Gruss, Peter

[["dc.bibliographiccitation.firstpage","83"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Gene Expression Patterns"],["dc.bibliographiccitation.lastpage","93"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Vogel, Tanja"],["dc.contributor.author","Gruss, Peter"],["dc.date.accessioned","2018-11-07T08:33:02Z"],["dc.date.available","2018-11-07T08:33:02Z"],["dc.date.issued","2009"],["dc.description.abstract","Mutations of leukaemia associated AF9/MLL73 are implicated in neurodevelopmental diseases such as epilepsia and ataxia. This study shows for the first time, that murine Af9 is transcribed in various CNS structures including the subventricular zone (SVZ) of the cerebral cortex, hippocampus, cerebellar cortex, septum and Various thalamic structures, the choroid plexus, and the midbrain/hindbrain boundary. Expression of Af9 in the SVZ overlaps with Svet1, Cux2, and partially with Tbr2, confining its activity to the neurogenic compartment of the SVZ. In contrast to Svet1 and Cux2 expression, Af9 transcription is not limited to upper layer neurons but is found in the entire cortical plate. As part of an extensive network of interacting proteins involved in epigenetic DNA modification, we Could show overlapping expression of Af9 with Af4/Aff1 and Fmr2/Aff2, two genes that are also related to neurodevelopmental diseases, as well as with the highly homologous Enl. (C) 2008 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.gep.2008.10.004"],["dc.identifier.isi","000263217500003"],["dc.identifier.pmid","19000783"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17479"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","1567-133X"],["dc.title","Expression of Leukaemia associated transcription factor Af9/Mllt3 in the cerebral cortex of the mouse"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","12016"],["dc.bibliographiccitation.issue","33"],["dc.bibliographiccitation.journal","Proceedings of the National Academy of Sciences"],["dc.bibliographiccitation.lastpage","12021"],["dc.bibliographiccitation.volume","105"],["dc.contributor.author","Balastik, M."],["dc.contributor.author","Ferraguti, F."],["dc.contributor.author","Pires-da Silva, A."],["dc.contributor.author","Lee, T. H."],["dc.contributor.author","Alvarez-Bolado, G."],["dc.contributor.author","Lu, K. P."],["dc.contributor.author","Gruss, P."],["dc.date.accessioned","2021-06-01T10:51:03Z"],["dc.date.available","2021-06-01T10:51:03Z"],["dc.date.issued","2008"],["dc.identifier.doi","10.1073/pnas.0802261105"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86878"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.eissn","1091-6490"],["dc.relation.issn","0027-8424"],["dc.title","Deficiency in ubiquitin ligase TRIM2 causes accumulation of neurofilament light chain and neurodegeneration"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","324"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Developmental Biology"],["dc.bibliographiccitation.lastpage","342"],["dc.bibliographiccitation.volume","227"],["dc.contributor.author","Thomas, Tim"],["dc.contributor.author","Voss, Anne K."],["dc.contributor.author","Petrou, Petros"],["dc.contributor.author","Gruss, Peter"],["dc.date.accessioned","2021-06-01T10:47:33Z"],["dc.date.available","2021-06-01T10:47:33Z"],["dc.date.issued","2000"],["dc.identifier.doi","10.1006/dbio.2000.9915"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85641"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.issn","0012-1606"],["dc.title","The Murine Gene, Traube, Is Essential for the Growth of Preimplantation Embryos"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","15"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Mechanisms of Development"],["dc.bibliographiccitation.lastpage","28"],["dc.bibliographiccitation.volume","113"],["dc.contributor.author","Faisst, Anja M"],["dc.contributor.author","Alvarez-Bolado, Gonzalo"],["dc.contributor.author","Treichel, Dieter"],["dc.contributor.author","Gruss, Peter"],["dc.date.accessioned","2021-06-01T10:50:18Z"],["dc.date.available","2021-06-01T10:50:18Z"],["dc.date.issued","2002"],["dc.identifier.doi","10.1016/S0925-4773(02)00003-5"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86608"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.issn","0925-4773"],["dc.title","Rotatin is a novel gene required for axial rotation and left–right specification in mouse embryos"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","319"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Developmental Biology"],["dc.bibliographiccitation.lastpage","328"],["dc.bibliographiccitation.volume","233"],["dc.contributor.author","Pires-daSilva, A."],["dc.contributor.author","Nayernia, K."],["dc.contributor.author","Engel, Wolfgang"],["dc.contributor.author","Torres, M."],["dc.contributor.author","Stoykova, A."],["dc.contributor.author","Chowdhury, K."],["dc.contributor.author","Gruss, P."],["dc.date.accessioned","2018-11-07T09:03:50Z"],["dc.date.available","2018-11-07T09:03:50Z"],["dc.date.issued","2001"],["dc.description.abstract","Spermatid perinuclear RNA-binding protein (SPNR) is a microtubule-associated RNA-binding protein that localizes to the manchette in developing spermatids. The Spur mRNA is expressed at high levels in testis, ovary, and brain and is present in these tissues in multiple forms. We have generated a gene trap allele of the murine Spur, named Spnr(+/GT). Spnr(GT/GT) mutants show a high rate of mortality, reduced weight, and an abnormal clutching reflex. In addition to minor anatomical abnormalities in the brain males exhibit defects in spermatogenesis that include a thin seminiferous epithelium and disorganization of spermatogenesis. Most of the sperm from mutant males display defects in the flagellum and consequently show decreased motility and transport within the oviducts. furthermore, sperm from mutant males achieve in vitro fertilization less frequently. Our findings suggest that SPNR plays an important role in normal spermatogenesis and sperm function. Thus, the Spnr(GT/GT) mutant male mouse provides a unique model for some human male infertility cases. (C) 2001 Academic Press."],["dc.identifier.doi","10.1006/dbio.2001.0169"],["dc.identifier.isi","000168931800006"],["dc.identifier.pmid","11336498"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24978"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Academic Press Inc"],["dc.relation.issn","0012-1606"],["dc.title","Mice deficient for spermatid perinuclear RNA-binding protein show neurologic, spermatogenic, and sperm morphological abnormalities"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","396"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Stem Cells"],["dc.bibliographiccitation.lastpage","404"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Baier, Paul Christian"],["dc.contributor.author","Schindehutte, J."],["dc.contributor.author","Thinyane, K."],["dc.contributor.author","Flugge, G."],["dc.contributor.author","Fuchs, E."],["dc.contributor.author","Mansouri, Ahmed"],["dc.contributor.author","Paulus, Walter J."],["dc.contributor.author","Gruss, P."],["dc.contributor.author","Trenkwalder, Claudia"],["dc.date.accessioned","2018-11-07T10:53:15Z"],["dc.date.available","2018-11-07T10:53:15Z"],["dc.date.issued","2004"],["dc.description.abstract","Objective. Transplantation of fetal mesencephalic cells into the striatum has been performed in about 350 patients with Parkinson's disease and has been intensively studied in rat models of Parkinson's disease. Limited access to this material has shifted the focus toward embryonic stem (ES) cells. The grafting of undifferentiated ES cells to 6-hydroxy-dopamine (6-OHDA)-lesioned rats leads to behavioral improvements but may induce teratoma-like structures. This risk might be avoided by using more differentiated ES cells. In this study, we aimed to investigate differentiated mouse ES cells regarding their in vivo development and fate after transplantation in the striatum in the 6-OHDA rat model and the behavioral changes induced after transplantation. Methods. Mouse ES cells were differentiated on PA6 feeder cells for 14 days before grafting. Twenty to twenty-five percent of the neurons obtained were positive for tyrosine-hydroxylase (TH). PKH26-labeled cells were transplanted in the striata of unilaterally 6-OHDA-lesioned rats. Results. Direct PKH26 fluorescence visualization and TH staining proved the existence of cell deposits in the striata of all grafted animals, indicating cell survival for at least 5 weeks posttransplantation. There was no evidence of tumor formation. Immunocytochemical staining showed glial immunoreactivity surrounding the grafted cell deposits, probably inhibiting axonal outgrowth into the surrounding host tissue. There was a significant reduction in amphetamine-induced rotational behavior seen in grafted animals, which was not observed in sham-operated animals. Conclusions. The findings of this study suggest that the amphetamine-induced rotational behavioral test without histological confirmation is not proof of morphological integration with axonal outgrowth within the first 4 weeks posttransplantation."],["dc.identifier.doi","10.1634/stemcells.22-3-396"],["dc.identifier.isi","000221869600019"],["dc.identifier.pmid","15153616"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/49315"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1066-5099"],["dc.title","Behavioral changes in unilaterally 6-hydroxy-dopamine lesioned rats after transplantation of differentiated mouse embryonic stem cells without morphological integration"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","658"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","European Journal of Neuroscience"],["dc.bibliographiccitation.lastpage","668"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Britanova, Olga"],["dc.contributor.author","Akopov, Sergey"],["dc.contributor.author","Lukyanov, Sergey"],["dc.contributor.author","Gruss, Peter"],["dc.contributor.author","Tarabykin, Victor"],["dc.date.accessioned","2021-06-01T10:47:18Z"],["dc.date.available","2021-06-01T10:47:18Z"],["dc.date.issued","2005"],["dc.identifier.doi","10.1111/j.1460-9568.2005.03897.x"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85551"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.eissn","1460-9568"],["dc.relation.issn","0953-816X"],["dc.title","Novel transcription factor Satb2 interacts with matrix attachment region DNA elements in a tissue-specific manner and demonstrates cell-type-dependent expression in the developing mouse CNS"],["dc.title.alternative","A novel transcription factor interacting with MARs"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["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","1121"],["dc.bibliographiccitation.issue","7148"],["dc.bibliographiccitation.journal","Nature"],["dc.bibliographiccitation.lastpage","U14"],["dc.bibliographiccitation.volume","447"],["dc.contributor.author","Fimia, Gian Maria"],["dc.contributor.author","Stoykova, Anastassia"],["dc.contributor.author","Romagnoli, Alessandra"],["dc.contributor.author","Giunta, Luigi"],["dc.contributor.author","Di Bartolomeo, Sabrina"],["dc.contributor.author","Nardacci, Roberta"],["dc.contributor.author","Corazzari, Marco"],["dc.contributor.author","Fuoco, Claudia"],["dc.contributor.author","Ucar, Ahmet"],["dc.contributor.author","Schwartz, Peter J."],["dc.contributor.author","Gruss, Peter"],["dc.contributor.author","Piacentini, Mauro"],["dc.contributor.author","Chowdhury, Kamal"],["dc.contributor.author","Cecconi, Francesco"],["dc.date.accessioned","2018-11-07T11:01:23Z"],["dc.date.available","2018-11-07T11:01:23Z"],["dc.date.issued","2007"],["dc.description.abstract","Autophagy is a self-degradative process involved both in basal turnover of cellular components and in response to nutrient starvation or organelle damage in a wide range of eukaryotes(1-3). During autophagy, portions of the cytoplasm are sequestered by double-membraned vesicles called autophagosomes, and are degraded after fusion with lysosomes for subsequent recycling(4). In vertebrates, this process acts as a pro-survival or pro-death mechanism in different physiological and pathological conditions, such as neurodegeneration and cancer(2,5-7); however, the roles of autophagy during embryonic development are still largely uncharacterized(3). Beclin1 (Becn1; coiled-coil, myosin-like BCL2-interacting protein) is a principal regulator in autophagosome formation, and its deficiency results in early embryonic lethality(8,9). Here we show that Ambra1 (activating molecule in Beclin1-regulated autophagy), a large, previously unknown protein bearing a WD40 domain at its amino terminus, regulates autophagy and has a crucial role in embryogenesis. We found that Ambra1 is a positive regulator of the Becn1-dependent programme of autophagy, as revealed by its overexpression and by RNA interference experiments in vitro. Notably, Ambra1 functional deficiency in mouse embryos leads to severe neural tube defects associated with autophagy impairment, accumulation of ubiquitinated proteins, unbalanced cell proliferation and excessive apoptotic cell death. In addition to identifying a new and essential element regulating the autophagy programme, our results provide in vivo evidence supporting the existence of a complex interplay between autophagy, cell growth and cell death required for neural development in mammals."],["dc.description.sponsorship","Telethon [TCR04004]"],["dc.identifier.doi","10.1038/nature05925"],["dc.identifier.isi","000247564600039"],["dc.identifier.pmid","17589504"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/51141"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","0028-0836"],["dc.title","Ambra1 regulates autophagy and development of the nervous system"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","405"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Gene Expression Patterns"],["dc.bibliographiccitation.lastpage","412"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Chang, Yuh-Shin"],["dc.contributor.author","Stoykova, Anastassia"],["dc.contributor.author","Chowdhury, Kamal"],["dc.contributor.author","Gruss, Peter"],["dc.date.accessioned","2021-06-01T10:49:47Z"],["dc.date.available","2021-06-01T10:49:47Z"],["dc.date.issued","2007"],["dc.identifier.doi","10.1016/j.modgep.2006.11.009"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86413"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.issn","1567-133X"],["dc.title","Graded expression of Zfp462 in the embryonic mouse cerebral cortex"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]