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  • 1
    Keywords: affymetrix, APOPTOSIS, ARRAYS, CDNA, CELL, CELLS, DIFFERENTIATION, DNA, ENZYMES, EXPRESSION, GENE, g
    Abstract: The transcription factors CREM, CREB, and ATF-1 constitute a subfamily of p-Zip, transcription factors. Several different kinase cascades regulate the activity of these proteins. The activator splice-isoform CREMtau is specifically and highly expressed in post-meiotic germ cells during mouse spermatogenesis. Male mice lacking CREMtau expression are sterile because of stage-specific arrest of sperm maturation as the spermatids undergo apoptosis.In order to characterize the genes that are controlled by CREM during post-meiotic differentiation of round spermatids, we compared the expression levels of mRNA prepared from testes of wild-type and CREM-deficient mice by suppression subtractive hybridization (SSH) and affymetrix oligonucleotide arrays.A set of 956 unique sequences found in the CREM SSH library was further characterized by generating stage-specific expression profiles during spermatogenesis by hybridization with cDNA from pre-pubertal mice at defined stages of spermatogenesis using nylon DNA arrays. The resulting expression profiles were arranged in a linear order according to similarity in their profile shapes to find co-regulation of functionally related genes.Our data shows that a large number of genes are transcriptionally activated in round spermatids when CREM activity is maximal, including functional groups like transcription factors, proteins involved in signal transduction, and metabolic enzymes, therefore providing novel information of post-meiotic expression of many known as well as novel genes that are either directly or indirectly influenced by CREM expression. (C) 2003 Elsevier Ireland Ltd. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 14654248
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  • 2
    Keywords: MINUTE VIRUS ; EPSTEIN-BARR-VIRUS ; TOLL-LIKE RECEPTORS ; NONSTRUCTURAL PROTEINS NS2 ; ADENOASSOCIATED VIRUS VECTORS ; NEWCASTLE-DISEASE-VIRUS ; PATHOGEN RECOGNITION ; INTERFERON-PRODUCING CELLS ; RIG-I ; I-LIKE RECEPTORS
    Abstract: The oncotropism of Minute Virus of Mice (MVMp) is partially related to the stimulation of an antiviral response mediated by type-I interferons (IFNs) in normal but not in transformed mouse cells. The present work was undertaken to assess whether the oncotropism displayed against human cells by MVMp and its rat homolog H-1PV also depends on antiviral mechanisms and to identify the pattern recognition receptor (PRR) involved. Despite their low proliferation rate which represents a drawback for parvovirus multiplication, we used human peripheral blood mononuclear cells (hPBMCs) as normal model specifically because all known PRRs are functional in this mixed cell population and moreover because some of its subsets are among the main IFN producers upon infections in mammals. Human transformed models consisted in lines and tumor cells more or less permissive to both parvoviruses. Our results show that irrespective of their permissiveness, transformed cells do not produce IFNs nor develop an antiviral response upon parvovirus infection. However, MVMp- or H-1PV-infected hPBMCs trigger such defense mechanisms despite an absence of parvovirus replication and protein expression, pointing to the viral genome as the activating element. Substantial reduction of an inhibitory oligodeoxynucleotide (iODN) of the latter IFN production identified TLR-9 as a potential PRR for parvoviruses in hPBMCs. However, neither the iODN treatment nor an antibody-induced neutralization of the IFN-triggered effects restored parvovirus multiplication in these cells as expected by their weak proliferation in culture. Finally, given that a TLR-9 activation could also not be observed in parvovirus-infected human lines reported to be endowed with a functional TLR-9 pathway (Namalwa, Raji, and HEK293-TLR9(+/+)), our data suggest that transformed human cells do not sense MVMp or H-1PV either because of an absence of PRR expression or an intrinsic, or virus-driven defect in the endosomal sensing of the parvovirus genomes by TLR-9.
    Type of Publication: Journal article published
    PubMed ID: 23383065
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  • 3
    Keywords: RISK ; EMBRYONIC STEM-CELLS ; bacterial ; IN-VITRO FERTILIZATION ; MOUSE HEPATITIS-VIRUS ; LIQUID-NITROGEN ; MICROBIAL-CONTAMINATION ; SPERM CRYOPRESERVATION ; CROSS-CONTAMINATION ; GERMPLASM
    Abstract: Genetically modified animals are unique models with enormous scientific potential. Cryopreservation of preimplantation embryos or of spermatozoa is a common approach to save those lines. The breeding of a line can be discontinued if a sufficient number of samples have been cryopreserved. To maintain the opportunity to recover a line, it is mandatory to assess the quality of the cryopreserved samples and to assure safe long-term storage conditions. Here, we investigated the revitalization rate of cryopreserved pre-implantation embryos stored inhouse up to 158 months, of imported (and shipped) embryos, and of embryos received after in vitro fertilization. The storage period did not affect the revitalization rate, whereas the recovery of imported embryos was significantly reduced, possibly due to shipment conditions. The genotypes of genetically modified pups received following embryo-transfer were slightly smaller than expected by Mendelian laws. Intensive investigations of the hygienic state of the cryopreserved samples and the equipment used never showed microbiological contamination of a sample within a cryo-tube. However, environmental organisms were found frequently in the permanent freezers and dry shippers used. Since such contamination cannot be completely excluded and an embryo-transfer might not lead in all cases to a secure rederivation, foster mothers and revitalized pups should be housed in an intermediate facility and their health assessed before introducing them into the target facility.
    Type of Publication: Journal article published
    PubMed ID: 25340944
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  • 4
  • 5
    Keywords: CELLS ; tumor ; Germany ; MICE ; NF-KAPPA-B ; ACTIVATION ; INFECTION ; MECHANISM ; mechanisms ; CYCLE ; IMMUNE-RESPONSES ; STIMULATION ; antibody ; MOUSE ; innate immunity ; INTERFERON ; FAILURE ; INFECTIONS ; DOUBLE-STRANDED-RNA ; S-PHASE ; VIRAL-INFECTION ; oncolytic virus ; LIFE ; PROTEIN-KINASE PKR ; TOLL-LIKE RECEPTOR-3 ; Intrinsic ; ALPHA/BETA INTERFERON ; KILHAM RAT VIRUS
    Abstract: Parvovirus minute virus of mice (MVMp) is endowed with oncotropic properties so far ascribed only to the dependency of the virus life cycle on cellular factors expressed during S phase and/or modulated by malignant transformation. For other viruses oncotropism relies on their inability to circumvent type I interferon (IFN)-induced innate antiviral mechanisms, the first line of defense triggered by normal cells against viral infections. These agents propagate, therefore, preferentially in transformed/tumor cells, which often lack functional antiviral mechanisms. The present study aimed at investigating whether antiviral processes also contribute to MVMp oncotropism. Our results demonstrate that in contrast to MVMp-permissive transformed mouse A9 fibroblasts, freshly isolated normal counterparts (mouse embryonic fibroblasts [MEFs]) mount, through production and release of type I IFNs upon their infection, an antiviral response against MVMp lytic multiplication. Pretreatment of MEFs with a type I IFN-beta-neutralizing antibody, prior to MVMp infection, inhibits the virus-triggered antiviral response and improves the fulfillment of the MVMp life cycle. Our results also show that part of the A9 permissiveness to MVMp relies on the inability to produce type I IFNs upon parvovirus infection, a feature related either to an A9 intrinsic deficiency of this process or to an MVMp-triggered inhibitory mechanism, since stimulation of these cells by exogenous IFN-beta strongly inhibits the parvovirus life cycle. Taken together, our results demonstrate for the first time that parvovirus infection triggers an innate antiviral response in normal cells and suggest that the MVMp oncotropism depends at least in part on the failure of infected transformed cells to mount such a response
    Type of Publication: Journal article published
    PubMed ID: 19864388
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  • 6
    Keywords: CELLS ; IN-VITRO ; CELL ; Germany ; KINASE ; SITE ; SITES ; GENOME ; PROTEIN ; PROTEINS ; MICE ; DNA ; INFECTION ; FAMILY ; IMPACT ; fibroblasts ; MEMBER ; MEMBERS ; PHOSPHORYLATION ; protein kinase ; PROTEIN-KINASE ; culture ; virus ; MOUSE ; PHENOTYPES ; MUTATION ; MODULATION ; REGION ; PRODUCT ; MUTATIONS ; POLYPEPTIDE ; INVOLVEMENT ; DNA-REPLICATION ; EXPORT FACTOR CRM1 ; KINASE-C ; MINUTE VIRUS ; MURINE CELLS ; NONSTRUCTURAL PROTEIN NS1 ; PARVOVIRUS H-1 ; PROTEIN-KINASE-C ; REPLICATION ; REPLICATIVE FUNCTIONS ; RESPONSIVE ELEMENT ; SITE-DIRECTED MUTAGENESIS ; TRANS-ACTIVATION
    Abstract: Late in infection, parvovirus minute virus of mice (MVMp) induces the lysis of mouse A9 fibroblasts. This effect depends on the large nonstructural phosphoprotein NS1, which plays in addition a major role in viral DNA replication and progeny particle production. Since the NS1 C-terminall region is subjected to late phosphorylation events and protein kinase C (PKC) family members regulate NS1 replicative activities, the present study was conducted to determine the impact of PKCs on NS1 cytotoxic functions. To this end, we performed site-directed mutagenesis, substituting alanine residues for two consensus PKC-phosphorylation sites located within the NS1 C-terminall region, T585 and S588. Although these substitutions had no detectable effect on virus multiplication in a single-round infection, the NS1-585A mutant virus was significantly less toxic to A9 cells than wild-type MVMp, whereas the NS1-588A mutant virus was endowed with a higher killing potential. These alterations correlated with specific changes in the late phosphoryllation pattern of the mutant NS1 proteins compared to the wild-type polypeptide. Since the mutations introduced in this region of the viral genome also made changes in the minor nonstructural protein NS2, a contribution of this polypeptide to the above-mentioned phenotypes of mutant viruses cannot be excluded at present. However, the involvement of NS1 in these phenotypes was directly supported by the respective reduced and enhanced capacity of NS1-585A and NS1-588A recombinant proteins for inducing morphological alterations and cell detachment in transfected A9 cultures. Altogether, these data suggest that late-occurring phosphoryllation of NS1 specifically regulates the cytotoxic functions of the viral product and that residues T585 and S588 contribute to this control in an antagonistic way
    Type of Publication: Journal article published
    PubMed ID: 14610171
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  • 7
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  48. Kongress für Allgemeinmedizin und Familienmedizin; 20140918-20140920; Hamburg; DOC14degam145 /20140911/
    Publication Date: 2014-09-12
    Keywords: Ärzte in Weiterbildung ; Weiterbildungsverbünde ; Zufriedenheit ; ddc: 610
    Language: German
    Type: conferenceObject
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  • 8
    ISSN: 1432-069X
    Keywords: In vitro study ; Procollagen peptide ; Collagen synthesis ; Scleroderma ; Fibroblastenkultur ; Procollagenpeptide ; Collagensynthese ; Scleroderma
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Skerodermie-Fibroblasten einer Patientin im sklerotischen Stadium zeigten unter in vitro Bedingungen eine erhöhte DNA-Syntheserate und eine gesteigerte Kollagensynthese. Durch Zugabe von Prokollagenpeptiden zum Inkubationsmedium konnte die Kollagensythese auf nahezu normales Niveau gebracht werden. Dieses Ergebnis läßt den Schlußzu, daß die Kontrolle der Kollagensynthese über einen »feed-back«-Mechanismus intakt ist. Es ist deshalb möglich, daß der Gehalt an Prokollagenpeptiden selbst in den Sklerodermie-Fibroblasten erniedrigt ist.
    Notes: Summary Fibroblasts derived from a skin biopsy of a patient with scleroderma in the sclerotic stage were shown to have a higher rate of DNA synthesis, and to synthesize more collagen than fibroblasts from a healthy control. The addition of procollagen peptides to the culture medium of scleroderma fibroblasts almost normalized the collagen synthesis. This observation indicates that the mechanism for the regulation of collagen synthesis by feed back inhibition of prollagen peptides is functioning in this disease. It is suggested that the level of biologically active procollagen peptides is lowered.
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Springer
    Archives of dermatological research 130 (1921), S. 334-340 
    ISSN: 1432-069X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] The differential response of RAR to activating ligands on DR +1 and DR + 5 response elements result from opposite polarities of heterodimer binding to the asymmetrically oriented half-sites6. On DR + 5 sites, RAR/RXR heterodimers bind such ...
    Type of Medium: Electronic Resource
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