يعرض 1 - 6 نتائج من 6 نتيجة بحث عن '"Paul Matteson"', وقت الاستعلام: 1.58s تنقيح النتائج
  1. 1
    دورية أكاديمية
    Dysregulation of mTOR signaling mediates common neurite and migration defects in both idiopathic and 16p11.2 deletion autism neural precursor cells

    المؤلفون: Smrithi Prem, Bharati Dev, Cynthia Peng, Monal Mehta, Rohan Alibutud, Robert J Connacher, Madeline St Thomas, Xiaofeng Zhou, Paul Matteson, Jinchuan Xing, James H Millonig, Emanuel DiCicco-Bloom

    المصدر: eLife, Vol 13 (2024)

    مصطلحات موضوعية: iPSC, autism, neurodevelopment, mTOR, neurites, cell migration, Medicine, Science, Biology (General), QH301-705.5

    وصف الملف: electronic resource

    Relation: https://elifesciences.org/articles/82809; https://doaj.org/toc/2050-084X

    URL الوصول: https://doaj.org/article/65ffe1bafb4a48f69a046dabc05f6f67

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  2. 2
    دورية أكاديمية
    Celf4 controls mRNA translation underlying synaptic development in the prenatal mammalian neocortex

    المؤلفون: Iva Salamon, Yongkyu Park, Terezija Miškić, Janja Kopić, Paul Matteson, Nicholas F. Page, Alfonso Roque, Geoffrey W. McAuliffe, John Favate, Marta Garcia-Forn, Premal Shah, Miloš Judaš, James H. Millonig, Ivica Kostović, Silvia De Rubeis, Ronald P. Hart, Željka Krsnik, Mladen-Roko Rasin

    المصدر: Nature Communications, Vol 14, Iss 1, Pp 1-22 (2023)

    مصطلحات موضوعية: Science

    وصف الملف: electronic resource

    Relation: https://doaj.org/toc/2041-1723

    URL الوصول: https://doaj.org/article/0ecc88f4fb9b43139559f4cbaf05e541

    Find this article in full text from Springer Verlag. Find this article in full text from ProQuest Full Text Finder
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  3. 3
    Autism NPCs from both idiopathic and CNV 16p11.2 deletion patients exhibit dysregulation of proliferation and mitogenic responses

    المؤلفون: Robert Connacher, Madeline Williams, Smrithi Prem, Percy L. Yeung, Paul Matteson, Monal Mehta, Anna Markov, Cynthia Peng, Xiaofeng Zhou, Courtney R. McDermott, Zhiping P. Pang, Judy Flax, Linda Brzustowicz, Che-Wei Lu, James H. Millonig, Emanuel DiCicco-Bloom

    المصدر: Stem Cell Reports. 17:1380-1394

    مصطلحات موضوعية: Phenotype, Induced Pluripotent Stem Cells, Genetics, Humans, Cell Biology, Autistic Disorder, Chromosome Deletion, Mitogens, Biochemistry, Cell Proliferation, Developmental Biology

    URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::378436bb9ff534bf06841d534220f8fb
    https://doi.org/10.1016/j.stemcr.2022.04.019

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  4. 4
    دورية أكاديمية
    Rapid Detection of Neurodevelopmental Phenotypes in Human Neural Precursor Cells (NPCs)

    المؤلفون: Madeline Williams, author1, Smrithi Prem, author1, Xiaofeng Zhou, author1, Paul Matteson, author2, Percy Luk Yeung, author3, Chi-Wei Lu, author3, Zhiping Pang, author4, Linda Brzustowicz, author5, James H. Millonig, author2, Emanuel Dicicco-Bloom, author1

    المصدر: Journal of Visualized Experiments. (133)

    الإتاحة: http://www.jove.com/video/56628

    View record at JoVE Journal
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  5. 5
    Dysregulation of mTOR Signaling Mediates Common Neurite and Migration Defects in Both Idiopathic and 16p11.2 Deletion Autism Neural Precursor Cells

    المؤلفون: Smrithi Prem, Bharati Dev, Cynthia Peng, Monal Mehta, Rohan Alibutud, Robert J. Connacher, Madeline St Thomas, Xiaofeng Zhou, Paul Matteson, Jinchuan Xing, James H. Millonig, Emanuel DiCicco-Bloom

    URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_________::196b46e72804ea6f06553fe566b88683
    https://doi.org/10.1101/2022.09.17.508382

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  6. 6
    Using iPSC-Based Models to Understand the Signaling and Cellular Phenotypes in Idiopathic Autism and 16p11.2 Derived Neurons

    المؤلفون: Luka, Turkalj, Monal, Mehta, Paul, Matteson, Smrithi, Prem, Madeline, Williams, Robert J, Connacher, Emanuel, DiCicco-Bloom, James H, Millonig

    المصدر: Advances in neurobiology. 25

    مصطلحات موضوعية: Neurons, Phenotype, Autism Spectrum Disorder, Induced Pluripotent Stem Cells, Humans, Autistic Disorder

    URL الوصول: https://explore.openaire.eu/search/publication?articleId=pmid________::58c04494c4b73cab439373e7486ce369
    https://pubmed.ncbi.nlm.nih.gov/32578145

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