Max-Planck-Institut für Experimentelle Medizin

[["dc.bibliographiccitation.firstpage","16522"],["dc.bibliographiccitation.issue","26"],["dc.bibliographiccitation.journal","Proceedings of the National Academy of Sciences"],["dc.bibliographiccitation.lastpage","16523"],["dc.bibliographiccitation.volume","99"],["dc.contributor.author","Brose, Nils"],["dc.contributor.author","Neher, Erwin"],["dc.date.accessioned","2017-09-07T11:45:11Z"],["dc.date.available","2017-09-07T11:45:11Z"],["dc.date.issued","2002"],["dc.identifier.doi","10.1073/pnas.022708199"],["dc.identifier.gro","3144145"],["dc.identifier.isi","000180101600006"],["dc.identifier.pmid","12486246"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1737"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Natl Acad Sciences"],["dc.relation.issn","0027-8424"],["dc.title","Specificity emerges in the dissection of diacylglycerol- and protein kinase C-mediated signalling pathways"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","letter_note"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1243"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Molecular Biology and Evolution"],["dc.bibliographiccitation.lastpage","1258"],["dc.bibliographiccitation.volume","37"],["dc.contributor.author","Maxeiner, Stephan"],["dc.contributor.author","Benseler, Fritz"],["dc.contributor.author","Krasteva-Christ, Gabriela"],["dc.contributor.author","Brose, Nils"],["dc.contributor.author","Südhof, Thomas C"],["dc.contributor.editor","Nowick, Katja"],["dc.date.accessioned","2022-03-01T11:46:46Z"],["dc.date.available","2022-03-01T11:46:46Z"],["dc.date.issued","2020"],["dc.description.abstract","Abstract Variants in genes encoding synaptic adhesion proteins of the neuroligin family, most notably neuroligin-4, are a significant cause of autism spectrum disorders in humans. Although human neuroligin-4 is encoded by two genes, NLGN4X and NLGN4Y, that are localized on the X-specific and male-specific regions of the two sex chromosomes, the chromosomal localization and full genomic sequence of the mouse Nlgn4 gene remain elusive. Here, we analyzed the neuroligin-4 genes of numerous rodent species by direct sequencing and bioinformatics, generated complete drafts of multiple rodent neuroligin-4 genes, and examined their evolution. Surprisingly, we find that the murine Nlgn4 gene is localized to the pseudoautosomal region (PAR) of the sex chromosomes, different from its human orthologs. We show that the sequence differences between various neuroligin-4 proteins are restricted to hotspots in which rodent neuroligin-4 proteins contain short repetitive sequence insertions compared with neuroligin-4 proteins from other species, whereas all other protein sequences are highly conserved. Evolutionarily, these sequence insertions initiate in the clade eumuroidea of the infraorder myomorpha and are additionally associated with dramatic changes in noncoding sequences and gene size. Importantly, these changes are not exclusively restricted to neuroligin-4 genes but reflect major evolutionary changes that substantially altered or even deleted genes from the PARs of both sex chromosomes. Our results show that despite the fact that the PAR in rodents and the neuroligin-4 genes within the rodent PAR underwent massive evolutionary changes, neuroligin-4 proteins maintained a highly conserved core structure, consistent with a substantial evolutionary pressure preserving its physiological function."],["dc.description.abstract","Abstract Variants in genes encoding synaptic adhesion proteins of the neuroligin family, most notably neuroligin-4, are a significant cause of autism spectrum disorders in humans. Although human neuroligin-4 is encoded by two genes, NLGN4X and NLGN4Y, that are localized on the X-specific and male-specific regions of the two sex chromosomes, the chromosomal localization and full genomic sequence of the mouse Nlgn4 gene remain elusive. Here, we analyzed the neuroligin-4 genes of numerous rodent species by direct sequencing and bioinformatics, generated complete drafts of multiple rodent neuroligin-4 genes, and examined their evolution. Surprisingly, we find that the murine Nlgn4 gene is localized to the pseudoautosomal region (PAR) of the sex chromosomes, different from its human orthologs. We show that the sequence differences between various neuroligin-4 proteins are restricted to hotspots in which rodent neuroligin-4 proteins contain short repetitive sequence insertions compared with neuroligin-4 proteins from other species, whereas all other protein sequences are highly conserved. Evolutionarily, these sequence insertions initiate in the clade eumuroidea of the infraorder myomorpha and are additionally associated with dramatic changes in noncoding sequences and gene size. Importantly, these changes are not exclusively restricted to neuroligin-4 genes but reflect major evolutionary changes that substantially altered or even deleted genes from the PARs of both sex chromosomes. Our results show that despite the fact that the PAR in rodents and the neuroligin-4 genes within the rodent PAR underwent massive evolutionary changes, neuroligin-4 proteins maintained a highly conserved core structure, consistent with a substantial evolutionary pressure preserving its physiological function."],["dc.identifier.doi","10.1093/molbev/msaa014"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/103791"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-531"],["dc.relation.eissn","1537-1719"],["dc.relation.issn","0737-4038"],["dc.title","Evolution of the Autism-Associated Neuroligin-4 Gene Reveals Broad Erosion of Pseudoautosomal Regions in Rodents"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1050"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Nature Neuroscience"],["dc.bibliographiccitation.lastpage","1059"],["dc.bibliographiccitation.volume","19"],["dc.contributor.author","Quintes, Susanne"],["dc.contributor.author","Brinkmann, Bastian G"],["dc.contributor.author","Ebert, Madlen"],["dc.contributor.author","Fröb, Franziska"],["dc.contributor.author","Kungl, Theresa"],["dc.contributor.author","Arlt, Friederike A"],["dc.contributor.author","Tarabykin, Victor"],["dc.contributor.author","Huylebroeck, Danny"],["dc.contributor.author","Meijer, Dies"],["dc.contributor.author","Suter, Ueli"],["dc.contributor.author","Wegner, Michael"],["dc.contributor.author","Sereda, Michael W"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.date.accessioned","2020-12-10T18:09:31Z"],["dc.date.available","2020-12-10T18:09:31Z"],["dc.date.issued","2016"],["dc.identifier.doi","10.1038/nn.4321"],["dc.identifier.eissn","1546-1726"],["dc.identifier.issn","1097-6256"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/73679"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Zeb2 is essential for Schwann cell differentiation, myelination and nerve repair"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","217"],["dc.bibliographiccitation.lastpage","236"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Krampe, Henning"],["dc.contributor.author","Sirén, Anna-Leena"],["dc.contributor.editor","Felthous, Alan"],["dc.contributor.editor","Sass, Henning"],["dc.date.accessioned","2017-09-07T11:46:20Z"],["dc.date.available","2017-09-07T11:46:20Z"],["dc.date.issued","2008"],["dc.identifier.gro","3150480"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7249"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.notes.submitter","chake"],["dc.publisher","Wiley"],["dc.publisher.place","Chichester"],["dc.relation.isbn","978-0-470-01185-0"],["dc.relation.ispartof","The International Handbook of Psychopathic Disorders and the Law, Vol. 1"],["dc.title","Brain trauma"],["dc.type","book_chapter"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2477"],["dc.bibliographiccitation.issue","13"],["dc.bibliographiccitation.journal","Cell Cycle"],["dc.bibliographiccitation.lastpage","2478"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Kawabe, Hiroshi"],["dc.contributor.author","Brose, Nils"],["dc.date.accessioned","2017-09-07T11:45:57Z"],["dc.date.available","2017-09-07T11:45:57Z"],["dc.date.issued","2010"],["dc.identifier.doi","10.4161/cc.9.13.12236"],["dc.identifier.gro","3142893"],["dc.identifier.isi","000281205400004"],["dc.identifier.pmid","20543564"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/348"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Landes Bioscience"],["dc.relation.issn","1538-4101"],["dc.title","The ubiquitin E3 ligase Nedd4-1 controls neurite development"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","letter_note"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","102"],["dc.bibliographiccitation.journal","Current Opinion in Neurobiology"],["dc.bibliographiccitation.lastpage","110"],["dc.bibliographiccitation.volume","42"],["dc.contributor.author","Schreiner, Dietmar"],["dc.contributor.author","Savas, Jeffrey N."],["dc.contributor.author","Herzog, Etienne"],["dc.contributor.author","Brose, Nils"],["dc.contributor.author","de Wit, Joris"],["dc.date.accessioned","2017-09-07T11:52:19Z"],["dc.date.available","2017-09-07T11:52:19Z"],["dc.date.issued","2017"],["dc.description.abstract","The neural connectome is a critical determinant of brain function. Circuits of precisely wired neurons, and the features of transmission at the synapses connecting them, are thought to dictate information processing in the brain. While recent technological advances now allow to define the anatomical and functional neural connectome at unprecedented resolution, the elucidation of the molecular mechanisms that establish the precise patterns of connectivity and the functional characteristics of synapses has remained challenging. Here, we describe the power and limitations of genetic approaches in the analysis of mechanisms that control synaptic connectivity and function, and discuss how recent methodological developments in proteomics might be used to elucidate the molecular synaptic connectome that is at the basis of the neural connectome."],["dc.identifier.doi","10.1016/j.conb.2016.12.004"],["dc.identifier.gro","3144893"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2568"],["dc.language.iso","en"],["dc.notes.intern","Crossref Import"],["dc.notes.status","final"],["dc.relation.issn","0959-4388"],["dc.title","Synapse biology in the ‘circuit-age’—paths toward molecular connectomics"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","427"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Journal of Cerebral Blood Flow and Metabolism"],["dc.bibliographiccitation.lastpage","430"],["dc.bibliographiccitation.volume","25"],["dc.contributor.author","Heyer, Andrea"],["dc.contributor.author","Hasselblatt, Martin"],["dc.contributor.author","von Ahsen, Nicolas"],["dc.contributor.author","Häfner, Heinz"],["dc.contributor.author","Sirén, Anna-Leena"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:46:18Z"],["dc.date.available","2017-09-07T11:46:18Z"],["dc.date.issued","2005"],["dc.description.abstract","Gender differences in neuropsychiatric disease are recognized but not well understood. Investigating the survival of primary rat hippocampal neurons in culture, we found significant and inverted gender differences on normoxia versus hypoxia. Male cells were more resistant under normoxia but more vulnerable under hypoxia than female cells. Male vulnerability pattern was acquired in cells from neonatally testosterone-primed females. Estrogens, acting via membrane receptors, had a higher neuroprotective power in male neurons, explained at least in part by the pronounced increase in estrogen receptor beta/alpha ratio during hypoxia in male cells only."],["dc.identifier.doi","10.1038/sj.jcbfm.9600056"],["dc.identifier.gro","3150469"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7237"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.issn","0271-678X"],["dc.subject","aromatase; estrogen receptor alpha; estrogen receptor beta; hippocampus; sex; testosterone"],["dc.title","In vitro gender differences in neuronal survival on hypoxia and in 17 beta-estradiol-mediated neuroprotection"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","411"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Nature Neuroscience"],["dc.bibliographiccitation.lastpage","413"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Nouvian, Régis"],["dc.contributor.author","Neef, Jakob"],["dc.contributor.author","Bulankina, Anna V"],["dc.contributor.author","Reisinger, Ellen"],["dc.contributor.author","Pangršič, Tina"],["dc.contributor.author","Frank, Thomas"],["dc.contributor.author","Sikorra, Stefan"],["dc.contributor.author","Brose, Nils"],["dc.contributor.author","Binz, Thomas"],["dc.contributor.author","Moser, Tobias"],["dc.date.accessioned","2017-09-07T11:44:19Z"],["dc.date.available","2017-09-07T11:44:19Z"],["dc.date.issued","2011"],["dc.description.abstract","SNARE proteins mediate membrane fusion. Neurosecretion depends on neuronal soluble NSF attachment protein receptors ( SNAREs; SNAP-25, syntaxin-1, and synaptobrevin-1 or synaptobrevin-2) and is blocked by neurotoxin-mediated cleavage or genetic ablation. We found that exocytosis in mouse inner hair cells (IHCs) was insensitive to neurotoxins and genetic ablation of neuronal SNAREs. mRNA, but no synaptically localized protein, of neuronal SNAREs was present in IHCs. Thus, IHC exocytosis is unconventional and may operate independently of neuronal SNAREs."],["dc.identifier.doi","10.1038/nn.2774"],["dc.identifier.gro","3142757"],["dc.identifier.isi","000288849400007"],["dc.identifier.pmid","21378973"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/196"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","1097-6256"],["dc.title","Exocytosis at the hair cell ribbon synapse apparently operates without neuronal SNARE proteins"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e51825"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Valero, María Ll."],["dc.contributor.author","Mello de Queiroz, Fernanda"],["dc.contributor.author","Stühmer, Walter"],["dc.contributor.author","Viana, Félix"],["dc.contributor.author","Pardo, Luis A."],["dc.date.accessioned","2019-07-09T11:54:06Z"],["dc.date.available","2019-07-09T11:54:06Z"],["dc.date.issued","2012-12-14"],["dc.description.abstract","Overexpression of the cation-permeable channel TRPM8 in prostate cancers might represent a novel opportunity for their treatment. Inhibitors of TRPM8 reduce the growth of prostate cancer cells. We have used two recently described and highly specific blockers, AMTB and JNJ41876666, and RNAi to determine the relevance of TRPM8 expression in the proliferation of non-tumor and tumor cells. Inhibition of the expression or function of the channel reduces proliferation rates and proliferative fraction in all tumor cells tested, but not of non-tumor prostate cells. We observed no consistent acceleration of growth after stimulation of the channel with menthol or icilin, indicating that basal TRPM8 expression is enough to sustain growth of prostate cancer cells."],["dc.format.extent","12"],["dc.identifier.doi","10.1371/journal.pone.0051825"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8457"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60572"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 2.5"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.5"],["dc.title","TRPM8 Ion Channels Differentially Modulate Proliferation and Cell Cycle Distribution of Normal and Cancer Prostate Cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","eLife"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Ripamonti, Silvia"],["dc.contributor.author","Ambrozkiewicz, Mateusz C."],["dc.contributor.author","Guzzi, Francesca"],["dc.contributor.author","Gravati, Marta"],["dc.contributor.author","Biella, Gerardo"],["dc.contributor.author","Bormuth, Ingo"],["dc.contributor.author","Hammer, Matthieu"],["dc.contributor.author","Tuffy, Liam P."],["dc.contributor.author","Sigler, Albrecht"],["dc.contributor.author","Kawabe, Hiroshi"],["dc.contributor.author","Nishimori, Katsuhiko"],["dc.contributor.author","Toselli, Mauro"],["dc.contributor.author","Brose, Nils"],["dc.contributor.author","Parenti, Marco"],["dc.contributor.author","Rhee, JeongSeop"],["dc.date.accessioned","2018-03-08T09:21:30Z"],["dc.date.available","2018-03-08T09:21:30Z"],["dc.date.issued","2017"],["dc.description.abstract","Beyond its role in parturition and lactation, oxytocin influences higher brain processes that control social behavior of mammals, and perturbed oxytocin signaling has been linked to the pathogenesis of several psychiatric disorders. However, it is still largely unknown how oxytocin exactly regulates neuronal function. We show that early, transient oxytocin exposure in vitro inhibits the development of hippocampal glutamatergic neurons, leading to reduced dendrite complexity, synapse density, and excitatory transmission, while sparing GABAergic neurons. Conversely, genetic elimination of oxytocin receptors increases the expression of protein components of excitatory synapses and excitatory synaptic transmission in vitro. In vivo, oxytocin-receptor-deficient hippocampal pyramidal neurons develop more complex dendrites, which leads to increased spine number and reduced γ-oscillations. These results indicate that oxytocin controls the development of hippocampal excitatory neurons and contributes to the maintenance of a physiological excitation/inhibition balance, whose disruption can cause neurobehavioral disturbances."],["dc.identifier.doi","10.7554/eLife.22466"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/12900"],["dc.language.iso","en"],["dc.notes.intern","GRO-Li-Import"],["dc.notes.status","final"],["dc.relation.doi","10.7554/eLife.22466"],["dc.relation.eissn","2050-084X"],["dc.title","Transient oxytocin signaling primes the development and function of excitatory hippocampal neurons"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]