Hammer, Christian

[["dc.bibliographiccitation.firstpage","738"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","American journal of human genetics"],["dc.bibliographiccitation.lastpage","743"],["dc.bibliographiccitation.volume","97"],["dc.contributor.author","Hammer, Christian"],["dc.contributor.author","Begemann, Martin"],["dc.contributor.author","McLaren, P. J."],["dc.contributor.author","Bartha, István"],["dc.contributor.author","Michel, Angelika"],["dc.contributor.author","Klose, Beate"],["dc.contributor.author","Schmitt, Corinna"],["dc.contributor.author","Waterboer, Tim"],["dc.contributor.author","Pawlita, Michael"],["dc.contributor.author","Schulz, Thomas F."],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Fellay, Jacques"],["dc.date.accessioned","2017-09-07T11:46:17Z"],["dc.date.available","2017-09-07T11:46:17Z"],["dc.date.issued","2015"],["dc.description.abstract","The magnitude of the human antibody response to viral antigens is highly variable. To explore the human genetic contribution to this variability, we performed genome-wide association studies of the immunoglobulin G response to 14 pathogenic viruses in 2,363 immunocompetent adults. Significant associations were observed in the major histocompatibility complex region on chromosome 6 for influenza A virus, Epstein-Barr virus, JC polyomavirus, and Merkel cell polyomavirus. Using local imputation and fine mapping, we identified specific amino acid residues in human leucocyte antigen (HLA) class II proteins as the most probable causal variants underlying these association signals. Common HLA-DRβ1 haplotypes showed virus-specific patterns of humoral-response regulation. We observed an overlap between variants affecting the humoral response to influenza A and EBV and variants previously associated with autoimmune diseases related to these viruses. The results of this study emphasize the central and pathogen-specific role of HLA class II variation in the modulation of humoral immune response to viral antigens in humans."],["dc.identifier.doi","10.1016/j.ajhg.2015.09.008"],["dc.identifier.gro","3150467"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12609"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7235"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation.issn","0002-9297"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Amino acid variation in HLA class II proteins is a major determinant of humoral response to common viruses"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1143"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Molecular Psychiatry"],["dc.bibliographiccitation.lastpage","1149"],["dc.bibliographiccitation.volume","19"],["dc.contributor.author","Hammer, Christian"],["dc.contributor.author","Stepniak, Beata"],["dc.contributor.author","Schneider, Anja"],["dc.contributor.author","Papiol, Sergi"],["dc.contributor.author","Tantra, Martesa"],["dc.contributor.author","Begemann, Martin"],["dc.contributor.author","Sirén, Anna-Leena"],["dc.contributor.author","Pardo, Luis A."],["dc.contributor.author","Sperling, Swetlana"],["dc.contributor.author","Mohd Jofrry, Sue"],["dc.contributor.author","Gurvich, Artem"],["dc.contributor.author","Jensen, Niels"],["dc.contributor.author","Ostmeier, Katrin"],["dc.contributor.author","Lühder, F."],["dc.contributor.author","Probst, Christian"],["dc.contributor.author","Martens, Henrik"],["dc.contributor.author","Gillis, M."],["dc.contributor.author","Saher, Gesine"],["dc.contributor.author","Assogna, F."],["dc.contributor.author","Spalletta, Gianfranco"],["dc.contributor.author","Stöcker, W."],["dc.contributor.author","Schulz, Thomas F."],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:46:37Z"],["dc.date.available","2017-09-07T11:46:37Z"],["dc.date.issued","2014"],["dc.description.abstract","In 2007, a multifaceted syndrome, associated with anti-NMDA receptor autoantibodies (NMDAR-AB) of immunoglobulin-G isotype, has been described, which variably consists of psychosis, epilepsy, cognitive decline and extrapyramidal symptoms. Prevalence and significance of NMDAR-AB in complex neuropsychiatric disease versus health, however, have remained unclear. We tested sera of 2817 subjects (1325 healthy, 1081 schizophrenic, 263 Parkinson and 148 affective-disorder subjects) for presence of NMDAR-AB, conducted a genome-wide genetic association study, comparing AB carriers versus non-carriers, and assessed their influenza AB status. For mechanistic insight and documentation of AB functionality, in vivo experiments involving mice with deficient blood-brain barrier (ApoE(-/-)) and in vitro endocytosis assays in primary cortical neurons were performed. In 10.5% of subjects, NMDAR-AB (NR1 subunit) of any immunoglobulin isotype were detected, with no difference in seroprevalence, titer or in vitro functionality between patients and healthy controls. Administration of extracted human serum to mice influenced basal and MK-801-induced activity in the open field only in ApoE(-/-) mice injected with NMDAR-AB-positive serum but not in respective controls. Seropositive schizophrenic patients with a history of neurotrauma or birth complications, indicating an at least temporarily compromised blood-brain barrier, had more neurological abnormalities than seronegative patients with comparable history. A common genetic variant (rs524991, P=6.15E-08) as well as past influenza A (P=0.024) or B (P=0.006) infection were identified as predisposing factors for NMDAR-AB seropositivity. The >10% overall seroprevalence of NMDAR-AB of both healthy individuals and patients is unexpectedly high. Clinical significance, however, apparently depends on association with past or present perturbations of blood-brain barrier function."],["dc.identifier.doi","10.1038/mp.2013.110"],["dc.identifier.gro","3150565"],["dc.identifier.pmid","23999527"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7339"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.title","Neuropsychiatric disease relevance of circulating anti-NMDA receptor autoantibodies depends on blood-brain barrier integrity"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","144"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Annals of Neurology"],["dc.bibliographiccitation.lastpage","151"],["dc.bibliographiccitation.volume","79"],["dc.contributor.author","Castillo-Gomez, Esther"],["dc.contributor.author","Kästner, Anne"],["dc.contributor.author","Steiner, Johann"],["dc.contributor.author","Schneider, Anja"],["dc.contributor.author","Hettling, Bilke"],["dc.contributor.author","Poggi, Giulia"],["dc.contributor.author","Ostehr, Kristin"],["dc.contributor.author","Uhr, Manfred"],["dc.contributor.author","Asif, Abdul R."],["dc.contributor.author","Matzke, Mike"],["dc.contributor.author","Schmidt, Ulrike"],["dc.contributor.author","Pfander, Viktoria"],["dc.contributor.author","Hammer, Christian"],["dc.contributor.author","Schulz, Thomas F."],["dc.contributor.author","Binder, Lutz"],["dc.contributor.author","Stöcker, Winfried"],["dc.contributor.author","Weber, Frank"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:46:35Z"],["dc.date.available","2017-09-07T11:46:35Z"],["dc.date.issued","2016"],["dc.description.abstract","Autoantibodies (AB) against N-methyl-D-aspartate receptor subunit NR1 (NMDAR1) are highly seroprevalent in health and disease. Symptomatic relevance may arise upon compromised blood–brain barrier (BBB). However, it remained unknown whether circulating NMDAR1 AB appear in the cerebrospinal fluid (CSF). Of n = 271 subjects with CSF–serum pairs, 26 were NMDAR1 AB seropositive, but only 1 was CSF positive. Contrariwise, tetanus AB (non–brain-binding) were present in serum and CSF of all subjects, with CSF levels higher upon BBB dysfunction. Translational mouse experiments proved the hypothesis that the brain acts as an ‘immunoprecipitator’; simultaneous injection of NMDAR1 AB and the non–brain-binding green fluorescent protein AB resulted in high detectability of the former in brain and the latter in CSF."],["dc.identifier.doi","10.1002/ana.24545"],["dc.identifier.gro","3150536"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7309"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.notes.submitter","chake"],["dc.relation.issn","0364-5134"],["dc.title","The brain as immunoprecipitator of serum autoantibodies against N-Methyl-D-aspartate receptor subunit NR1"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","26"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Molecular Medicine"],["dc.bibliographiccitation.lastpage","37"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Hammer, Christian"],["dc.contributor.author","Wanitchakool, Podchanart"],["dc.contributor.author","Sirianant, Lalida"],["dc.contributor.author","Papiol, Sergi"],["dc.contributor.author","Monnheimer, Mathieu"],["dc.contributor.author","Faria, Diana"],["dc.contributor.author","Ousingsawat, Jiraporn"],["dc.contributor.author","Schramek, Natalie"],["dc.contributor.author","Schmitt, Corinna"],["dc.contributor.author","Margos, Gabriele"],["dc.contributor.author","Michel, Angelika"],["dc.contributor.author","Kraiczy, Peter"],["dc.contributor.author","Pawlita, Michael"],["dc.contributor.author","Schreiber, Rainer"],["dc.contributor.author","Schulz, Thomas F."],["dc.contributor.author","Fingerle, Volker"],["dc.contributor.author","Tumani, Hayrettin"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Kunzelmann, Karl"],["dc.date.accessioned","2017-09-07T11:46:14Z"],["dc.date.available","2017-09-07T11:46:14Z"],["dc.date.issued","2015"],["dc.description.abstract","In a first genome-wide association study (GWAS) approach to anti-Borrelia seropositivity, we identified two significant single nucleotide polymorphisms (SNPs) (rs17850869, P = 4.17E-09; rs41289586, P = 7.18E-08). Both markers, located on chromosomes 16 and 3, respectively, are within or close to genes previously connected to spinocerebellar ataxia. The risk SNP rs41289586 represents a missense variant (R263H) of anoctamin 10 (ANO10), a member of a protein family encoding Cl(-) channels and phospholipid scramblases. ANO10 augments volume-regulated Cl(-) currents (IHypo) in Xenopus oocytes, HEK293 cells, lymphocytes and macrophages and controls volume regulation by enhancing regulatory volume decrease (RVD). ANO10 supports migration of macrophages and phagocytosis of spirochetes. The R263H variant is inhibitory on IHypo, RVD and intracellular Ca(2+) signals, which may delay spirochete clearance, thereby sensitizing adaptive immunity. Our data demonstrate for the first time that ANO10 has a central role in innate immune defense against Borrelia infection."],["dc.identifier.doi","10.2119/molmed.2014.00219"],["dc.identifier.gro","3150465"],["dc.identifier.pmid","25730773"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7233"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.title","A coding variant of ANO10, affecting volume regulation of macrophages, is associated with Borrelia seropositivity"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","213"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","CardioVascular and interventional radiology"],["dc.bibliographiccitation.lastpage","219"],["dc.bibliographiccitation.volume","42"],["dc.contributor.author","Uller, W."],["dc.contributor.author","Hammer, S."],["dc.contributor.author","Wildgruber, M."],["dc.contributor.author","Müller-Wille, R."],["dc.contributor.author","Goessmann, H."],["dc.contributor.author","Wohlgemuth, W. A."],["dc.date.accessioned","2020-12-10T14:10:01Z"],["dc.date.available","2020-12-10T14:10:01Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1007/s00270-018-2099-5"],["dc.identifier.eissn","1432-086X"],["dc.identifier.issn","0174-1551"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/70641"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Radiofrequency Ablation of the Marginal Venous System in Patients with Venous Malformations"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e254"],["dc.bibliographiccitation.journal","Translational Psychiatry"],["dc.bibliographiccitation.volume","3"],["dc.contributor.author","El-Kordi, Ahmed"],["dc.contributor.author","Kästner, Anne"],["dc.contributor.author","Grube, Sabrina"],["dc.contributor.author","Klugmann, M."],["dc.contributor.author","Begemann, Martin"],["dc.contributor.author","Sperling, Swetlana"],["dc.contributor.author","Hammerschmidt, Kurt"],["dc.contributor.author","Hammer, Christian"],["dc.contributor.author","Stepniak, Beata"],["dc.contributor.author","Patzig, Julia"],["dc.contributor.author","Monasterio-Schrader, P. D."],["dc.contributor.author","Strenzke, N."],["dc.contributor.author","Flügge, G."],["dc.contributor.author","Werner, Hauke B."],["dc.contributor.author","Pawlak, R."],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:46:37Z"],["dc.date.available","2017-09-07T11:46:37Z"],["dc.date.issued","2013"],["dc.description.abstract","Claustrophobia, the well-known fear of being trapped in narrow/closed spaces, is often considered a conditioned response to traumatic experience. Surprisingly, we found that mutations affecting a single gene, encoding a stress-regulated neuronal protein, can cause claustrophobia. Gpm6a-deficient mice develop normally and lack obvious behavioral abnormalities. However, when mildly stressed by single-housing, these mice develop a striking claustrophobia-like phenotype, which is not inducible in wild-type controls, even by severe stress. The human GPM6A gene is located on chromosome 4q32-q34, a region linked to panic disorder. Sequence analysis of 115 claustrophobic and non-claustrophobic subjects identified nine variants in the noncoding region of the gene that are more frequent in affected individuals (P=0.028). One variant in the 3'untranslated region was linked to claustrophobia in two small pedigrees. This mutant mRNA is functional but cannot be silenced by neuronal miR124 derived itself from a stress-regulated transcript. We suggest that loosing dynamic regulation of neuronal GPM6A expression poses a genetic risk for claustrophobia."],["dc.format.extent","12"],["dc.identifier.doi","10.1038/tp.2013.28"],["dc.identifier.gro","3150562"],["dc.identifier.pmid","23632458"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10616"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7336"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.rights","CC BY-NC-SA 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-sa/3.0"],["dc.subject","chromosome 4; GPM6A; human pedigree; miR124; mouse mutant; panic disorder"],["dc.title","A single gene defect causing claustrophobia"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","82"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Annals of Neurology"],["dc.bibliographiccitation.lastpage","94"],["dc.bibliographiccitation.volume","76"],["dc.contributor.author","Dahm, Liane"],["dc.contributor.author","Ott, Christoph"],["dc.contributor.author","Steiner, Johann"],["dc.contributor.author","Stepniak, Beata"],["dc.contributor.author","Teegen, Bianca"],["dc.contributor.author","Saschenbrecker, Sandra"],["dc.contributor.author","Hammer, Christian"],["dc.contributor.author","Borowski, Kathrin"],["dc.contributor.author","Begemann, Martin"],["dc.contributor.author","Lemke, Sandra"],["dc.contributor.author","Rentzsch, Kristin"],["dc.contributor.author","Probst, Christian"],["dc.contributor.author","Martens, Henrik"],["dc.contributor.author","Wienands, Jürgen"],["dc.contributor.author","Spalletta, Gianfranco"],["dc.contributor.author","Weißenborn, Karin"],["dc.contributor.author","Stöcker, Winfried"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:46:34Z"],["dc.date.available","2017-09-07T11:46:34Z"],["dc.date.issued","2014"],["dc.description.abstract","ObjectiveWe previously reported an unexpectedly high seroprevalence (∼10%) of N-methyl-D-aspartate-receptor subunit-NR1 (NMDAR1) autoantibodies (AB) in healthy and neuropsychiatrically ill subjects (N = 2,817). This finding challenges an unambiguous causal relationship of serum AB with brain disease. To test whether similar results would be obtained for other brain antigen-directed AB previously connected with pathological conditions, we systematically screened serum samples of 4,236 individuals.MethodsSerum samples of healthy (n = 1,703) versus neuropsychiatrically ill subjects (schizophrenia, affective disorders, stroke, Parkinson disease, amyotrophic lateral sclerosis, personality disorder; total n = 2,533) were tested. For analysis based on indirect immunofluorescence, we used biochip mosaics of frozen brain sections (rat, monkey) and transfected HEK293 cells expressing respective recombinant target antigens.ResultsSeroprevalence of all screened AB was comparable in healthy and ill individuals. None of them, however, reached the abundance of NMDAR1 AB (again ∼10%; immunoglobulin [Ig] G ∼1%). Appreciable frequency was noted for AB against amphiphysin (2.0%), ARHGAP26 (1.3%), CASPR2 (0.9%), MOG (0.8%), GAD65 (0.5%), Ma2 (0.5%), Yo (0.4%), and Ma1 (0.4%), with titers and Ig class distribution similar among groups. All other AB were found in ≤0.1% of individuals (anti–AMPAR-1/2, AQP4, CV2, Tr/DNER, DPPX-IF1, GABAR-B1/B2, GAD67, GLRA1b, GRM1, GRM5, Hu, LGl1, recoverin, Ri, ZIC4). The predominant Ig class depended on antigen location, with intracellular epitopes predisposing to IgG (chi-square = 218.91, p = 2.8 × 10−48).InterpretationTo conclude, the brain antigen-directed AB tested here are comparably detectable in healthy subjects and the disease groups studied here, thus questioning an upfront pathological role of these serum AB."],["dc.identifier.doi","10.1002/ana.24189"],["dc.identifier.gro","3150539"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7312"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.title","Seroprevalence of autoantibodies against brain antigens in health and disease"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1054"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Molecular Psychiatry"],["dc.bibliographiccitation.lastpage","1056"],["dc.bibliographiccitation.volume","19"],["dc.contributor.author","Hammer, Christian"],["dc.contributor.author","Zerche, M."],["dc.contributor.author","Schneider, A."],["dc.contributor.author","Begemann, Martin"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:46:21Z"],["dc.date.available","2017-09-07T11:46:21Z"],["dc.date.issued","2014"],["dc.identifier.doi","10.1038/mp.2014.52"],["dc.identifier.gro","3150495"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7266"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.title","Apolipoprotein E4 carrier status plus circulating anti-NMDAR1 autoantibodies: association with schizoaffective disorder"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e362"],["dc.bibliographiccitation.journal","Translational Psychiatry"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Papiol, Sergi"],["dc.contributor.author","Mitjans, Marina"],["dc.contributor.author","Assogna, F."],["dc.contributor.author","Piras, F."],["dc.contributor.author","Hammer, Christian"],["dc.contributor.author","Caltagirone, Carlo"],["dc.contributor.author","Arias, B."],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Spalletta, Gianfranco"],["dc.date.accessioned","2017-09-07T11:46:23Z"],["dc.date.available","2017-09-07T11:46:23Z"],["dc.date.issued","2014"],["dc.description.abstract","A recent publication reported an exciting polygenic effect of schizophrenia (SCZ) risk variants, identified by a large genome-wide association study (GWAS), on total brain and white matter volumes in schizophrenic patients and, even more prominently, in healthy subjects. The aim of the present work was to replicate and then potentially extend these findings. According to the original publication, polygenic risk scores-using single nucleotide polymorphism (SNP) information of SCZ GWAS-(polygenic SCZ risk scores; PSS) were calculated in 122 healthy subjects, enrolled in a structural magnetic resonance imaging (MRI) study. These scores were computed based on P-values and odds ratios available through the Psychiatric GWAS Consortium. In addition, polygenic white matter scores (PWM) were calculated, using the respective SNP subset in the original publication. None of the polygenic scores, either PSS or PWM, were found to be associated with total brain, white matter or gray matter volume in our replicate sample. Minor differences between the original and the present study that might have contributed to lack of reproducibility (but unlikely explain it fully), are number of subjects, ethnicity, age distribution, array technology, SNP imputation quality and MRI scanner type. In contrast to the original publication, our results do not reveal the slightest signal of association of the described sets of GWAS-identified SCZ risk variants with brain volumes in adults. Caution is indicated in interpreting studies building on polygenic risk scores without replication sample."],["dc.identifier.doi","10.1038/tp.2013.126"],["dc.identifier.gro","3150493"],["dc.identifier.pmid","24548877"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11921"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7263"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.rights","CC BY-NC-ND 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/3.0"],["dc.title","Polygenic determinants of white matter volume derived from GWAS lack reproducibility in a replicate sample"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","662"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","EMBO Molecular Medicine"],["dc.bibliographiccitation.lastpage","684"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Tantra, Martesa"],["dc.contributor.author","Hammer, Christian"],["dc.contributor.author","Kästner, Anne"],["dc.contributor.author","Dahm, Liane"],["dc.contributor.author","Begemann, Martin"],["dc.contributor.author","Bodda, Chiranjeevi"],["dc.contributor.author","Hammerschmidt, Kurt"],["dc.contributor.author","Giegling, Ina"],["dc.contributor.author","Stepniak, Beata"],["dc.contributor.author","Castillo Venzor, Aracely"],["dc.contributor.author","Konte, Bettina"],["dc.contributor.author","Erbaba, Begun"],["dc.contributor.author","Hartmann, Annette M."],["dc.contributor.author","Tarami, Asieh"],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Rujescu, Dan"],["dc.contributor.author","Mannan, Ashraf U."],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:46:35Z"],["dc.date.available","2017-09-07T11:46:35Z"],["dc.date.issued","2014"],["dc.description.abstract","The X-chromosomal MECP2/Mecp2 gene encodes methyl-CpG-binding protein 2, a transcriptional activator and repressor regulating many other genes. We discovered in male FVB/N mice that mild (~50%) transgenic overexpression of Mecp2 enhances aggression. Surprisingly, when the same transgene was expressed in C57BL/6N mice, transgenics showed reduced aggression and social interaction. This suggests that Mecp2 modulates aggressive social behavior. To test this hypothesis in humans, we performed a phenotype-based genetic association study (PGAS) in >1000 schizophrenic individuals. We found MECP2 SNPs rs2239464 (G/A) and rs2734647 (C/T; 3'UTR) associated with aggression, with the G and C carriers, respectively, being more aggressive. This finding was replicated in an independent schizophrenia cohort. Allele-specific MECP2 mRNA expression differs in peripheral blood mononuclear cells by ~50% (rs2734647: C > T). Notably, the brain-expressed, species-conserved miR-511 binds to MECP2 3'UTR only in T carriers, thereby suppressing gene expression. To conclude, subtle MECP2/Mecp2 expression alterations impact aggression. While the mouse data provides evidence of an interaction between genetic background and mild Mecp2 overexpression, the human data convey means by which genetic variation affects MECP2 expression and behavior."],["dc.identifier.doi","10.1002/emmm.201303744"],["dc.identifier.gro","3150551"],["dc.identifier.pmid","24648499"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11691"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7325"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Mild expression differences of MECP2 influencing aggressive social behavior"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]