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    Wyświetlanie 1-6 z 6
    Tytuł:
    Prenatal folic acid and vitamin B 12 imbalance alter neuronal morphology and synaptic density in the mouse neocortex.
    Autorzy:
    Tat L; Department of Pathology and Laboratory Medicine, University of California, Davis, CA, 95817, USA.
    Cannizzaro N; Department of Pathology and Laboratory Medicine, University of California, Davis, CA, 95817, USA.
    Schaaf Z; Department of Pathology and Laboratory Medicine, University of California, Davis, CA, 95817, USA.
    Racherla S; Department of Pathology and Laboratory Medicine, University of California, Davis, CA, 95817, USA.
    Bottiglieri T; Baylor Scott & White Research Institute, Center of Metabolomics, 3434 Live Oak, Dallas, TX, 75204, USA.
    Green R; Department of Pathology and Laboratory Medicine, University of California, Davis, CA, 95817, USA. .; Institute for Pediatric Regenerative Medicine, Shriners Hospitals for Children, Northern California, 2425 Stockton Boulevard, Sacramento, CA, 95817, USA. .
    Zarbalis KS; Department of Pathology and Laboratory Medicine, University of California, Davis, CA, 95817, USA. .; Institute for Pediatric Regenerative Medicine, Shriners Hospitals for Children, Northern California, 2425 Stockton Boulevard, Sacramento, CA, 95817, USA. .; MIND Institute, University of California, Davis, CA, 95817, USA. .
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    Źródło:
    Communications biology [Commun Biol] 2023 Nov 08; Vol. 6 (1), pp. 1133. Date of Electronic Publication: 2023 Nov 08.
    Typ publikacji:
    Journal Article; Research Support, Non-U.S. Gov't; Research Support, N.I.H., Extramural
    MeSH Terms:
    Vitamin B 12*
    Neocortex*
    Female ; Pregnancy ; Animals ; Mice ; Folic Acid/pharmacology ; Vitamins ; Neurons
    Czasopismo naukowe
    Pełny tekst  Link otwiera się w nowym oknie Pełny tekstSzczegóły
    Tytuł:
    Correction: WDFY3 mutation alters laminar position and morphology of cortical neurons.
    Autorzy:
    Schaaf ZA; Department of Pathology and Laboratory Medicine, University of California at Davis, Sacramento, CA, 95817, USA.; Shriners Hospitals for Children Northern California, Sacramento, CA, 95817, USA.
    Tat L; Department of Pathology and Laboratory Medicine, University of California at Davis, Sacramento, CA, 95817, USA.
    Cannizzaro N; Department of Pathology and Laboratory Medicine, University of California at Davis, Sacramento, CA, 95817, USA.
    Panoutsopoulos AA; Shriners Hospitals for Children Northern California, Sacramento, CA, 95817, USA.; Department of Physiology and Membrane Biology, University of California at Davis, Sacramento, CA, 95817, USA.
    Green R; Department of Pathology and Laboratory Medicine, University of California at Davis, Sacramento, CA, 95817, USA.
    Rülicke T; Department of Biomedical Sciences, University of Veterinary Medicine Vienna, 1210, Vienna, Austria.
    Hippenmeyer S; Institute of Science and Technology Austria, Am Campus 1, 3400, Klosterneuburg, Austria.
    Zarbalis KS; Department of Pathology and Laboratory Medicine, University of California at Davis, Sacramento, CA, 95817, USA. .; Shriners Hospitals for Children Northern California, Sacramento, CA, 95817, USA. .; UC Davis MIND Institute, Sacramento, CA, 95817, USA. .
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    Źródło:
    Molecular autism [Mol Autism] 2023 Jan 31; Vol. 14 (1), pp. 4. Date of Electronic Publication: 2023 Jan 31.
    Typ publikacji:
    Published Erratum
    Pełny tekst  Link otwiera się w nowym oknie Pełny tekstSzczegóły
    Tytuł:
    WDFY3 mutation alters laminar position and morphology of cortical neurons.
    Autorzy:
    Schaaf ZA; University of California at Davis, Department of Pathology and Laboratory Medicine, Sacramento, CA, 95817, USA.; Shriners Hospitals for Children Northern California, Sacramento, CA, 95817, USA.
    Tat L; University of California at Davis, Department of Pathology and Laboratory Medicine, Sacramento, CA, 95817, USA.
    Cannizzaro N; University of California at Davis, Department of Pathology and Laboratory Medicine, Sacramento, CA, 95817, USA.
    Panoutsopoulos AA; Shriners Hospitals for Children Northern California, Sacramento, CA, 95817, USA.; University of California at Davis, Department of Physiology and Membrane Biology, Sacramento, CA, 95817, USA.
    Green R; University of California at Davis, Department of Pathology and Laboratory Medicine, Sacramento, CA, 95817, USA.
    Rülicke T; Department of Biomedical Sciences, University of Veterinary Medicine Vienna, 1210, Vienna, Austria.
    Hippenmeyer S; Institute of Science and Technology Austria, Am Campus 1, 3400, Klosterneuburg, Austria.
    Zarbalis KS; University of California at Davis, Department of Pathology and Laboratory Medicine, Sacramento, CA, 95817, USA. .; Shriners Hospitals for Children Northern California, Sacramento, CA, 95817, USA. .; UC Davis MIND Institute, Sacramento, CA, 95817, USA. .
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    Źródło:
    Molecular autism [Mol Autism] 2022 Jun 22; Vol. 13 (1), pp. 27. Date of Electronic Publication: 2022 Jun 22.
    Typ publikacji:
    Journal Article; Research Support, Non-U.S. Gov't; Research Support, N.I.H., Extramural
    MeSH Terms:
    Adaptor Proteins, Signal Transducing*/genetics
    Autistic Disorder*/genetics
    Autophagy-Related Proteins*/genetics
    Cerebral Cortex*/cytology
    Neurons*/cytology
    Animals ; Humans ; Mice ; Mutation ; Neurogenesis/genetics
    Czasopismo naukowe
    Pełny tekst  Link otwiera się w nowym oknie Pełny tekstSzczegóły
    Tytuł:
    Beyond autophagy: a novel role for autism-linked Wdfy3 in brain mitophagy.
    Autorzy:
    Napoli E; Department of Molecular Biosciences, School of Veterinary Medicine, University of California, Davis, CA, 95616, USA.
    Song G; Department of Molecular Biosciences, School of Veterinary Medicine, University of California, Davis, CA, 95616, USA.
    Panoutsopoulos A; Department of Pathology and Laboratory Medicine, University of California Davis, Davis, USA.; Institute for Pediatric Regenerative Medicine, Shriners Hospitals for Children, Northern California, 2425 Stockton Boulevard, Sacramento, CA, 95817, USA.
    Riyadh MA; Department of Pathology and Laboratory Medicine, University of California Davis, Davis, USA.; Institute for Pediatric Regenerative Medicine, Shriners Hospitals for Children, Northern California, 2425 Stockton Boulevard, Sacramento, CA, 95817, USA.
    Kaushik G; Department of Pathology and Laboratory Medicine, University of California Davis, Davis, USA.; Institute for Pediatric Regenerative Medicine, Shriners Hospitals for Children, Northern California, 2425 Stockton Boulevard, Sacramento, CA, 95817, USA.
    Halmai J; Department of Molecular Biosciences, School of Veterinary Medicine, University of California, Davis, CA, 95616, USA.
    Levenson R; Department of Pathology and Laboratory Medicine, University of California Davis, Davis, USA.
    Zarbalis KS; Department of Pathology and Laboratory Medicine, University of California Davis, Davis, USA. .; Institute for Pediatric Regenerative Medicine, Shriners Hospitals for Children, Northern California, 2425 Stockton Boulevard, Sacramento, CA, 95817, USA. .; Medical Investigations of Neurodevelopmental Disorders (MIND) Institute, University of California Davis, Davis, CA, 95817, USA. .
    Giulivi C; Department of Molecular Biosciences, School of Veterinary Medicine, University of California, Davis, CA, 95616, USA. .; Medical Investigations of Neurodevelopmental Disorders (MIND) Institute, University of California Davis, Davis, CA, 95817, USA. .
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    Źródło:
    Scientific reports [Sci Rep] 2018 Jul 27; Vol. 8 (1), pp. 11348. Date of Electronic Publication: 2018 Jul 27.
    Typ publikacji:
    Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
    MeSH Terms:
    Autophagy*
    Mitophagy*
    Autistic Disorder/*pathology
    Brain/*metabolism
    Vesicular Transport Proteins/*metabolism
    Adaptor Proteins, Signal Transducing ; Animals ; Autophagy-Related Proteins ; Axon Guidance ; Cytoskeleton/metabolism ; Energy Metabolism ; Haploinsufficiency ; Mice, Inbred C57BL ; Mitochondria/metabolism ; Neural Stem Cells/metabolism ; Neurons/metabolism ; Nonsense Mediated mRNA Decay ; Protein Domains ; Vesicular Transport Proteins/chemistry ; Vesicular Transport Proteins/deficiency
    Czasopismo naukowe
    Pełny tekst  Link otwiera się w nowym oknie Pełny tekstSzczegóły
    Tytuł:
    Neural crest-derived mesenchymal cells require Wnt signaling for their development and drive invagination of the telencephalic midline.
    Autorzy:
    Choe Y; Department of Neurology, University of California San Francisco, San Francisco, California, United States of America.
    Zarbalis KS; Department of Pathology and Laboratory Medicine, University of California at Davis, Davis, California, United States of America ; Institute for Pediatric Regenerative Medicine, Shriners Hospitals for Children, Sacramento, California, United States of America.
    Pleasure SJ; Department of Neurology, University of California San Francisco, San Francisco, California, United States of America ; Program in Neuroscience, University of California San Francisco, San Francisco, California, United States of America ; Program in Developmental Stem Cell Biology, University of California San Francisco, San Francisco, California, United States of America ; Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research and University of California San Francisco, San Francisco, California, United States of America.
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    Źródło:
    PloS one [PLoS One] 2014 Feb 06; Vol. 9 (2), pp. e86025. Date of Electronic Publication: 2014 Feb 06 (Print Publication: 2014).
    Typ publikacji:
    Journal Article; Research Support, N.I.H., Extramural
    MeSH Terms:
    Wnt Signaling Pathway*
    Mesenchymal Stem Cells/*cytology
    Mesenchymal Stem Cells/*metabolism
    Neural Crest/*cytology
    Neural Crest/*growth & development
    Telencephalon/*growth & development
    Animals ; Cell Lineage ; Cell Proliferation ; Gene Deletion ; Meninges/cytology ; Mice ; Myocytes, Smooth Muscle/cytology ; Myocytes, Smooth Muscle/metabolism ; Telencephalon/pathology ; beta Catenin/metabolism
    Czasopismo naukowe
    Pełny tekst  Link otwiera się w nowym oknieSzczegóły
    Tytuł:
    A mutation in mouse Pak1ip1 causes orofacial clefting while human PAK1IP1 maps to 6p24 translocation breaking points associated with orofacial clefting.
    Autorzy:
    Ross AP; Department of Pathology and Laboratory Medicine, University of California Davis, Sacramento, California, United States of America.
    Mansilla MA
    Choe Y
    Helminski S
    Sturm R
    Maute RL
    May SR
    Hozyasz KK
    Wójcicki P
    Mostowska A
    Davidson B
    Adamopoulos IE
    Pleasure SJ
    Murray JC
    Zarbalis KS
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    Źródło:
    PloS one [PLoS One] 2013 Jul 25; Vol. 8 (7), pp. e69333. Date of Electronic Publication: 2013 Jul 25 (Print Publication: 2013).
    Typ publikacji:
    Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
    MeSH Terms:
    Chromosomes, Human, Pair 6*
    Mutation*
    Translocation, Genetic*
    Cleft Lip/*genetics
    Cleft Palate/*genetics
    Intracellular Signaling Peptides and Proteins/*genetics
    Nuclear Proteins/*genetics
    Alleles ; Amino Acid Sequence ; Animals ; Chromosome Breakpoints ; Chromosome Mapping ; Cleft Lip/pathology ; Cleft Palate/pathology ; Female ; Homozygote ; Humans ; Male ; Mice ; Molecular Sequence Data ; Polymorphism, Single Nucleotide ; Protein Isoforms/genetics
    Czasopismo naukowe
    Pełny tekst  Link otwiera się w nowym oknieSzczegóły
      Wyświetlanie 1-6 z 6

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