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5 results on '"University of Cincinnati (UC)-Cincinnati Children's Hospital Medical Center"'

1. Significant variation between SNP-based HLA imputations in diverse populations: the last mile is the hardest

Author

Derek J. Pappas, Jarek Meller, Pierre-Antoine Gourraud, Vanja Paunic, Antoine Lizee, Steven J. Mack, Jill A. Hollenbach, Damjan Vukcevic, Karl R. Beutner, Lue Ping Zhao, Jacek Biesiada, Xiuwen Zheng, Martin Maiers, Stephen Leslie, Allan Motyer, Kent D. Taylor, Center for Genetics [Oakland, CA, USA], Children's Hospital Oakland Research Institute, Department of Neurology [San Francisco, CA, USA], University of California [San Francisco] (UC San Francisco), University of California (UC)-University of California (UC), Bioinformatics Research [Minneapolis, MN, USA] (National Marrow Donor Program), National Marrow Donor Program [Minneapolis], Centre for Systems Genomics [Melbourne, Australia] (Schools of Mathematics and Statistics, and BioSciences), University of Melbourne-Schools of Mathematics and Statistics, and BioSciences [Melbourne, Australia], Murdoch Children’s Research Institute [Melbourne, Australia], Department of Biomedical Informatics [Cincinnati, OH, USA], University of Cincinnati (UC)-Cincinnati Children's Hospital Medical Center, Los Angeles Biomedical Research Institute (LA BioMed), Department of Biostatistics [Seattle, WA, USA], University of Washington [Seattle], Fred Hutchinson Cancer Research Center [Seattle] (FHCRC), Centre de Recherche en Transplantation et Immunologie (U1064 Inserm - CRTI), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), Université de Nantes (UN)-Université de Nantes (UN), Département de Santé Publique [CHU Nantes], Centre hospitalier universitaire de Nantes (CHU Nantes), ONR grant N00014-08-1-1207 (KB, DP, PAG, JAH, AL, SJM, MM and VP), NIH grants U01AI067068 (JAH and SJM) and U19AI067152 (ARRA administrative supplement) (PAG) awarded by the NIAID, R01GM109030 (JAH, SJM and DJP) and P01GM099568 (XZ) awarded by the NIGMS, RO1NS076492 (PAG), RO1NS046297 (PAG) and R01NS049477 (PAG) awarded by the NINDS, NMSS grant RG 2899-D11 (PAG), the Australian National Health and Medical Research Council (NHMRC) Career Development Fellowship ID 1053756 (SL), and by the Victorian Life Sciences Computation Initiative (VLSCI) grant number VR0240 on its Peak Computing Facility at the University of Melbourne, an initiative of the Victorian Government, Australia (SL). Research at the Murdoch Childrens Research Institute was supported by the Victorian Government’s Operational Infrastructure Support Program. PAG is a recipient of the Race to Erase MS Junior Investigator Award and the European Federation for Immunogenetics Julia Bodmer Award., Le Bihan, Sylvie, University of California [San Francisco] (UCSF), and University of California-University of California

Subjects
0301 basic medicine, Linkage disequilibrium, Genotype, Genome-wide association study, Human leukocyte antigen, HLA-C Antigens, Biology, Polymorphism, Single Nucleotide, White People, Article, 03 medical and health sciences, HLA Antigens, Genetics, HLA-B Antigens, SNP, Humans, Pharmacology & Pharmacy, Imputation (statistics), Polymorphism, 1000 Genomes Project, HLA Complex, Alleles, Pharmacology, Genome, [SDV.MHEP] Life Sciences [q-bio]/Human health and pathology, HLA-A Antigens, Genome, Human, Human Genome, Genetic Variation, Single Nucleotide, Pharmacology and Pharmaceutical Sciences, 030104 developmental biology, Haplotypes, Molecular Medicine, Generic health relevance, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology, Human, Genome-Wide Association Study, HLA-DRB1 Chains
Abstract

International audience; Four single nucleotide polymorphism (SNP)-based human leukocyte antigen (HLA) imputation methods (e-HLA, HIBAG, HLA*IMP:02 and MAGPrediction) were trained using 1000 Genomes SNP and HLA genotypes and assessed for their ability to accurately impute molecular HLA-A, -B, -C and -DRB1 genotypes in the Human Genome Diversity Project cell panel. Imputation concordance was high (>89%) across all methods for both HLA-A and HLA-C, but HLA-B and HLA-DRB1 proved generally difficult to impute. Overall

Published
2018
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2. Sp8 and COUP-TF1 Reciprocally Regulate Patterning and Fgf Signaling in Cortical Progenitors

Author

Alessandra Pierani, Kenneth Campbell, Ilya Vilinsky, Andrea Faedo, John L.R. Rubenstein, Mayur Madhavan, Ugo Borello, Institut cellule souche et cerveau (U846 Inserm - UCBL1), Institut National de la Recherche Agronomique (INRA)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM), Division of Developmental Biology, University of Cincinnati (UC)-Cincinnati Children's Hospital Medical Center, Nina Ireland Laboratory of Developmental Neurobiology, Department of Psychiatry, University of California [San Francisco] (UCSF), University of California-University of California, Institut Jacques Monod (IJM (UMR_7592)), Université Paris Diderot - Paris 7 (UPD7)-Centre National de la Recherche Scientifique (CNRS), following grants: NIH MH069643, NIH F30-DC008928, Nina Ireland, Weston Havens Foundation, NIH NS34661, Neurodis Foundation (U.B.), Institut cellule souche et cerveau / Stem Cell and Brain Research Institute (SBRI), and Université Claude Bernard Lyon 1 (UCBL)

Subjects
Telencephalon, Fibroblast growth factor, Transgenic, Mice, 0302 clinical medicine, Neural Stem Cells, Models, Psychology, Cerebral Cortex, 0303 health sciences, patterning, Cell Death, COUP Transcription Factor I, Experimental Psychology, Articles, Neural stem cell, DNA-Binding Proteins, Corticogenesis, Neurological, Cognitive Sciences, [SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], Signal transduction, Signal Transduction, Fibroblast Growth Factor 8, Fgf signaling, Cognitive Neuroscience, proliferation, Neurogenesis, Models, Neurological, Mice, Transgenic, Biology, Globus Pallidus, 03 medical and health sciences, Cellular and Molecular Neuroscience, FGF8, Sp8, Genetics, Animals, Transcription factor, 030304 developmental biology, Body Patterning, Cell Proliferation, Neurosciences, [SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Molecular biology, Stem Cell Research, Fibroblast Growth Factors, Neuron differentiation, Neuroscience, 030217 neurology & neurosurgery, corticogenesis, Transcription Factors
Abstract

International audience; To gain new insights into the transcriptional regulation of cortical development, we examined the role of the transcription factor Sp8, which is downstream of Fgf8 signaling and known to promote rostral cortical development. We have used a binary transgenic system to express Sp8 throughout the mouse telencephalon in a temporally restricted manner. Our results show that misexpression of Sp8 throughout the telencephalon, at early but not late embryonic stages, results in cortical hypoplasia, which is accompanied by increased cell death, reduced proliferation, and precocious neuronal differentiation. Misexpression of Sp8 at early developmental stages represses COUP-TF1 expression, a negative effector of Fgf signaling and a key promoter of posterior cortical identity, while ablation of Sp8 has the opposite effect. In addition, transgenic misexpression of COUP-TF1 resulted in downregulation of Sp8, indicating a reciprocal cross-regulation between these 2 transcription factors. Although Sp8 has been suggested to induce and/or maintain Fgf8 expression in the embryonic telencephalon, neither Fgf8 nor Fgf15 was upregulated using our gain-of-function approach. However, misexpression of Sp8 greatly increased the expression of Fgf target molecules, suggesting enhanced Fgf signaling. Thus, we propose that Sp8 promotes rostral and dorsomedial cortical development by repressing COUP-TF1 and promoting Fgf signaling in pallial progenitors.

Published
2013
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3. Distinct ATOH1 and Neurog3 requirements define tuft cells as a new secretory cell type in the intestinal epithelium

Author

Béatrice Romagnolo, François Gerbe, Leila Makrini, Noah F. Shroyer, Johan H. van Es, Christine Pignodel, Sylvie Robine, Georg Mellitzer, Philippe Jay, Bénédicte Brulin, Hans Clevers, Jean-François Bourgaux, Institut de Génomique Fonctionnelle (IGF), Université de Montpellier (UM)-Université Montpellier 1 (UM1)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Montpellier 2 - Sciences et Techniques (UM2)-Centre National de la Recherche Scientifique (CNRS), Interface de Recherche Fondamentale et Appliquée en Cancérologie (IRFAC - Inserm U1113), Université de Strasbourg (UNISTRA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre Paul Strauss : Centre Régional de Lutte contre le Cancer (CRLCC)-Fédération de Médecine Translationelle de Strasbourg (FMTS), Compartimentation et dynamique cellulaires (CDC), Centre National de la Recherche Scientifique (CNRS)-Institut Curie [Paris]-Université Pierre et Marie Curie - Paris 6 (UPMC), Institut Cochin (IC UM3 (UMR 8104 / U1016)), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Division of Gastroenterology, Hepatology and Nutrition, University of Cincinnati (UC)-Cincinnati Children's Hospital Medical Center, Centre Hospitalier Universitaire de Nîmes (CHU Nîmes), Service d'Anatomopathologie, Hubrecht Institute for Developmental Biology and Stem Cell Research, Physiopathologie de la Résorption Osseuse et Thérapie des Tumeurs Osseuses Primitives, Université de Nantes (UN)-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre National de la Recherche Scientifique (CNRS)-Institut Curie-Université Pierre et Marie Curie - Paris 6 (UPMC), Centre Hospitalier Régional Universitaire de Nîmes (CHRU Nîmes), Université Montpellier 1 (UM1)-Université Montpellier 2 - Sciences et Techniques (UM2)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), and Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut Curie [Paris]-Centre National de la Recherche Scientifique (CNRS)

Subjects
Adenoma, Cell type, Cellular differentiation, Nerve Tissue Proteins, Enteroendocrine cell, [SDV.CAN]Life Sciences [q-bio]/Cancer, SOX9, Adenocarcinoma, Protein Serine-Threonine Kinases, Biology, Article, Mice, 03 medical and health sciences, Doublecortin-Like Kinases, 0302 clinical medicine, Intestinal mucosa, Intestinal Neoplasms, Intestine, Small, Basic Helix-Loop-Helix Transcription Factors, Animals, Humans, Intestine, Large, Intestinal Mucosa, Isomerases, Research Articles, ComputingMilieux_MISCELLANEOUS, 030304 developmental biology, 0303 health sciences, Membrane Proteins, Cell Differentiation, SOX9 Transcription Factor, Cell Biology, Intestinal epithelium, Cell biology, Intramolecular Oxidoreductases, Mice, Inbred C57BL, Cyclooxygenase 2, 030220 oncology & carcinogenesis, Cyclooxygenase 1, Tuft cell, Stem cell, Biomarkers
Abstract

Tuft cells represent a fourth type of intestinal secretory cell that constitutes the primary source of endogenous intestinal opioids and are the only epithelial cell that constitutively express cyclooxygenases., The unique morphology of tuft cells was first revealed by electron microscopy analyses in several endoderm-derived epithelia. Here, we explore the relationship of these cells with the other cell types of the intestinal epithelium and describe the first marker signature allowing their unambiguous identification. We demonstrate that although mature tuft cells express DCLK1, a putative marker of quiescent stem cells, they are post-mitotic, short lived, derive from Lgr5-expressing epithelial stem cells, and are found in mouse and human tumors. We show that whereas the ATOH1/MATH1 transcription factor is essential for their differentiation, Neurog3, SOX9, GFI1, and SPDEF are dispensable, which distinguishes these cells from enteroendocrine, Paneth, and goblet cells, and raises from three to four the number of secretory cell types in the intestinal epithelium. Moreover, we show that tuft cells are the main source of endogenous intestinal opioids and are the only epithelial cells that express cyclooxygenase enzymes, suggesting important roles for these cells in the intestinal epithelium physiopathology.

Published
2011
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4. Complex interplay between {beta}-catenin signalling and Notch effectors in intestinal tumorigenesis

Author

Grégory Peignon, Tasuku Honjo, Olivier Ayrault, Pierre Laurent-Puig, Béatrice Romagnolo, Christine Perret, Benoit Terris, Isabelle Van Seuningen, Noah F. Shroyer, Wulfran Cacheux, Aurélie Durand, Institut Cochin ( UM3 (UMR 8104 / U1016) ), Université Paris Descartes - Paris 5 ( UPD5 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Centre National de la Recherche Scientifique ( CNRS ), Department of Genetics and Tumour Cell Biology, St Jude Children's Research Hospital, Bases moléculaires de la réponse aux xénobiotiques ( U775 (IFR95) ), Division of Gastroenterology, Hepatology and Nutrition, Cincinnati Children's Hospital Medical Center-University of Cincinnati, Centre de recherche Jean-Pierre Aubert-Neurosciences et Cancer, Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Université de Lille, Droit et Santé, Department of Immunology and Genomic Medicine, Kyoto University [Kyoto], This work was supported by grants from INCa, ARC, the Ligue Nationale Contre le Cancer, Inserm and the CNRS., Institut Cochin (IC UM3 (UMR 8104 / U1016)), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Bases moléculaires de la réponse aux xénobiotiques (U775 (IFR95)), University of Cincinnati (UC)-Cincinnati Children's Hospital Medical Center, Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer - U837 (JPArc), Université Lille Nord de France (COMUE)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille, Kyoto University, Romagnolo, Béatrice, Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer - U1172 Inserm - U837 (JPArc), and Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Lille Nord de France (COMUE)-Université de Lille

Subjects
ATOH1, DNA Mutational Analysis, molecular carcinogenesis, [ SDV.CAN ] Life Sciences [q-bio]/Cancer, Mice, 0302 clinical medicine, GSK-3, colorectal cancer genes, Basic Helix-Loop-Helix Transcription Factors, HES1, beta Catenin, Mice, Knockout, 0303 health sciences, biology, Receptors, Notch, Gastroenterology, cell signalling, differentiation, DNA, Neoplasm, 3. Good health, Cell biology, Intestine, Neoplasm Proteins, Cell Transformation, Neoplastic, 030220 oncology & carcinogenesis, Immunoglobulin J Recombination Signal Sequence-Binding Protein, RNA Interference, Signal transduction, Colorectal Neoplasms, Signal Transduction, Beta-catenin, Genes, APC, proliferation, Adenomatous Polyposis Coli Protein, Notch signaling pathway, [SDV.CAN]Life Sciences [q-bio]/Cancer, 03 medical and health sciences, Downregulation and upregulation, [SDV.CAN] Life Sciences [q-bio]/Cancer, Animals, Humans, 030304 developmental biology, Homeodomain Proteins, RBP-J, Atoh1, β-catenin, Molecular biology, GI cancer, Hes1, cell proliferation, Catenin, biology.protein, Transcription Factor HES-1, Genes, Neoplasm
Abstract

International audience; Aims The activation of β-catenin signalling is a key step in intestinal tumorigenesis. Interplay between the β-catenin and Notch pathways during tumorigenesis has been reported, but the mechanisms involved and the role of Notch remain unclear. Methods Notch status was analysed by studying expression of the Notch effector Hes1 and Notch ligands/receptors in human colorectal cancer (CRC) and mouse models of Apc mutation. A genetic approach was used, deleting the Apc and RBP-J or Atoh1 genes in murine intestine. CRC cell lines were used to analyse the control of Hes1 and Atoh1 by β-catenin signalling. Results Notch signalling was found to be activated downstream from β-catenin. It was rapidly induced and maintained throughout tumorigenesis. Hes1 induction was mediated by β-catenin and resulted from both the induction of the Notch ligand/receptor and Notch-independent control of the Hes1 promoter by β-catenin. Surprisingly, the strong phenotype of unrestricted proliferation and impaired differentiation induced by acute Apc deletion in the intestine was not rescued by conditional Notch inactivation. Hyperactivation of β-catenin signalling overrode the forced differention induced by Notch inhibition, through the downregulation of Atoh1, a key secretory determinant factor downstream of Notch. This process involves glycogen synthase kinase 3 β (GSK3β) and proteasome-mediated degradation. The restoration of Atoh1 expression in CRC cell lines displaying β-catenin activation was sufficient to increase goblet cell differentiation, whereas genetic ablation of Atoh1 greatly increased tumour formation in Apc mutant mice. Conclusion Notch signalling is a downstream target of β-catenin hyperactivation in intestinal tumorigenesis. However, its inhibition had no tumour suppressor effect in the context of acute β-catenin activation probably due to the downregulation of Atoh1. This finding calls into question the use of γ-secretase inhibitors for the treatment of CRC and suggests that the restoration of Atoh1 expression in CRC should be considered as a therapeutic approach.

Published
2011
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5. Upregulation of costimulatory molecules induced by lipopolysaccharide and double-stranded RNA occurs by Trif-dependent and Trif-independent pathways

Author

Lena Alexopoulou, Jiahuai Han, Edith M. Janssen, Richard A. Flavell, Bruce Beutler, Kasper Hoebe, Sung Ouk Kim, Division of Molecular Immunology, University of Cincinnati (UC)-Cincinnati Children's Hospital Medical Center, University of Maryland [Baltimore], Centre d'Immunologie de Marseille - Luminy (CIML), Aix Marseille Université (AMU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Department of Immunology, The Scripps Research Institute [La Jolla, San Diego], and Department of Immunology and Microbial Science

Subjects
Lipopolysaccharides, viruses, [SDV]Life Sciences [q-bio], Molecular Sequence Data, Immunology, Receptors, Cell Surface, Receptor, Interferon alpha-beta, Biology, Mice, eIF-2 Kinase, Paracrine signalling, Adjuvants, Immunologic, Downregulation and upregulation, Antigens, CD, Animals, Immunology and Allergy, CD40 Antigens, Receptors, Immunologic, Autocrine signalling, Receptor, Adaptor Proteins, Signal Transducing, RNA, Double-Stranded, Receptors, Interferon, Immunity, Cellular, Membrane Glycoproteins, Macrophages, Toll-Like Receptors, Membrane Proteins, Signal transducing adaptor protein, Antigens, Differentiation, Molecular biology, Toll-Like Receptor 3, Up-Regulation, Toll-Like Receptor 4, Adaptor Proteins, Vesicular Transport, TRIF, Mutation, Myeloid Differentiation Factor 88, TLR3, B7-1 Antigen, TLR4, B7-2 Antigen, Signal Transduction
Abstract

Both lipopolysaccharide (LPS) and double-stranded RNA (dsRNA) are adjuvants for the adaptive immune response, inducing upregulation of costimulatory molecules (UCM) on antigen-presenting cells. Trif, an adapter protein that transduces signals from Toll-like receptor 4 (TLR4) and TLR3, permits the induction of many cytokines, including interferon-beta, which signals through the type I interferon receptor. We show here that LPS-induced UCM was strictly dependent on the TLR4-->Trif axis, whereas dsRNA-induced UCM was only partly dependent on the TLR3-->Trif axis. But both LPS- and dsRNA-induced UCM were entirely dependent on type I interferon receptor signaling. These findings show that UCM involves an autocrine or paracrine loop, and indicate that an alternative TLR3-independent, Trif-independent pathway contributes to dsRNA-induced UCM.

Published
2003
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