Dressel, Ralf

[["dc.bibliographiccitation.firstpage","3957"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","The Journal of Immunology"],["dc.bibliographiccitation.lastpage","3965"],["dc.bibliographiccitation.volume","166"],["dc.contributor.author","Ioannidu, S."],["dc.contributor.author","Walter, L."],["dc.contributor.author","Dressel, Ralf"],["dc.contributor.author","Gunther, E."],["dc.date.accessioned","2018-11-07T09:16:35Z"],["dc.date.available","2018-11-07T09:16:35Z"],["dc.date.issued","2001"],["dc.description.abstract","The rat is an important model for studying organ graft rejection and susceptibility to certain complex diseases. The MHC, the RT1 complex, plays a decisive role in controlling these traits. We have cloned the telomeric class I region of the RT1 complex, RT1-C/E/M, of the BN inbred rat strain in a contig of overlapping pi-derived artificial chromosome clones encompassing similar to2 Mb, and present a physical map of this MHC region, Forty-five class I exon ii-hybridizing BamHI fragments were detected, including the previously known rat class I genes RT1-E, RT-BM1, RT1-N, RT1-M2, RT1-M3 and RT1-M4, Twenty-six non-class I genes known to map to the corresponding part of the human and mouse MHC were tested and could be fine mapped in the RT1-C/E/M region at orthologous position. Four previously known microsatellite markers were fine mapped in the RT1-C/E/M region and found to occur in multiple copies. In addition, a new, single-copy polymorphic microsatellite has been defined. The expression profiles of several class I genes and the 26 non-class I genes were determined in 13 different tissues and exhibited restricted patterns in most cases. The data provide further molecular information on the MHC for analyzing disease susceptibility and underline the usefulness of the rat model."],["dc.identifier.isi","000167437700044"],["dc.identifier.pmid","11238641"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27965"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Assoc Immunologists"],["dc.relation.issn","0022-1767"],["dc.title","Physical map and expression profile of genes of the telomeric class I gene region of the rat MHC"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","970"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","The Journal of Immunology"],["dc.bibliographiccitation.lastpage","975"],["dc.bibliographiccitation.volume","174"],["dc.contributor.author","Roos, Christian"],["dc.contributor.author","Dressel, Ralf"],["dc.contributor.author","Schmidt, Bernhard"],["dc.contributor.author","Günther, Eberhard"],["dc.contributor.author","Walter, Lutz"],["dc.date.accessioned","2022-10-06T13:26:53Z"],["dc.date.available","2022-10-06T13:26:53Z"],["dc.date.issued","2005"],["dc.identifier.doi","10.4049/jimmunol.174.2.970"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/115191"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-602"],["dc.relation.eissn","1550-6606"],["dc.relation.issn","0022-1767"],["dc.relation.orgunit","Deutsches Primatenzentrum"],["dc.title","The Rat Expresses Two Complement Factor C4 Proteins, but Only One Isotype Is Expressed in the Liver"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Wiener klinische Wochenschrift"],["dc.bibliographiccitation.volume","120"],["dc.contributor.author","Novota, P."],["dc.contributor.author","Sviland, Lisbet"],["dc.contributor.author","Opitz, Lennart"],["dc.contributor.author","Hitt, Reiner"],["dc.contributor.author","Dickinson, Anne M."],["dc.contributor.author","Walter, L."],["dc.contributor.author","Dressel, Ralf"],["dc.date.accessioned","2018-11-07T11:12:51Z"],["dc.date.available","2018-11-07T11:12:51Z"],["dc.date.issued","2008"],["dc.format.extent","124"],["dc.identifier.isi","000259367100404"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53754"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Wien"],["dc.relation.issn","0043-5325"],["dc.title","Major histocompatibility complex (MHC) gene expression profiling of the graft versus host reaction in skin explant assays"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","5523"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","The Journal of Immunology"],["dc.bibliographiccitation.lastpage","5533"],["dc.bibliographiccitation.volume","179"],["dc.contributor.author","Elsner, Leslie"],["dc.contributor.author","Muppala, Vijayakumar"],["dc.contributor.author","Gehrmann, Mathias"],["dc.contributor.author","Lozano, Jingky"],["dc.contributor.author","Malzahn, Dörthe"],["dc.contributor.author","Bickeböller, Heike"],["dc.contributor.author","Brunner, Edgar"],["dc.contributor.author","Zientkowska, Marta"],["dc.contributor.author","Herrmann, Thomas"],["dc.contributor.author","Walter, Lutz"],["dc.contributor.author","Dressel, Ralf"],["dc.date.accessioned","2022-06-08T07:57:36Z"],["dc.date.available","2022-06-08T07:57:36Z"],["dc.date.issued","2007"],["dc.description.abstract","The stress-inducible heat shock protein (HSP) 70 is known to function as an endogenous danger signal that can increase the immunogenicity of tumors and induce CTL responses. We show in this study that HSP70 also activates mouse NK cells that recognize stress-inducible NKG2D ligands on tumor cells. Tumor size and the rate of metastases derived from HSP70-overexpressing human melanoma cells were found to be reduced in T and B cell-deficient SCID mice, but not in SCID/beige mice that lack additionally functional NK cells. In the SCID mice with HSP70-overexpressing tumors, NK cells were activated so that they killed ex vivo tumor cells that expressed NKG2D ligands. In the tumors, the MHC class I chain-related (MIC) A and B molecules were found to be expressed. Interestingly, a counter selection was observed against the expression of MICA/B in HSP70-overexpressing tumors compared with control tumors in SCID, but not in SCID/beige mice, suggesting a functional relevance of MICA/B expression. The melanoma cells were found to release exosomes. HSP70-positive exosomes from the HSP70-overexpressing cells, in contrast to HSP70-negative exosomes from the control cells, were able to activate mouse NK cells in vitro to kill YAC-1 cells, which express NKG2D ligands constitutively, or the human melanoma cells, in which MICA/B expression was induced. Thus, HSP70 and inducible NKG2D ligands synergistically promote the activation of mouse NK cells resulting in a reduced tumor growth and suppression of metastatic disease."],["dc.identifier.doi","10.4049/jimmunol.179.8.5523"],["dc.identifier.isi","000250099400061"],["dc.identifier.pmid","17911639"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/110150"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-575"],["dc.notes.status","final"],["dc.notes.submitter","Najko"],["dc.relation.eissn","1550-6606"],["dc.relation.issn","0022-1767"],["dc.title","The Heat Shock Protein HSP70 Promotes Mouse NK Cell Activity against Tumors That Express Inducible NKG2D Ligands"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Frontiers in Immunology"],["dc.bibliographiccitation.volume","13"],["dc.contributor.affiliation","Hasan, Mohammad Zahidul; 1Primate Genetics Laboratory, German Primate Center, Leibniz Institute for Primate Research, Göttingen, Germany"],["dc.contributor.affiliation","Höltermann, Charlotte; 1Primate Genetics Laboratory, German Primate Center, Leibniz Institute for Primate Research, Göttingen, Germany"],["dc.contributor.affiliation","Petersen, Beatrix; 1Primate Genetics Laboratory, German Primate Center, Leibniz Institute for Primate Research, Göttingen, Germany"],["dc.contributor.affiliation","Schrod, Annette; 3Animal Husbandry, German Primate Center, Leibniz Institute for Primate Research, Göttingen, Germany"],["dc.contributor.affiliation","Mätz-Rensing, Kerstin; 4Pathology Unit, German Primate Center, Leibniz Institute for Primate Research, Göttingen, Germany"],["dc.contributor.affiliation","Kaul, Artur; 5Infection Biology Unit, German Primate Center, Leibniz Institute for Primate Research, Göttingen, Germany"],["dc.contributor.affiliation","Salinas, Gabriela; 6NGS Core Unit for Integrative Genomics, Institute of Human Genetics, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Dressel, Ralf; 7Institute for Cellular and Molecular Immunology, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Walter, Lutz; 1Primate Genetics Laboratory, German Primate Center, Leibniz Institute for Primate Research, Göttingen, Germany"],["dc.contributor.author","Hasan, Mohammad Zahidul"],["dc.contributor.author","Höltermann, Charlotte"],["dc.contributor.author","Petersen, Beatrix"],["dc.contributor.author","Schrod, Annette"],["dc.contributor.author","Mätz-Rensing, Kerstin"],["dc.contributor.author","Kaul, Artur"],["dc.contributor.author","Salinas, Gabriela"],["dc.contributor.author","Dressel, Ralf"],["dc.contributor.author","Walter, Lutz"],["dc.date.accessioned","2022-12-12T08:41:47Z"],["dc.date.available","2022-12-12T08:41:47Z"],["dc.date.issued","2022-11-25"],["dc.date.updated","2022-12-12T08:18:36Z"],["dc.description.abstract","Previous research on adaptive NK cells in rhesus macaques suffered from the lack of specific antibodies to differentiate between inhibitory CD94/NKG2A and stimulatory CD94/NKG2C heterodimeric receptors. Recently we reported an expansion of NKG2C receptor-encoding genes in rhesus macaques, but their expression and functional role on primary NK cells remained unknown due to this deficit. Thus, we established monoclonal antibodies 4A8 and 7B1 which show identical specificities and bind to both NKG2C-1 and NKG2C-2 but neither react with NKG2C-3 nor NKG2A on transfected cells. Using a combination of 4A8 and Z199 antibodies in multicolor flow cytometry we detected broad expression (4-73%) of NKG2C-1 and/or NKG2C-2 (NKG2C-1/2) on primary NK cells in rhesus macaques from our breeding colony. Stratifying our data to CMV-positive and CMV-negative animals, we noticed a higher proportion (23-73%) of primary NK cells expressing NKG2C-1/2 in CMV+ as compared to CMV- macaques (4-5%). These NKG2C-1/2-positive NK cells in CMV+ macaques are characterized by lower expression of IL12RB2, ZBTB16, SH2D1B, but not FCER1G, as well as high expression of IFNG, indicating that antibody 4A8 detects CMV-associated adaptive NK cells. Single cell RNA seq data of 4A8-positive NK cells from a rhCMV-positive macaque demonstrated that a high proportion of these adaptive NK cells transcribe in addition to NKG2C-1 and NKG2C-2 also NKG2C-3, but interestingly NKG2A as well. Remarkably, in comparison to NKG2A, NKG2C-1 and in particular NKG2C-2 bind Mamu-E with higher avidity. Primary NK cells exposed to Mamu-E-expressing target cells displayed strong degranulation as well as IFN-gamma expression of 4A8+ adaptive NK cells from rhCMV+ animals. Thus, despite co-expression of inhibitory and stimulatory CD94/NKG2 receptors the higher number of different stimulatory NKG2C receptors and their higher binding avidity to Mamu-E outreach inhibitory signaling via NKG2A. These data demonstrate the evolutionary conservation of the CMV-driven development of NKG2C-positive adaptive NK cells with particular molecular signatures in primates and with changes in gene copy numbers and ligand-binding strength of NKG2C isotypes. Thus, rhesus macaques represent a suitable and valuable nonhuman primate animal model to study the CMV-NKG2C liaison in vivo."],["dc.identifier.doi","10.3389/fimmu.2022.1028788"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/118501"],["dc.language.iso","en"],["dc.relation.eissn","1664-3224"],["dc.rights","CC BY 4.0"],["dc.rights.uri","http://creativecommons.org/licenses/by/4.0/"],["dc.title","Detailed phenotypic and functional characterization of CMV-associated adaptive NK cells in rhesus macaques"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","109"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Immunogenetics"],["dc.bibliographiccitation.lastpage","123"],["dc.bibliographiccitation.volume","68"],["dc.contributor.author","Isernhagen, Antje"],["dc.contributor.author","Schilling, Daniela"],["dc.contributor.author","Monecke, Sebastian"],["dc.contributor.author","Shah, Pranali"],["dc.contributor.author","Elsner, Leslie"],["dc.contributor.author","Walter, Lutz"],["dc.contributor.author","Multhoff, Gabriele"],["dc.contributor.author","Dressel, Ralf"],["dc.date.accessioned","2018-11-07T10:18:55Z"],["dc.date.available","2018-11-07T10:18:55Z"],["dc.date.issued","2016"],["dc.description.abstract","The MHC class I chain-related molecule A (MICA) is a ligand for the activating natural killer (NK) cell receptor NKG2D. A polymorphism causing a valine to methionine exchange at position 129 affects binding to NKG2D, cytotoxicity, interferon-gamma release by NK cells and activation of CD8(+) T cells. It is known that tumors can escape NKG2D-mediated immune surveillance by proteolytic shedding of MICA. Therefore, we investigated whether this polymorphism affects plasma membrane expression (pmMICA) and shedding of MICA. Expression of pmMICA was higher in a panel of tumor (n = 16, P = 0.0699) and melanoma cell lines (n = 13, P = 0.0429) carrying the MICA-129Val/Val genotype. MICA-129Val homozygous melanoma cell lines released more soluble MICA (sMICA) by shedding (P = 0.0015). MICA-129Met or MICA-129Val isoforms differing only in this amino acid were expressed in the MICA-negative melanoma cell line Malme, and clones with similar pmMICA expression intensity were selected. The MICA-129Met clones released more sMICA (P = 0.0006), and a higher proportion of the MICA-129Met than the MICA-129Val variant was retained in intracellular compartments (P = 0.0199). The MICA-129Met clones also expressed more MICA messenger RNA (P = 0.0047). The latter phenotype was also observed in mouse L cells transfected with the MICA expression constructs (P = 0.0212). In conclusion, the MICA-129Met/Val dimorphism affects the expression density of MICA on the plasma membrane. More of the MICA-129Met variants were retained intracellularly. If expressed at the cell surface, the MICA-129Met isoform was more susceptible to shedding. Both processes appear to limit the cell surface expression of MICA-129Met variants that have a high binding avidity to NKG2D."],["dc.identifier.doi","10.1007/s00251-015-0884-8"],["dc.identifier.isi","000369012800002"],["dc.identifier.pmid","26585323"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12585"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41550"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/128"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C05: Bedeutung von zellulären Immunreaktionen für das kardiale Remodeling und die Therapie der Herzinsuffizienz durch Stammzelltransplantation"],["dc.relation.issn","1432-1211"],["dc.relation.issn","0093-7711"],["dc.relation.workinggroup","RG Dressel"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","The MICA-129Met/Val dimorphism affects plasma membrane expression and shedding of the NKG2D ligand MICA"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","82"],["dc.bibliographiccitation.journal","Immunological Reviews"],["dc.bibliographiccitation.lastpage","95"],["dc.bibliographiccitation.volume","184"],["dc.contributor.author","Dressel, Ralf"],["dc.contributor.author","Walter, L."],["dc.contributor.author","Gunther, E."],["dc.date.accessioned","2018-11-07T11:21:08Z"],["dc.date.available","2018-11-07T11:21:08Z"],["dc.date.issued","2001"],["dc.description.abstract","The major histocompatibility complex (MHC) plays a central role in controlling immune responsiveness, susceptibility to certain diseases and histo-incompatibility, A physical map of the complete rat MHC, the RT1 complex, is presented based on a PAC clonal contig (RT1(n) haplotype). Expression profiling of various tissues of different inbred strains has been carried out for genes of the RT1-C/E/M region, and different types of variability of expression are shown. As an example of single gene analysis, the RT1-linked heat shock-inducible heat shock genes Hsp70-1 and Hsp70-2 have been studied. It is demonstrated that their gene products are able to increase lysability of target cells by cytotoxic T lymphocytes."],["dc.identifier.doi","10.1034/j.1600-065x.2001.1840108.x"],["dc.identifier.isi","000173738900007"],["dc.identifier.pmid","11918680"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55701"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Blackwell Munksgaard"],["dc.relation.issn","0105-2896"],["dc.title","Genomic and funtional aspects of the rat MHC, the RT1 complex"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1480"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","EMBO Molecular Medicine"],["dc.bibliographiccitation.lastpage","1502"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Isernhagen, Antje"],["dc.contributor.author","Malzahn, Doerthe"],["dc.contributor.author","Viktorova, Elena"],["dc.contributor.author","Elsner, Leslie"],["dc.contributor.author","Monecke, Sebastian"],["dc.contributor.author","von Bonin, Frederike"],["dc.contributor.author","Kilisch, Markus"],["dc.contributor.author","Wermuth, Janne Marieke"],["dc.contributor.author","Walther, Neele"],["dc.contributor.author","Balavarca, Yesilda"],["dc.contributor.author","Stahl-Hennig, Christiane"],["dc.contributor.author","Engelke, Michael"],["dc.contributor.author","Walter, Lutz"],["dc.contributor.author","Bickeboeller, Heike"],["dc.contributor.author","Kube, Dieter"],["dc.contributor.author","Wulf, Gerald"],["dc.contributor.author","Dressel, Ralf"],["dc.date.accessioned","2018-11-07T09:49:36Z"],["dc.date.available","2018-11-07T09:49:36Z"],["dc.date.issued","2015"],["dc.description.abstract","The MHC class I chain-related molecule A (MICA) is a highly polymorphic ligand for the activating natural killer (NK)-cell receptor NKG2D. A single nucleotide polymorphism causes a valine to methionine exchange at position 129. Presence of a MICA-129Met allele in patients (n=452) undergoing hematopoietic stem cell transplantation (HSCT) increased the chance of overall survival (hazard ratio [HR]=0.77, P=0.0445) and reduced the risk to die due to acute graft-versus-host disease (aGVHD) (odds ratio [OR]=0.57, P=0.0400) although homozygous carriers had an increased risk to experience this complication (OR=1.92, P=0.0371). Overall survival of MICA-129Val/Val genotype carriers was improved when treated with anti-thymocyte globulin (HR=0.54, P=0.0166). Functionally, the MICA-129Met isoform was characterized by stronger NKG2D signaling, triggering more NK-cell cytotoxicity and interferon- release, and faster co-stimulation of CD8(+) T cells. The MICA-129Met variant also induced a faster and stronger down-regulation of NKG2D on NK and CD8(+) T cells than the MICA-129Val isoform. The reduced cell surface expression of NKG2D in response to engagement by MICA-129Met variants appeared to reduce the severity of aGVHD."],["dc.description.sponsorship","Open-Access Publikationsfonds 2015"],["dc.identifier.doi","10.15252/emmm.201505246"],["dc.identifier.isi","000364320100008"],["dc.identifier.pmid","26483398"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12462"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35542"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/127"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C05: Bedeutung von zellulären Immunreaktionen für das kardiale Remodeling und die Therapie der Herzinsuffizienz durch Stammzelltransplantation"],["dc.relation.issn","1757-4684"],["dc.relation.issn","1757-4676"],["dc.relation.workinggroup","RG Dressel"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","The MICA-129 dimorphism affects NKG2D signaling and outcome of hematopoietic stem cell transplantation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","8212"],["dc.bibliographiccitation.issue","23"],["dc.bibliographiccitation.journal","Cancer Research"],["dc.bibliographiccitation.lastpage","8220"],["dc.bibliographiccitation.volume","63"],["dc.contributor.author","Dressel, Ralf"],["dc.contributor.author","Grzeszik, C."],["dc.contributor.author","Kreiss, M."],["dc.contributor.author","Lindemann, D."],["dc.contributor.author","Herrmann, Thomas R."],["dc.contributor.author","Walter, L."],["dc.contributor.author","Gunther, E."],["dc.date.accessioned","2018-11-07T10:34:17Z"],["dc.date.available","2018-11-07T10:34:17Z"],["dc.date.issued","2003"],["dc.description.abstract","We have shown previously that acute heat shock protein (Hsp) 70 induction in a human melanoma cell line containing a doxycycline-inducible Hsp70 expression construct increases lysability of these tumor cells by cytotoxic T lymphocyte (CTL) without interfering with MHC class I expression and antigen presentation. The same parental melanoma cell line has now been transduced retrovirally to overexpress Hsp70 permanently. Here we demonstrate that MHC class I cell surface expression is again not altered and that these cells, in contrast with acutely Hsp70 overexpressing cells, do not show augmentation of CTL-mediated apoptosis. Also, long-term induction of Hsp70 in cells with the doxycycline-inducible Hsp70 construct leads to abrogation of increased lysability. Because, furthermore, after heat shock the same permanently Hsp70 overexpressing cells show Hsp70 induction and increased lysability, it is hypothesized that acutely available Hsp70 is able to chaperone proteins that are involved in CTL-mediated apoptosis of target cells and to thereby improve their lysability. We also observed that permanent but not acute Hsp70 overexpression resulted in decreased levels of Hsc70, the constitutively expressed member of the Hsp70 family. Down-regulation of Hsc70 occurs at the post-transcriptional level and can be observed also after long-term induction of Hsp70 in cells containing the doxycycline-inducible expression system. Hsc70 down-regulation might reflect a functional integration of the overexpressed Hsp70 on the basis of a chaperone network so that only acute induction will provide Hsp70 that can improve tumor cell lysability. The implications of the differential effect of acute versus permanent Hsp70 overexpression for tumor therapy are discussed."],["dc.identifier.isi","000187450900023"],["dc.identifier.pmid","14678977"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/44826"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Assoc Cancer Research"],["dc.relation.issn","0008-5472"],["dc.title","Differential effect of acute and permanent heat shock protein 70 overexpression in tumor cells on lysability by cytotoxic T lymphocytes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","970"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","The Journal of Immunology"],["dc.bibliographiccitation.lastpage","975"],["dc.bibliographiccitation.volume","174"],["dc.contributor.author","Roos, Christian"],["dc.contributor.author","Dressel, Ralf"],["dc.contributor.author","Schmidt, B."],["dc.contributor.author","Gunther, E."],["dc.contributor.author","Walter, L."],["dc.date.accessioned","2018-11-07T08:32:31Z"],["dc.date.available","2018-11-07T08:32:31Z"],["dc.date.issued","2005"],["dc.description.abstract","The complement component C4 is well known for its complex genetics inhuman and mouse where it is part of a tandemly duplicated module. For the rat, no such information had been available until recently. A C4 gene duplication could be identified also in the rat, but the duplicated module maps similar to200 kb centromerically from the canonical C4-1 gene. In this study, we present the genomic organization of the two C4 gene-containing modules and the expression of the two C4 genes in the rat (Rattus norvegicus). The duplicated module contains an intact C4 gene as well as Cyp21 and Stk19 pseudogenes. Quantitative mRNA expression analyses revealed that both C4 genes are transcribed in various organs and tissues, but displaying ample differences of C4-1 and C4-2 expression. Most notably, C4-2 is not expressed in the liver. At variance to the mouse, the expression of the rat C4 genes does not exhibit any sex dependency. By using two-dimensional gel electrophoresis and mass spectrometry, products of both C4 genes could be identified in rat serum samples. These two rat C4 isotypes are nearly identical, but differ in a functionally important amino acid residue that is known to influence the functional properties of the C4 isotypes in human."],["dc.identifier.isi","000226360500048"],["dc.identifier.pmid","15634920"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17358"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Assoc Immunologists"],["dc.relation.issn","0022-1767"],["dc.title","The rat expresses two complement factor C4 proteins, but only one isotype is expressed in the liver"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]