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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: transcription ; MESSENGER-RNA ; ELEMENT ; NERVOUS-SYSTEM ; CYCLIC-AMP ; TYROSINE AMINOTRANSFERASE GENE ; mineralocorticoid receptor ; SERINE DEHYDRATASE GENE ; HORMONAL-CONTROL ; CORTICOTROPIN
    Abstract: The role of the glucocorticoid receptor (GR) in glucocorticoid physiology and during development was investigated by generation of GR-deficient mice by gene targeting. GR -/- mice die within a few hours after birth because of respiratory failure. The lungs at birth are severely atelectatic, and development is impaired from day 15.5 p.c. Newborn livers have a reduced capacity to activate genes for key gluconeogenic enzymes. Feedback regulation via the hypothalamic-pituitary-adrenal axis is severely impaired resulting in elevated levels of plasma adrenocorticotrophic hormone (15-fold) and plasma corticosterone (2.5-fold). Accordingly, adrenal glands are enlarged because of hypertrophy of the cortex, resulting in increased expression of key cortical steroid biosynthetic enzymes, such as side-chain cleavage enzyme, steroid 11 beta-hydroxylase, and aldosterone synthase. Adrenal glands lack a central medulla and synthesize no adrenaline. They contain no adrenergic chromaffin cells and only scattered noradrenergic chromaffin cells even when analyzed from the earliest stages of medulla development. These results suggest that the adrenal medulla may be formed from two different cell populations: adrenergic-specific cells that require glucocorticoids for proliferation and/or survival, and a smaller noradrenergic population that differentiates normally in the absence of glucocorticoid signaling.
    Type of Publication: Journal article published
    PubMed ID: 7628695
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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 ; EXPRESSION ; BLOOD ; CELL ; Germany ; IN-VIVO ; liver ; ENZYMES ; GENE ; GENES ; transcription ; METABOLISM ; MICE ; ACTIVATION ; kidney ; TRANSCRIPTION FACTOR ; INDUCTION ; hepatocytes ; MUTANT ; hormone ; DISRUPTION ; TANDEM MASS-SPECTROMETRY ; inactivation ; Jun ; GLUCOSE ; glucocorticoid receptor ; GLUCOCORTICOID-RECEPTOR ; ANTAGONIST ; insulin ; ABSENCE ; ADULT ; ENDOCRINE ; LEADS ; development ; CARBOXYKINASE GTP GENE ; HEPATIC GLUCONEOGENESIS ; PHOSPHOENOLPYRUVATE CARBOXYKINASE ; TYROSINE AMINOTRANSFERASE GENE
    Abstract: Hepatic glucose production by gluconeogenesis is the main source of glucose during fasting and contributes significantly to hyperglycemia in diabetes mellitus. Accordingly, glucose metabolism is tightly controlled by a variety of hormones including insulin, epinephrine, glucagon, and glucocorticoids (GCs) acting on various cell types. GC effects are mediated by the GC receptor (GR), a ligand-dependent transcription factor, which in the liver and kidney controls gluconeogenesis by induction of gluconeogenic enzymes. To specifically study the contribution of GC on liver carbohydrate metabolism, we generated mice with an inactivation of the GR gene exclusively in hepatocytes using the Cre/loxP technology. Half of the mutant mice die within the first 2 d after birth most likely due to hypoglycemia. Adult mice have normal blood sugar under basal conditions but show hypoglycemia after prolonged starvation due to reduced expression of genes involved in gluconeogenesis. We further demonstrate that absence of GR in hepatocytes limits the development of hyperglycemia in streptozotocin-induced diabetes mellitus probably due to impaired induction of gluconeogenesis. These findings show the essential role of GR function in liver glucose metabolism during fasting and in diabetic mice and indicate that liver-specific GC antagonists could be beneficial in control of diabetic hyperglycemia
    Type of Publication: Journal article published
    PubMed ID: 15031319
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  • 5
    Keywords: RECEPTOR ; GROWTH ; CELL ; Germany ; IN-VIVO ; MODEL ; VIVO ; SUPPORT ; liver ; GENE ; GENE-EXPRESSION ; PROTEIN ; PROTEINS ; transcription ; MICE ; ACTIVATION ; TRANSCRIPTION FACTOR ; REDUCTION ; hepatocytes ; TRANSCRIPTION FACTORS ; hormone ; inactivation ; DNA-BINDING ; REGION ; REGIONS ; TARGETED DISRUPTION ; BINDING PROTEIN-3 ; I IGF-I ; postnatal body growth,glucocorticoid receptor,growth hormone signaling,Stat5 ; STAT5B
    Abstract: Mice carrying a hepatocyte-specific inactivation of the glucorticoid receptor (GR) gene show a dramatic reduction in body size. Growth hormone signaling mediated by the Stat5 transcription factors is impaired. We show that Stat5 proteins physically interact with GR and GR is present in vivo on Stat5-dependent IGF-I and ALS regulatory regions. Interestingly, mice with a DNA-binding-deficient GR but an unaltered ability to interact with STAT5(GR(dim/dim)) have a normal body size and normal levels of Stat5-dependent mRNAs. These findings strongly support the model in which GR acts as a coactivator for Stat5-dependent transcription upon GH stimulation and reveal an essential role of hepatic GR in the control of body growth
    Type of Publication: Journal article published
    PubMed ID: 15037546
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