Walter, Lutz

[["dc.bibliographiccitation.firstpage","409"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Immunogenetics"],["dc.bibliographiccitation.lastpage","418"],["dc.bibliographiccitation.volume","62"],["dc.contributor.author","Rosner, Cornelia"],["dc.contributor.author","Kruse, Philip H."],["dc.contributor.author","Luebke, Torben"],["dc.contributor.author","Walter, Lutz"],["dc.date.accessioned","2018-11-07T08:42:46Z"],["dc.date.available","2018-11-07T08:42:46Z"],["dc.date.issued","2010"],["dc.description.abstract","The MHC class I gene family of rhesus macaques is characterised by considerable gene duplications. While a HLA-C-orthologous gene is absent, the Mamu-A and in particular the Mamu-B genes have expanded, giving rise to plastic haplotypes with differential gene content. Although some of the rhesus macaque MHC class I genes are known to be associated with susceptibility/resistance to infectious diseases, the functional significance of duplicated Mamu-A and Mamu-B genes and the expression pattern of their encoded proteins are largely unknown. Here, we present data of the subcellular localization of AcGFP-tagged Mamu-A and Mamu-B molecules. We found strong cell surface and low intracellular expression for Mamu-A1, Mamu-A2 and Mamu-A3-encoded molecules as well as for Mamu-B 01704, Mamu-B 02101, Mamu-B 04801, Mamu-B 06002 and Mamu-B 13401. In contrast, weak cell surface and strong intracellular expression was seen for Mamu-A4 1403, Mamu-B 01202, Mamu-B 02804, Mamu-B 03002, Mamu-B 05704, Mamu-I 010201 and Mamu-I 0121. The different expression patterns were assigned to the antigen-binding alpha 1 and alpha 2 domains, suggesting failure of peptide binding is responsible for retaining 'intracellular' Mamu class I molecules in the endoplasmic reticulum. These findings indicate a diverse functional role of the duplicated rhesus macaque MHC class I genes."],["dc.identifier.doi","10.1007/s00251-010-0447-y"],["dc.identifier.isi","000278026700006"],["dc.identifier.pmid","20445972"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6705"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19777"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0093-7711"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Rhesus macaque MHC class I molecules show differential subcellular localizations (vol 62, pg 149, 2010)"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","149"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Immunogenetics"],["dc.bibliographiccitation.lastpage","158"],["dc.bibliographiccitation.volume","62"],["dc.contributor.author","Rosner, Cornelia"],["dc.contributor.author","Kruse, Philip H."],["dc.contributor.author","Luebke, Torben"],["dc.contributor.author","Walter, Lutz"],["dc.date.accessioned","2018-11-07T08:45:28Z"],["dc.date.available","2018-11-07T08:45:28Z"],["dc.date.issued","2010"],["dc.description.abstract","The MHC class I gene family of rhesus macaques is characterised by considerable gene duplications. While a HLA-C-orthologous gene is absent, the Mamu-A and in particular the Mamu-B genes have expanded, giving rise to plastic haplotypes with differential gene content. Although some of the rhesus macaque MHC class I genes are known to be associated with susceptibility/resistance to infectious diseases, the functional significance of duplicated Mamu-A and Mamu-B genes and the expression pattern of their encoded proteins are largely unknown. Here, we present data of the subcellular localization of AcGFP-tagged Mamu-A and Mamu-B molecules. We found strong cell surface and low intracellular expression for Mamu-A1, Mamu-A2 and Mamu-A3-encoded molecules as well as for Mamu-B 01704, Mamu-B 02101, Mamu-B 04801, Mamu-B 06002 and Mamu-B 13401. In contrast, weak cell surface and strong intracellular expression was seen for Mamu-A4 1403, Mamu-B 01202, Mamu-B 02804, Mamu-B 03002, Mamu-B 05704, Mamu-I 010201 and Mamu-I 0121. The different expression patterns were assigned to the antigen-binding alpha 1 and alpha 2 domains, suggesting failure of peptide binding is responsible for retaining 'intracellular' Mamu class I molecules in the endoplasmic reticulum. These findings indicate a diverse functional role of the duplicated rhesus macaque MHC class I genes."],["dc.identifier.doi","10.1007/s00251-010-0424-5"],["dc.identifier.isi","000274903800003"],["dc.identifier.pmid","20151120"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?goescholar/4144"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20447"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0093-7711"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Rhesus macaque MHC class I molecules show differential subcellular localizations"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["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","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.artnumber","600"],["dc.bibliographiccitation.journal","Frontiers in Immunology"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Albrecht, Christina"],["dc.contributor.author","Brameier, Markus"],["dc.contributor.author","Hermes, Meike"],["dc.contributor.author","Ansari, Aftab A."],["dc.contributor.author","Walter, Lutz"],["dc.contributor.author","Malzahn, Dörthe"],["dc.date.accessioned","2018-11-07T09:32:24Z"],["dc.date.available","2018-11-07T09:32:24Z"],["dc.date.issued","2014"],["dc.description.abstract","Killer cell immunoglobulin-like receptors (KIR) regulate the activity of natural killer (NK) cells and have been shown to be associated with susceptibility to a number of human infectious diseases. Here, we analyzed NK cell function and genetic associations in a cohort of 52 rhesus macaques experimentally infected with SIVmac and subsequently stratified into high viral load (HVL) and low viral load (LVL) plasma viral loads at set point. This stratification coincided with fast (HVL) and slow (LVL) disease progression indicated by the disease course and critical clinical parameters including CD4+ T cell counts. HVL animals revealed sustained proliferation of NK cells but distinct loss of peripheral blood NK cell numbers and lytic function. Genetic analyses revealed that KIR genes 3DL05, 3DS05, and 3DL10 as well as 3DSW08, 3DLW03, and 3DSW09 are correlated, most likely due to underlying haplotypes. SIV-infection outcome associated with presence of transcripts for two inhibitory KIR genes (KIR3DL02, KIR3DL10) and three activating KIR genes (KIR3DSW08, KIR3DS02, KIR3DS05). Presence of KIR3DLO2 and KIR3DSW08 was associated with LVL outcome, whereas presence of KIR3DS02 was associated with HVL outcome. Furthermore, we identified epistasis between KIR and MHC class I alleles as the transcript presence of the correlated genes KIR3DL05, KIR3DS05, and KIR3DL10 increased HVL risk when Mamu-B 012 transcripts were also present or when Mamu-Al 001 transcripts were absent. These genetic associations were mirrored by changes in the numbers, the level of proliferation, and lytic capabilities of NK cells as well as overall survival time and gastro-intestinal tissue viral load."],["dc.description.sponsorship","NIH HHS [P51 OD011132]"],["dc.identifier.doi","10.3389/fimmu.2014.00600"],["dc.identifier.isi","000354531900001"],["dc.identifier.pmid","25506344"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11789"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31752"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Frontiers Media S.A."],["dc.relation.eissn","1664-3224"],["dc.relation.issn","1664-3224"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Progression to AIDS in SIV-infected rhesus macaques is associated with distinct KIR and MHC class 1 polymorphisms and NK cell dysfunction"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","79"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Frontiers in zoology"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Liu, Guangjian"],["dc.contributor.author","Walter, Lutz"],["dc.contributor.author","Tang, Suni"],["dc.contributor.author","Tan, Xinxin"],["dc.contributor.author","Shi, Fanglei"],["dc.contributor.author","Pan, Huijuan"],["dc.contributor.author","Roos, Christian"],["dc.contributor.author","Liu, Zhijin"],["dc.contributor.author","Li, Ming"],["dc.date.accessioned","2019-07-09T11:41:12Z"],["dc.date.available","2019-07-09T11:41:12Z"],["dc.date.issued","2014"],["dc.description.abstract","BACKGROUND: Umami and sweet tastes are two important basic taste perceptions that allow animals to recognize diets with nutritious carbohydrates and proteins, respectively. Until recently, analyses of umami and sweet taste were performed on various domestic and wild animals. While most of these studies focused on the pseudogenization of taste genes, which occur mostly in carnivores and species with absolute feeding specialization, omnivores and herbivores were more or less neglected. Catarrhine primates are a group of herbivorous animals (feeding mostly on plants) with significant divergence in dietary preference, especially the specialized folivorous Colobinae. Here, we conducted the most comprehensive investigation to date of selection pressure on sweet and umami taste genes (TAS1Rs) in catarrhine primates to test whether specific adaptive evolution occurred during their diversification, in association with particular plant diets. RESULTS: We documented significant relaxation of selective constraints on sweet taste gene TAS1R2 in the ancestral branch of Colobinae, which might correlate with their unique ingestion and digestion of leaves. Additionally, we identified positive selection acting on Cercopithecidae lineages for the umami taste gene TAS1R1, on the Cercopithecinae and extant Colobinae and Hylobatidae lineages for TAS1R2, and on Macaca lineages for TAS1R3. Our research further identified several site mutations in Cercopithecidae, Colobinae and Pygathrix, which were detected by previous studies altering the sensitivity of receptors. The positively selected sites were located mostly on the extra-cellular region of TAS1Rs. Among these positively selected sites, two vital sites for TAS1R1 and four vital sites for TAS1R2 in extra-cellular region were identified as being responsible for the binding of certain sweet and umami taste molecules through molecular modelling and docking. CONCLUSIONS: Our results suggest that episodic and differentiated adaptive evolution of TAS1Rs pervasively occurred in catarrhine primates, most concentrated upon the extra-cellular region of TAS1Rs."],["dc.format.extent","16"],["dc.identifier.doi","10.1186/s12983-014-0079-4"],["dc.identifier.pmid","25389445"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11833"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58372"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1742-9994"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Differentiated adaptive evolution, episodic relaxation of selective constraints, and pseudogenization of umami and sweet taste genes TAS1Rs in catarrhine primates."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e64936"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Hermes, Meike"],["dc.contributor.author","Albrecht, Christina"],["dc.contributor.author","Schrod, Annette"],["dc.contributor.author","Brameier, Markus"],["dc.contributor.author","Walter, Lutz"],["dc.date.accessioned","2019-07-09T11:54:24Z"],["dc.date.available","2019-07-09T11:54:24Z"],["dc.date.issued","2013-05-22"],["dc.description.abstract","The expression of killer cell immunoglobulin-like receptors (KIR) on lymphocytes of rhesus macaques and other Old World monkeys was unknown so far. We used our recently established monoclonal anti-rhesus macaque KIR antibodies in multicolour flow cytometry for phenotypic characterization of KIR protein expression on natural killer (NK) cells and T cell subsets of rhesus macaques, cynomolgus macaques, hamadryas baboons, and African green monkeys. Similar to human KIR, we found clonal expression patterns of KIR on NK and T cell subsets in rhesus macaques and differences between individuals using pan-KIR3D antibody 1C7 and antibodies specific for single KIR. Similar results were obtained with lymphocytes from the other studied species. Notably, African green monkeys show only a low frequency of KIR3D expressed on CD8+ abT cells. Contrasting human NK cells are KIR-positive CD56bright NK cells and frequencies of KIR-expressing NK cells that are independent of the presence of their cognate MHC class I ligands in rhesus macaques. Interestingly, the frequency of KIR-expressing cells and the expression strength of KIR3D are correlated in cd T cells of rhesus macaques and CD8+ abT cells of baboons."],["dc.format.extent","10"],["dc.identifier.doi","10.1371/journal.pone.0064936"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9109"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60652"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY-NC-ND 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/3.0"],["dc.title","Expression Patterns of Killer Cell Immunoglobulin-Like Receptors (KIR) of NK-Cell and T-Cell Subsets in Old World Monkeys"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","19"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Genome Medicine"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Wilson, Gareth A"],["dc.contributor.author","Butcher, Lee M"],["dc.contributor.author","Foster, Holly R"],["dc.contributor.author","Feber, Andrew"],["dc.contributor.author","Roos, Christian"],["dc.contributor.author","Walter, Lutz"],["dc.contributor.author","Woszczek, Grzegorz"],["dc.contributor.author","Beck, Stephan"],["dc.contributor.author","Bell, Christopher G"],["dc.date.accessioned","2019-07-09T11:39:42Z"],["dc.date.available","2019-07-09T11:39:42Z"],["dc.date.issued","2014"],["dc.description.abstract","Background Common human diseases are caused by the complex interplay of genetic susceptibility as well as environmental factors. Due to the environment’s influence on the epigenome, and therefore genome function, as well as conversely the genome’s facilitative effect on the epigenome, analysis of this level of regulation may increase our knowledge of disease pathogenesis. Methods In order to identify human-specific epigenetic influences, we have performed a novel genome-wide DNA methylation analysis comparing human, chimpanzee and rhesus macaque. Results We have identified that the immunological Leukotriene B4 receptor (LTB4R, BLT1 receptor) is the most epigenetically divergent human gene in peripheral blood in comparison with other primates. This difference is due to the co-ordinated active state of human-specific hypomethylation in the promoter and human-specific increased gene body methylation. This gene is significant in innate immunity and the LTB4/LTB4R pathway is involved in the pathogenesis of the spectrum of human inflammatory diseases. This finding was confirmed by additional neutrophil-only DNA methylome and lymphoblastoid H3K4me3 chromatin comparative data. Additionally we show through functional analysis that this receptor has increased expression and a higher response to the LTB4 ligand in human versus rhesus macaque peripheral blood mononuclear cells. Genome-wide we also find human species-specific differentially methylated regions (human s-DMRs) are more prevalent in CpG island shores than within the islands themselves, and within the latter are associated with the CTCF motif. Conclusions This result further emphasises the exclusive nature of the human immunological system, its divergent adaptation even from very closely related primates, and the power of comparative epigenomics to identify and understand human uniqueness."],["dc.identifier.doi","10.1186/gm536"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12726"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58027"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 2.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.0"],["dc.title","Human-specific epigenetic variation in the immunological Leukotriene B4 Receptor (LTB4R/BLT1) implicated in common inflammatory diseases"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.issue","17"],["dc.bibliographiccitation.journal","BMC evolutionary biology"],["dc.bibliographiccitation.lastpage","13"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Andriaholinirina, Nicole"],["dc.contributor.author","Fausser, Jean-Luc"],["dc.contributor.author","Roos, Christian"],["dc.contributor.author","Zinner, Dietmar"],["dc.contributor.author","Thalmann, Urs"],["dc.contributor.author","Rabarivola, Clément"],["dc.contributor.author","Ravoarimanana, Iary"],["dc.contributor.author","Ganzhorn, Jörg U."],["dc.contributor.author","Meier, Bernhard"],["dc.contributor.author","Hilgartner, Roland"],["dc.contributor.author","Walter, Lutz"],["dc.contributor.author","Zaramody, Alphonse"],["dc.contributor.author","Langer, Christoph"],["dc.contributor.author","Hahn, Thomas"],["dc.contributor.author","Zimmermann, Elke"],["dc.contributor.author","Radespiel, Ute"],["dc.contributor.author","Craul, Mathias"],["dc.contributor.author","Tomiuk, Jürgen"],["dc.contributor.author","Tattersall, Ian"],["dc.contributor.author","Rumpler, Yves"],["dc.date.accessioned","2019-07-09T11:52:29Z"],["dc.date.available","2019-07-09T11:52:29Z"],["dc.date.issued","2006"],["dc.description.abstract","Background: The number of species within the Malagasy genus Lepilemur and their phylogenetic relationships is disputed and controversial. In order to establish their evolutionary relationships, a comparative cytogenetic and molecular study was performed. We sequenced the complete mitochondrial cytochrome b gene (1140 bp) from 68 individuals representing all eight sportive lemur species and most major populations, and compared the results with those obtained from cytogenetic studies derived from 99 specimens. Results: Interspecific genetic variation, diagnostic characters and significantly supported phylogenetic relationships were obtained from the mitochondrial sequence data and are in agreement with cytogenetic information. The results confirm the distinctiveness of Lepilemur ankaranensis, L. dorsalis, L. edwardsi, L. leucopus, L. microdon, L. mustelinus, L. ruficaudatus and L. septentrionalis on species level. Additionally, within L. ruficaudatus large genetic differences were observed among different geographic populations. L. dorsalis from Sahamalaza Peninsula and from the Ambanja/Nosy Be region are paraphyletic, with the latter forming a sister group to L. ankaranensis."],["dc.identifier.doi","10.1186/1471-2148-6-17"],["dc.identifier.fs","42806"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/4397"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60200"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","590"],["dc.subject.ddc","599"],["dc.subject.ddc","610"],["dc.subject.ddc","599.8"],["dc.title","Molecular phylogeny and taxonomic revision of the sportive lemurs (Lepilemur, Primates)"],["dc.title.alternative","Research article"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]