Zhou, Xunlei

[["dc.bibliographiccitation.firstpage","412"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Disease Models & Mechanisms"],["dc.bibliographiccitation.lastpage","418"],["dc.bibliographiccitation.volume","2"],["dc.contributor.author","Miró, Xavier"],["dc.contributor.author","Zhou, Xunlei"],["dc.contributor.author","Boretius, Susann"],["dc.contributor.author","Michaelis, Thomas"],["dc.contributor.author","Kubisch, Christian"],["dc.contributor.author","Alvarez-Bolado, Gonzalo"],["dc.contributor.author","Gruss, Peter"],["dc.date.accessioned","2017-09-07T11:45:25Z"],["dc.date.available","2017-09-07T11:45:25Z"],["dc.date.issued","2009"],["dc.description.abstract","Polycomb proteins are epigenetic regulators of gene expression. Human central nervous system (CNS) malformations are congenital defects of the brain and spinal cord. One example of a human CNS malformation is Chiari malformation (CM), which presents as abnormal brainstem growth and cerebellar herniation, sometimes accompanied by spina bifida and cortical defects; it can occur in families. Clinically, CM ranges from an asymptomatic condition to one with incapacitating or lethal symptoms, including neural tube defects and hydrocephalus. However, no genes that are causally involved in any manifestation of CM or similar malformations have been identified. Here, we show that a pathway that involves Zac1 (also known as Plagl1 or Lot1) and controls neuronal proliferation is altered in mice that are heterozygous for the polycomb gene Suz12, resulting in a phenotype that overlaps with some clinical manifestations of the CM spectrum. Suz12 heterozygotes show cerebellar herniation and an enlarged brainstem, accompanied by occipital cortical alterations and spina bifida. Downward displacement of the cerebellum causes hydrocephalus in the most severely impaired cases. Although the involvement of polycomb genes in human disease is starting to be recognized, this is the first demonstration of their role in nervous system malformations. Our work strongly suggests that brain malformations such as CM can result from altered epigenetic regulation of genes involved in cell proliferation in the brain."],["dc.identifier.doi","10.1242/dmm.001602"],["dc.identifier.gro","3150365"],["dc.identifier.pmid","19535498"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7122"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.issn","1754-8403"],["dc.title","Haploinsufficiency of the murine polycomb gene Suz12 results in diverse malformations of the brain and neural tube"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","e178"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","PLoS Genetics"],["dc.bibliographiccitation.volume","3"],["dc.contributor.author","Visel, Axel"],["dc.contributor.author","Carson, James"],["dc.contributor.author","Oldekamp, Judit"],["dc.contributor.author","Warnecke, Marei"],["dc.contributor.author","Jakubcakova, Vladimira"],["dc.contributor.author","Zhou, Xunlei"],["dc.contributor.author","Shaw, Chad A"],["dc.contributor.author","Alvarez-Bolado, Gonzalo"],["dc.contributor.author","Eichele, Gregor"],["dc.contributor.editor","Beier, David"],["dc.date.accessioned","2021-06-01T10:48:18Z"],["dc.date.available","2021-06-01T10:48:18Z"],["dc.date.issued","2007"],["dc.identifier.doi","10.1371/journal.pgen.0030178"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85889"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.eissn","1553-7404"],["dc.title","Regulatory Pathway Analysis by High-Throughput In Situ Hybridization"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","379"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Journal of Biological Rhythms"],["dc.bibliographiccitation.lastpage","389"],["dc.bibliographiccitation.volume","26"],["dc.contributor.author","Husse, Jana"],["dc.contributor.author","Zhou, Xunlei"],["dc.contributor.author","Shostak, Anton"],["dc.contributor.author","Oster, Henrik"],["dc.contributor.author","Eichele, Gregor"],["dc.date.accessioned","2021-06-01T10:47:54Z"],["dc.date.available","2021-06-01T10:47:54Z"],["dc.date.issued","2011"],["dc.description.abstract","Surgical lesion of the suprachiasmatic nuclei (SCN) profoundly affects the circadian timing system. A complication of SCN ablations is the concomitant scission of SCN afferents and efferents. Genetic disruption of the molecular clockwork in the SCN provides a complementary, less invasive experimental approach. The authors report the generation and functional analysis of a new Cre recombinase driver mouse that evokes homologous recombination with high efficiency in the SCN. They inserted the Cre recombinase cDNA into the Synaptotagmin10 ( Syt10) locus, a gene strongly expressed in the SCN. Heterozygous Synaptotagmin10-Cre ( Syt10 Cre ) mice have no obvious circadian locomotor phenotype, and homozygous animals show slightly reduced light-induced phase delays. Crosses of Syt10 Cre mice with β-galactosidase reporter animals revealed strong Cre activity in the vast majority of SCN cells. Cre activity is not detected in nonneuronal tissues with the exception of the testis. The authors demonstrate that conditionally deleting the clock gene Bmal1 using the Syt10 Cre driver renders animals arrhythmic."],["dc.identifier.doi","10.1177/0748730411415363"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85760"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.eissn","1552-4531"],["dc.relation.issn","0748-7304"],["dc.title","Synaptotagmin10-Cre, a Driver to Disrupt Clock Genes in the SCN"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Scientific Reports"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Urban, Inga"],["dc.contributor.author","Kerimoglu, Cemil"],["dc.contributor.author","Sakib, M. Sadman"],["dc.contributor.author","Wang, Haifang"],["dc.contributor.author","Benito, Eva"],["dc.contributor.author","Thaller, Christina"],["dc.contributor.author","Zhou, Xunlei"],["dc.contributor.author","Yan, Jun"],["dc.contributor.author","Fischer, André"],["dc.contributor.author","Eichele, Gregor"],["dc.date.accessioned","2020-12-10T18:11:07Z"],["dc.date.available","2020-12-10T18:11:07Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1038/s41598-019-50927-1"],["dc.identifier.eissn","2045-2322"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16897"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/73903"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","TIP60/KAT5 is required for neuronal viability in hippocampal CA1"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]