Stoykova, Anastassia S.

[["dc.bibliographiccitation.firstpage","256"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Developmental Cell"],["dc.bibliographiccitation.lastpage","269"],["dc.bibliographiccitation.volume","25"],["dc.contributor.author","Tuoc, Tran Cong"],["dc.contributor.author","Boretius, Susann"],["dc.contributor.author","Sansom, Stephen N."],["dc.contributor.author","Pitulescu, Mara-Elena"],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","Livesey, Frederick J."],["dc.contributor.author","Stoykova, Anastassia"],["dc.date.accessioned","2017-09-07T11:44:52Z"],["dc.date.available","2017-09-07T11:44:52Z"],["dc.date.issued","2013"],["dc.description.abstract","Increased cortical size is essential to the enhanced intellectual capacity of primates during mammalian evolution. The mechanisms that control cortical size are largely unknown. Here, we show that mammalian BAF170, a subunit of the chromatin remodeling complex mSWI/SNF, is an intrinsic factor that controls cortical size. We find that conditional deletion of BAF170 promotes indirect neurogenesis by increasing the pool of intermediate progenitors (IPs) and results in an enlarged cortex, whereas cortex-specific BAF170 overexpression results in the opposite phenotype. Mechanistically, BAF170 competes with BAF155 subunit in the BAF complex, affecting euchromatin structure and thereby modulating the binding efficiency of the Pax6/REST-corepressor complex to Pax6 target genes that regulate the generation of IPs and late cortical progenitors. Our findings reveal a molecular mechanism mediated by the mSWI/SNF chromatin-remodeling complex that controls cortical architecture."],["dc.identifier.doi","10.1016/j.devcel.2013.04.005"],["dc.identifier.gro","3150356"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7111"],["dc.language.iso","en"],["dc.notes.status","zu prüfen"],["dc.relation.issn","1534-5807"],["dc.title","Chromatin Regulation by BAF170 Controls Cerebral Cortical Size and Thickness"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2144"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Hippocampus"],["dc.bibliographiccitation.lastpage","2156"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Rosenthal, Eva H."],["dc.contributor.author","Tonchev, Anton B."],["dc.contributor.author","Stoykova, Anastassia"],["dc.contributor.author","Chowdhury, Kamal"],["dc.date.accessioned","2021-06-01T10:50:36Z"],["dc.date.available","2021-06-01T10:50:36Z"],["dc.date.issued","2012"],["dc.identifier.doi","10.1002/hipo.22035"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86721"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.issn","1050-9631"],["dc.title","Regulation of archicortical arealization by the transcription factor Zbtb20"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","567"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Molecular Neurobiology"],["dc.bibliographiccitation.lastpage","582"],["dc.bibliographiccitation.volume","56"],["dc.contributor.author","Doeppner, Thorsten R."],["dc.contributor.author","Herz, Josephine"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Tonchev, Anton B."],["dc.contributor.author","Stoykova, Anastassia"],["dc.date.accessioned","2020-12-10T14:14:28Z"],["dc.date.available","2020-12-10T14:14:28Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1007/s12035-018-1104-y"],["dc.identifier.eissn","1559-1182"],["dc.identifier.issn","0893-7648"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/71350"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Zbtb20 Regulates Developmental Neurogenesis in the Olfactory Bulb and Gliogenesis After Adult Brain Injury"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1795"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Cellular and Molecular Life Sciences"],["dc.bibliographiccitation.lastpage","1809"],["dc.bibliographiccitation.volume","72"],["dc.contributor.author","Tylkowski, Marco Andreas"],["dc.contributor.author","Yang, Kefei"],["dc.contributor.author","Hoyer-Fender, Sigrid"],["dc.contributor.author","Stoykova, Anastassia"],["dc.date.accessioned","2018-11-07T09:58:04Z"],["dc.date.available","2018-11-07T09:58:04Z"],["dc.date.issued","2015"],["dc.description.abstract","Cortical glutamatergic neurons are generated by radial glial cells (RGCs), specified by the expression of transcription factor (TF) Pax6, in the germinative zones of the dorsal telencephalon. Here, we demonstrate that Pax6 regulates the structural assembly of the interphase centrosomes. In the cortex of the Pax6-deficient Small eye (Sey/Sey) mutant, we find a defect of the appendages of the mother centrioles, indicating incomplete centrosome maturation. Consequently, RGCs fail to generate primary cilia, and instead of staying in the germinative zone for renewal, RGCs detach from the ventricular surface thus affecting the interkinetic nuclear migration and they exit prematurely from mitosis. Mechanistically, we show that TF Pax6 directly regulates the activity of the Odf2 gene encoding for the appendage-specific protein Odf2 with a role for the assembly of mother centriole. Our findings demonstrate a molecular mechanism that explains important characteristics of the centrosome disassembly and malfunctioning in developing cortex lacking Pax6."],["dc.identifier.doi","10.1007/s00018-014-1766-1"],["dc.identifier.isi","000352791200011"],["dc.identifier.pmid","25352170"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37296"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Basel"],["dc.relation.issn","1420-9071"],["dc.relation.issn","1420-682X"],["dc.title","Pax6 controls centriole maturation in cortical progenitors through Odf2"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","109"],["dc.bibliographiccitation.journal","iScience"],["dc.bibliographiccitation.lastpage","126"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Narayanan, Ramanathan"],["dc.contributor.author","Pham, Linh"],["dc.contributor.author","Kerimoglu, Cemil"],["dc.contributor.author","Watanabe, Takashi"],["dc.contributor.author","Castro Hernandez, Ricardo"],["dc.contributor.author","Sokpor, Godwin"],["dc.contributor.author","Ulmke, Pauline Antonie"],["dc.contributor.author","Kiszka, Kamila A."],["dc.contributor.author","Tonchev, Anton B."],["dc.contributor.author","Rosenbusch, Joachim"],["dc.contributor.author","Seong, Rho H."],["dc.contributor.author","Teichmann, Ulrike"],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","Fischer, Andre"],["dc.contributor.author","Bonn, Stefan"],["dc.contributor.author","Stoykova, Anastassia"],["dc.contributor.author","Staiger, Jochen F."],["dc.contributor.author","Tuoc, Tran"],["dc.date.accessioned","2020-12-10T14:24:42Z"],["dc.date.available","2020-12-10T14:24:42Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1016/j.isci.2018.05.014"],["dc.identifier.issn","2589-0042"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/72326"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Chromatin Remodeling BAF155 Subunit Regulates the Genesis of Basal Progenitors in Developing Cortex"],["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","1579"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Oncology Reports"],["dc.bibliographiccitation.lastpage","1592"],["dc.bibliographiccitation.volume","37"],["dc.contributor.author","Pavlakis, Evangelos"],["dc.contributor.author","Tonchev, Anton B."],["dc.contributor.author","Kaprelyan, Ara"],["dc.contributor.author","Enchev, Yavor"],["dc.contributor.author","Stoykova, Anastassia"],["dc.date.accessioned","2018-11-07T10:26:47Z"],["dc.date.available","2018-11-07T10:26:47Z"],["dc.date.issued","2017"],["dc.description.abstract","A misbalance between proliferation and differentiation of neural stem cells in niches for adult brain neurogenesis is a key mechanism in glioma pathogenesis. In the adult brain, the expression of Pax6 marks stem cells in the forebrain neurogenic niche. We analyzed the expression profile of the two active in vertebrates Pax6 isoforms, Pax6 and Pax6-5a, along with the expression of microRNA cluster miR-183-96-182 in a large set of glioma patient specimens and glioma cell lines which showed opposite expression level, low and high, respectively, with the progression of tumor malignancy. Our results from biochemical and in vitro studies in glioma cell lines disclosed a specific regulation of the PAX6-5a isoform by miR-183. Mechanistically, we show that the downregulation of the lipid kinase SPHK1 by both PAX6 isoforms and the simultaneous induction of CTNDD2 expression, specifically by PAX6-5a, results in reduced glioma cell survival, decreased migration and invasion and increased cell death, in glioma cell lines. Taken together, our findings point towards the important role of PAX6 and define PAX6-5a as a new essential player in glioma development. Finally, we propose that the expression level of TFs PAX6/PAX6-5a and miR-183-96-182 may potentially serve as prognostic markers for the progression of glioma tumors from low- to high-grade with a potential to identify new therapeutic approaches."],["dc.identifier.doi","10.3892/or.2017.5411"],["dc.identifier.isi","000396186600033"],["dc.identifier.pmid","28184912"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/43118"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Spandidos Publ Ltd"],["dc.relation.issn","1791-2431"],["dc.relation.issn","1021-335X"],["dc.title","Interaction between transcription factors PAX6/PAX6-5a and specific members of miR-183-96-182 cluster, may contribute to glioma progression in glioblastoma cell lines"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["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"]]

[["dc.bibliographiccitation.firstpage","2574"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Developmental Dynamics"],["dc.bibliographiccitation.lastpage","2585"],["dc.bibliographiccitation.volume","235"],["dc.contributor.author","Vogel, Tanja"],["dc.contributor.author","Stoykova, Anastassia"],["dc.contributor.author","Gruss, Peter"],["dc.date.accessioned","2018-11-07T09:18:13Z"],["dc.date.available","2018-11-07T09:18:13Z"],["dc.date.issued","2006"],["dc.description.abstract","Polycomb group (PcG) genes are regulators of body segmentation and cell growth, therefore being important players during development. PcG proteins form large complexes (PRC) that fulfil mostly repressive regulative functions on homeotic gene expression. Although expression of PcG genes in the brain has been noticed, the involvement of PcG genes in the processes of brain development is not understood. In this study, we analysed the expression patterns of PRC1 complex members to reveal PcG proteins that might be relevant for mouse brain development. Using in situ hybridisation, we show PRC1 activity in proliferative progenitor cells during neurogenesis, but also in maturated neuronal structures. PRC1 complex compositions vary in a spatial and temporal controlled manner during mouse brain development, providing cellular tools to act in different developmental contexts of cell proliferation, cell fate determination, and differentiation. Developmental Dynamics 235:2574-2585, 2006. (c) 2006 Wiley-Liss, Inc."],["dc.identifier.doi","10.1002/dvdy.20876"],["dc.identifier.isi","000240262000025"],["dc.identifier.pmid","16786585"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28357"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.relation.issn","1058-8388"],["dc.title","Differential expression of polycomb repression complex 1 (PRC1) members in the developing mouse brain reveals multiple complexes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]