Triple play of DYRK1A kinase in cortical progenitor cells of Trisomy 21

[1]  B. Delatour,et al.  DYRK1A inhibition and cognitive rescue in a Down syndrome mouse model are induced by new fluoro-DANDY derivatives , 2018, Scientific Reports.

[2]  M. Hagiwara,et al.  Prenatal neurogenesis induction therapy normalizes brain structure and function in Down syndrome mice , 2017, Proceedings of the National Academy of Sciences.

[3]  Guillaume Pavlovic,et al.  Efficient and rapid generation of large genomic variants in rats and mice using CRISMERE , 2017, Scientific Reports.

[4]  R. Bartesaghi,et al.  Short- and long-term effects of neonatal pharmacotherapy with epigallocatechin-3-gallate on hippocampal development in the Ts65Dn mouse model of Down syndrome , 2016, Neuroscience.

[5]  K. Kula,et al.  Influence of prenatal EGCG treatment and Dyrk1a dosage reduction on craniofacial features associated with Down syndrome. , 2016, Human molecular genetics.

[6]  A. Dhanasekaran,et al.  Mouse models of Down syndrome: gene content and consequences , 2016, Mammalian Genome.

[7]  Tora K. Smulders-Srinivasan,et al.  Understanding the Multifaceted Role of Human Down Syndrome Kinase DYRK1A. , 2016, Advances in protein chemistry and structural biology.

[8]  N. Kurabayashi,et al.  DYRK1A overexpression enhances STAT activity and astrogliogenesis in a Down syndrome mouse model , 2015, EMBO reports.

[9]  S. Antonarakis,et al.  Brief Report: Isogenic Induced Pluripotent Stem Cell Lines From an Adult With Mosaic Down Syndrome Model Accelerated Neuronal Ageing and Neurodegeneration , 2015, Stem cells.

[10]  S. Cook,et al.  DYRK1A-mediated Cyclin D1 Degradation in Neural Stem Cells Contributes to the Neurogenic Cortical Defects in Down Syndrome , 2015, EBioMedicine.

[11]  C. Chen,et al.  Role of astroglia in Down’s syndrome revealed by patient-derived human-induced pluripotent stem cells , 2014, Nature Communications.

[12]  Y. Hérault,et al.  Epigallocatechin-3-gallate, a DYRK1A inhibitor, rescues cognitive deficits in Down syndrome mouse models and in humans. , 2014, Molecular nutrition & food research.

[13]  S. Antonarakis,et al.  Modelling and rescuing neurodevelopmental defect of Down syndrome using induced pluripotent stem cells from monozygotic twins discordant for trisomy 21 , 2013, EMBO molecular medicine.

[14]  N. Kurabayashi,et al.  Increased dosage of DYRK1A and DSCR1 delays neuronal differentiation in neocortical progenitor cells , 2013, Genes & development.

[15]  Jia-Ren Lin,et al.  Dosage of Dyrk1a shifts cells within a p21-cyclin D1 signaling map to control the decision to enter the cell cycle. , 2013, Molecular cell.

[16]  James Briggs,et al.  Integration‐Free Induced Pluripotent Stem Cells Model Genetic and Neural Developmental Features of Down Syndrome Etiology , 2013, Stem cells.

[17]  Giuseppe Esposito,et al.  OLIG2 over-expression impairs proliferation of human Down syndrome neural progenitors. , 2012, Human molecular genetics.

[18]  Y. Hérault,et al.  DYRK1A: A master regulatory protein controlling brain growth , 2012, Neurobiology of Disease.

[19]  V. Tybulewicz,et al.  Down syndrome: searching for the genetic culprits , 2011, Disease Models & Mechanisms.

[20]  B. Dickinson,et al.  S100B and APP Promote a Gliocentric Shift and Impaired Neurogenesis in Down Syndrome Neural Progenitors , 2011, PloS one.

[21]  P. Rakic,et al.  Neural Stem Cells: Historical Perspective and Future Prospects , 2011, Neuron.

[22]  R. Bartesaghi,et al.  APP-dependent up-regulation of Ptch1 underlies proliferation impairment of neural precursors in Down syndrome. , 2011, Human molecular genetics.

[23]  G. Guy,et al.  Direct Association of Sprouty-related Protein with an EVH1 Domain (SPRED) 1 or SPRED2 with DYRK1A Modifies Substrate/Kinase Interactions* , 2010, The Journal of Biological Chemistry.

[24]  K. Yamakawa,et al.  Enlarged brain ventricles and impaired neurogenesis in the Ts1Cje and Ts2Cje mouse models of Down syndrome. , 2010, Cerebral cortex.

[25]  G. D’Arcangelo,et al.  Dyrk1A Overexpression Inhibits Proliferation and Induces Premature Neuronal Differentiation of Neural Progenitor Cells , 2010, The Journal of Neuroscience.

[26]  Y. Hérault,et al.  Proliferation deficits and gene expression dysregulation in Down's syndrome (Ts1Cje) neural progenitor cells cultured from neurospheres , 2009, Journal of neuroscience research.

[27]  C. Englund,et al.  Intermediate neuronal progenitors (basal progenitors) produce pyramidal-projection neurons for all layers of cerebral cortex. , 2009, Cerebral cortex.

[28]  M. Gerstein,et al.  The genetic architecture of Down syndrome phenotypes revealed by high-resolution analysis of human segmental trisomies , 2009, Proceedings of the National Academy of Sciences.

[29]  Arnold Kriegstein,et al.  The glial nature of embryonic and adult neural stem cells. , 2009, Annual review of neuroscience.

[30]  Y. Hérault,et al.  Gene expression signature of cerebellar hypoplasia in a mouse model of Down syndrome during postnatal development , 2009, BMC Genomics.

[31]  B. Pakkenberg,et al.  Reduced cell number in the neocortical part of the human fetal brain in Down syndrome. , 2008, Annals of anatomy = Anatomischer Anzeiger : official organ of the Anatomische Gesellschaft.

[32]  P. Sylvester.  The hippocampus in Down's syndrome. , 2008, Journal of mental deficiency research.

[33]  Colin Blakemore,et al.  Development of the human cerebral cortex: Boulder Committee revisited , 2008, Nature Reviews Neuroscience.

[34]  R. Bartesaghi,et al.  RESEARCH ARTICLE: Neurogenesis Impairment and Increased Cell Death Reduce Total Neuron Number in the Hippocampal Region of Fetuses with Down Syndrome , 2007, Brain pathology.

[35]  T. Haydar,et al.  Defects in Embryonic Neurogenesis and Initial Synapse Formation in the Forebrain of the Ts65Dn Mouse Model of Down Syndrome , 2007, The Journal of Neuroscience.

[36]  A. Contestabile,et al.  Cell cycle alteration and decreased cell proliferation in the hippocampal dentate gyrus and in the neocortical germinal matrix of fetuses with down syndrome and in Ts65Dn mice , 2007, Hippocampus.

[37]  Li-Huei Tsai,et al.  Trekking across the Brain: The Journey of Neuronal Migration , 2007, Cell.

[38]  Xin Gao,et al.  NFAT dysregulation by increased dosage of DSCR1 and DYRK1A on chromosome 21 , 2006, Nature.

[39]  Y. Gwack,et al.  A genome-wide Drosophila RNAi screen identifies DYRK-family kinases as regulators of NFAT , 2006, Nature.

[40]  K. Wisniewski,et al.  Down syndrome children often have brain with maturation delay, retardation of growth, and cortical dysgenesis. , 2005, American journal of medical genetics. Supplement.

[41]  Sara G. Becker-Catania,et al.  A positive autoregulatory loop of Jak-STAT signaling controls the onset of astrogliogenesis , 2005, Nature Neuroscience.

[42]  Stylianos E. Antonarakis,et al.  Chromosome 21 and Down syndrome: from genomics to pathophysiology , 2004, Nature Reviews Genetics.

[43]  C. Ananth,et al.  Fetal transcerebellar diameter measurement with particular emphasis in the third trimester: a reliable predictor of gestational age. , 2004, American journal of obstetrics and gynecology.

[44]  Katheleen Gardiner,et al.  Mouse models of Down syndrome: how useful can they be? Comparison of the gene content of human chromosome 21 with orthologous mouse genomic regions. , 2003, Gene.

[45]  J. Darnell,et al.  Signalling: STATs: transcriptional control and biological impact , 2002, Nature Reviews Molecular Cell Biology.

[46]  X. Estivill,et al.  Dyrk1A Haploinsufficiency Affects Viability and Causes Developmental Delay and Abnormal Brain Morphology in Mice , 2002, Molecular and Cellular Biology.

[47]  A. Reiss,et al.  Neuroanatomy of Down's syndrome: a high-resolution MRI study. , 2001, The American journal of psychiatry.

[48]  Rick B. Vega,et al.  A Protein Encoded within the Down Syndrome Critical Region Is Enriched in Striated Muscles and Inhibits Calcineurin Signaling* , 2000, The Journal of Biological Chemistry.

[49]  T. Winter,et al.  Cerebellar and frontal lobe hypoplasia in fetuses with trisomy 21: usefulness as combined US markers. , 2000, Radiology.

[50]  K. Deisseroth,et al.  L-type calcium channels and GSK-3 regulate the activity of NF-ATc4 in hippocampal neurons , 1999, Nature.

[51]  K. Miyazono,et al.  Synergistic signaling in fetal brain by STAT3-Smad1 complex bridged by p300. , 1999, Science.

[52]  G. Crabtree.  Generic Signals and Specific Outcomes Signaling through Ca2+, Calcineurin, and NF-AT , 1999, Cell.

[53]  W. Griffin,et al.  Life-long overexpression of S100β in Down’s syndrome: implications for Alzheimer pathogenesis , 1998, Neurobiology of Aging.

[54]  C. Epstein,et al.  Ts1Cje, a partial trisomy 16 mouse model for Down syndrome, exhibits learning and behavioral abnormalities. , 1998, Proceedings of the National Academy of Sciences of the United States of America.

[55]  R. McKay,et al.  Multiple Routes to Astrocytic Differentiation in the CNS , 1998, The Journal of Neuroscience.

[56]  M. Greenberg,et al.  Regulation of gliogenesis in the central nervous system by the JAK-STAT signaling pathway. , 1997, Science.

[57]  J. Darnell,et al.  Maximal activation of transcription by statl and stat3 requires both tyrosine and serine phosphorylation , 1995, Cell.

[58]  B T Hyman,et al.  Development of the Superior Temporal Neocortex Is Anomalous in Trisomy 21 , 1994, Journal of neuropathology and experimental neurology.

[59]  C. Disteche,et al.  Down syndrome phenotypes: the consequences of chromosomal imbalance. , 1994, Proceedings of the National Academy of Sciences of the United States of America.

[60]  L. Becker,et al.  Developmental Changes of S-100 Protein and Glial Fibrillary Acidic Protein in the Brain in Down Syndrome , 1993, Experimental Neurology.

[61]  U Bellugi,et al.  Cerebral morphologic distinctions between Williams and Down syndromes. , 1993, Archives of neurology.

[62]  S. Pulst,et al.  Molecular definition of a region of chromosome 21 that causes features of the Down syndrome phenotype. , 1990, American journal of human genetics.

[63]  K. Wisniewski,et al.  Brain growth in Down syndrome subjects 15 to 22 weeks of gestational age and birth to 60 months. , 1990, Clinical neuropathology.

[64]  A. Aurias,et al.  Critical role of the D21S55 region on chromosome 21 in the pathogenesis of Down syndrome. , 1989, Proceedings of the National Academy of Sciences of the United States of America.

[65]  D. J. Driscoll,et al.  Molecular genetic approach to the characterization of the "Down syndrome region" of chromosome 21. , 1989, Genomics.

[66]  T. Petit,et al.  Synaptic development in the human fetus: A morphometric analysis of normal and Down's syndrome neocortex , 1984, Experimental Neurology.

[67]  Sachio Takashima,et al.  Abnormal neuronal development in the visual cortex of the human fetus and infant with down's syndrome. A quantitative and qualitative golgi study , 1981, Brain Research.

[68]  K. Servick.  Observations on an Ethnic Classification of Idiots , 2014 .

[69]  Y. Hérault,et al.  The in vivo Down syndrome genomic library in mouse. , 2012, Progress in brain research.

[70]  F. Ménez,et al.  Biometry of Face and Brain in Fetuses with Trisomy 21 , 2006, Pediatric Research.

[71]  K. Nakashima,et al.  A new expression cloning strategy for isolation of substrate-specific kinases by using phosphorylation site-specific antibody. , 2001, Journal of immunological methods.

[72]  J. Delabar,et al.  Molecular Mapping of Twenty-Four Features of Down Syndrome on Chromosome 21 , 1993, European journal of human genetics : EJHG.

[73]  M. Davisson,et al.  Segmental trisomy of murine chromosome 16: a new model system for studying Down syndrome. , 1990, Progress in clinical and biological research.