoresis. The resulting approximately 4300-kb physical map covers the entire region absent from the prototypic alf/hsdr-1 deletion c14CoS, estimated as approximately 3600 kb. Since the deletion c11DSD complements and overlaps most of c14CoS, alf/hsdr-1 was mapped at the proximal extreme of c14CoS, approximately 3000 kb from the albino locus. The density of CpG islands was found to be very heterogeneous across the region mapped.
    Type of Publication: Journal article published
    PubMed ID: 1427844
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  • 6
    Keywords: CANCER ; CELLS ; EXPRESSION ; SURVIVAL ; BLOOD ; CLINICAL-TRIAL ; Germany ; DISEASE ; GENE ; GENE-EXPRESSION ; GENES ; RNA ; TIME ; PATIENT ; treatment ; TRIAL ; TRIALS ; gene expression ; CLINICAL-TRIALS ; PREDICTION ; PERIPHERAL-BLOOD ; gene expression profiling ; B-CELL LYMPHOMA ; MONONUCLEAR-CELLS ; ACUTE MYELOID-LEUKEMIA ; clinical trials ; analysis ; PROFILES ; GENDER ; TECHNOLOGY ; MOLECULAR CLASSIFICATION ; MICROARRAY PLATFORMS ; WHOLE-BLOOD ; peripheral blood ; peripheral blood mononuclear cells ; transcriptome
    Abstract: The use of peripheral blood mononuclear cells (PBMC) for transcriptome analysis has already been proven valuable for assessing disease-associated and drug-response-related gene signatures. While these proof-of-principle studies have been critically important, the instability of RNA within PBMC prohibits their use in large-scale multicenter trials for which samples have to be transported for a prolonged time prior to RNA isolation. Therefore, a prerequisite for transcriptome analysis of peripheral blood in clinical trials will be a standardized and valid method to stabilize the RNA profile immediately after blood withdrawal. Moreover, to be able to perform such large-scale clinical studies routinely in several hundred patients more cost-effective array technologies are required. To address these critical issues, we have combined a whole-blood RNA stabilization technology with a method to reduce globin mRNA, followed by genome-wide transcriptome analysis using a newly introduced BeadChip oligonucleotide technology. We demonstrate that the globin mRNA reduction method results in significantly improved data quality of stabilized RNA samples with low intragroup variance and a detection rate of expressed genes similar to that in PBMC. More important, even small differences in gene expression such as are observed between females and males were detected and sufficient to predict gender in whole-blood samples. We therefore propose the combination of globin mRNA reduction after whole-blood RNA stabilization with a newly introduced cost-effective BeadChip array as the preferred approach for large-scale multicenter trials, especially when establishing predictive markers for disease and treatment outcome in peripheral blood. (c) 2005 Elsevier Inc. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 16387473
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  • 7
    Keywords: RECEPTOR ; EXPRESSION ; NETWORK ; GENE ; GENE-EXPRESSION ; GENES ; MICE ; MESSENGER-RNA ; primary ; MR ; culture ; MOUSE ; IDENTIFICATION ; gene expression ; CELL-DEATH ; genetics ; INVOLVEMENT ; glucocorticoid receptor ; specificity ; heredity ; genomics ; HEART-FAILURE ; mineralocorticoid receptor ; analysis ; USA ; corticosteroids ; GLUCOCORTICOIDS ; genomic ; microbiology ; SET ; transcriptome ; biotechnology ; PERIPHERAL-TISSUES ; aldosterone ; CA2+ CURRENT ; cardiomyocytes ; gene networks ; NEONATAL-RAT ; SODIUM-TRANSPORT
    Abstract: Corticosteroids (aldosterone, cortisol/corticosterone) exert direct functional effects on cardiomyocytes. However, gene networks activated by corticosteroids in cardiomyocytes, as well as the involvement of the mineralocorticoid receptor (MR) vs the glueocorticoid receptor (GR) in these effects, remain largely unknown. Here we characterized the corticosteroid-dependent transcriptome in primary culture of neonatal mouse cardiomyocytes treated with 10(-6) M aldosterone, a concentration predicted to occupy both MR and GR. Serial analysis of gene expression revealed 101 alclosterone-regulated genes. The MR/GR specificity was characterized for one regulated transcript, namely ecto-ADP-ribosyltransferase-3 (Art3). Using cardiomyocytes from GR(null/null) or MR(null/null) mice we demonstrate that in GR(null/null) cardiomyocytes the response is abrogated, but it is fully maintained in MR(null/null) cardiomyocytes. We conclude that Art3 expression is regulated exclusively via the GR. Our study identifies a new set of corticosteroid-regulated genes in cardiomyocytes and demonstrates a new approach to studying the selectivity of MR- vs GR-dependent effects. (c) 2006 Elsevier Inc. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 17174066
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  • 8
    Keywords: CANCER ; EXPRESSION ; carcinoma ; Germany ; PATHWAY ; PATHWAYS ; PROSTATE ; GENE ; GENE-EXPRESSION ; microarray ; RNA ; SAMPLE ; SAMPLES ; TISSUE ; MARKER ; IMPACT ; gene expression ; MICROARRAY DATA ; EXPRESSION ANALYSIS ; genetics ; meta-analysis ; prostate cancer ; PROSTATE-CANCER ; NUCLEOTIDES ; SIGNALING PATHWAY ; VARIABILITY ; DEGRADATION ; POLYMERASE-CHAIN-REACTION ; MICROARRAY ANALYSIS ; heredity ; signaling ; molecular ; RE ; genomics ; METAANALYSIS ; LEVEL ; analysis ; methods ; PROFILES ; TESTS ; ANDROGEN RECEPTOR ; USA ; microbiology ; biotechnology ; NUCLEOTIDE ; breakpoint ; constant cut-off ; degradation plot ; formalin-fixed paraffin embedded tissue ; METHYLACYL-COA RACEMASE
    Abstract: Microarray analysis of formalin-fixed and paraffin-embedded (FFPE) tissue seems to be of importance for the detection of molecular marker sets in prostate cancer (PC). The compromised RNA integrity of FFPE tissue results in a high degree of variability at the probe level of microarray data as shown by degradation plot. We tested methods that reduce the variability by including all probes within 300 nucleotides, within 600 nucleotides, or up to a calculated breakpoint with reference to the 3'-end. Accepted PC pathways such as the Wnt signaling pathway could be observed to be significantly regulated within FFPE microarray datasets. The best representation of PC gene expression, as well as better comparability to meta-analysis and fresh-frozen microarray data, could be obtained with a 600-nucleotide cutoff. Beyond the specific impact for PC microarray data analysis we propose a cutoff of 600 nucleotides for samples for which the integrity of the RNA cannot be guaranteed. (C) 2008 Elsevier Inc. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 18490134
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  • 9
    Abstract: Paralemmin is a newly identified protein that is associated with the plasma membrane and with intracellular membranes through a lipid anchor. It is abundant in brain, is expressed at intermediate levels in the kidney and in endocrine cells, and occurs at low levels in many other tissues. As it is a candidate for genetic disorders that affect membrane functions, we have determined the structure of the human paralemmin gene, PALM, showing that it is organized into nine exons. Moreover, we have performed chromosomal assignments of the human and mouse paralemmin genes, localizing them to regions of homology at human 19p13.3 and the central mouse chromosome 10. Finally, mutation analysis using RNA from mice homozygous for the mutant genes grizzled (gr), mocha (mh), mocha 2J (mh2J), jittery (ji) and hesitant (ji(hes)), which map to this area, excluded mutations in their Palm coding sequences.
    Type of Publication: Journal article published
    PubMed ID: 9615234
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  • 10
    Abstract: The rat HNF-3 (hepatocyte nuclear factor 3) gene family encodes three transcription factors known to be important in the regulation of gene expression in liver and lung. We have cloned and characterized the mouse genes and cDNAs for HNF-3 alpha, beta, and gamma and analyzed their expression patterns in various adult tissues and mouse embryonic stages. The HNF-3 proteins are highly conserved between mouse and rat, with the exception of the amino terminus of HNF-3 gamma, which in mouse is more similar to those of HNF-3 alpha and beta than to the amino termini of the rat HNF-3 gamma protein. The mouse HNF-3 genes are small and contain only two or three (HNF-3 beta) exons with conserved intron-exon boundaries. The proximal promoter of the mouse HNF-3 beta gene is remarkably similar to that of the previously cloned rat HNF-3 beta gene, but is different from the promoters of the HNF-3 alpha and gamma genes. The mRNA distribution of the mouse HNF-3 genes was analyzed by quantitative RNase protection with gene-specific probes. While HNF-3 alpha and beta are restricted mainly to endoderm-derived tissues (lung, liver, stomach, and small intestine), HNF-3 gamma is more extensively expressed, being present additionally in ovary, testis, heart, and adipose tissue, but missing from lung. Transcripts for HNF-3 beta and alpha are detected most abundantly in midgestation embryos (Day 9.5), while HNF-3 gamma expression peaks around Day 15.5 of gestation.
    Type of Publication: Journal article published
    PubMed ID: 8034310
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