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  1. Book ; Online ; E-Book: Huntington's Disease

    Yang, X. William / Heiman, Myriam / Thompson, Leslie M.

    Pathogenic Mechanisms and Implications for Therapeutics

    2024  

    Author's details edited by X. William Yang, Myriam Heiman, and Leslie M. Thompson
    Keywords Huntington's disease
    Subject code 616.851
    Language English
    Size 1 online resource (620 pages)
    Edition First edition.
    Publisher Academic Press
    Publishing place London, England
    Document type Book ; Online ; E-Book
    Remark Zugriff für angemeldete ZB MED-Nutzerinnen und -Nutzer
    ISBN 0-323-95673-4 ; 9780323956727 ; 978-0-323-95673-4 ; 0323956726
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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  2. Article ; Online: Group dynamics goes awry: PolyQ-expanded huntingtin gains unwanted partners.

    Dionisio, Leonardo E / Yang, X William

    Cell systems

    2022  Volume 13, Issue 4, Page(s) 268–270

    Abstract: In this issue of Cell Systems, Greco et al. define high-confidence polyglutamine-dependent huntingtin interactors using AP-MS and complementary approaches and categorize them based on their interaction abundance and stability. The study reveals that a ... ...

    Abstract In this issue of Cell Systems, Greco et al. define high-confidence polyglutamine-dependent huntingtin interactors using AP-MS and complementary approaches and categorize them based on their interaction abundance and stability. The study reveals that a toxic gain of polyQ-dependent Htt interacting partners is a robust feature of HD pathogenesis.
    MeSH term(s) Huntingtin Protein/genetics ; Nuclear Proteins/genetics ; Peptides/genetics
    Chemical Substances Huntingtin Protein ; Nuclear Proteins ; Peptides ; polyglutamine (26700-71-0)
    Language English
    Publishing date 2022-04-21
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 2854138-8
    ISSN 2405-4720 ; 2405-4712
    ISSN (online) 2405-4720
    ISSN 2405-4712
    DOI 10.1016/j.cels.2022.03.003
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Life and death rest on a bivalent chromatin state.

    Yang, X William

    Nature neuroscience

    2016  Volume 19, Issue 10, Page(s) 1271–1273

    Language English
    Publishing date 2016-09-27
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1420596-8
    ISSN 1546-1726 ; 1097-6256
    ISSN (online) 1546-1726
    ISSN 1097-6256
    DOI 10.1038/nn.4396
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  4. Article ; Online: Huntington Disease's Glial Progenitor Cells Hit the Pause Button in the Mouse Brain.

    Wang, Nan / Yang, X William

    Cell stem cell

    2019  Volume 24, Issue 1, Page(s) 3–4

    Abstract: White matter abnormalities are prominent neuropathological features in Huntington's disease (HD); however, the cellular culprits are unclear. In this issue of Cell Stem Cell, Osipovitch et al. (2019) show that patient-derived glial progenitor cells fail ... ...

    Abstract White matter abnormalities are prominent neuropathological features in Huntington's disease (HD); however, the cellular culprits are unclear. In this issue of Cell Stem Cell, Osipovitch et al. (2019) show that patient-derived glial progenitor cells fail to properly differentiate and myelinate in the mouse brain due to cell-intrinsic transcriptional defects.
    MeSH term(s) Animals ; Brain ; Cell Differentiation ; Humans ; Huntington Disease ; Mice ; Neuroglia ; Stem Cells
    Language English
    Publishing date 2019-01-23
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 2375354-7
    ISSN 1875-9777 ; 1934-5909
    ISSN (online) 1875-9777
    ISSN 1934-5909
    DOI 10.1016/j.stem.2018.12.004
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  5. Article ; Online: Huntington's Disease: Genome-wide Neuroprotection Screening Goes Viral.

    Lee, C Y Daniel / Yang, X William

    Neuron

    2020  Volume 106, Issue 1, Page(s) 4–6

    Abstract: Forward genetic screen, typically performed in invertebrates or mammalian cell lines, has been instrumental in discovering genes essential for neural function. In this issue of Neuron, Wertz et al. (2020) demonstrate the first viral-mediated, genome-wide ...

    Abstract Forward genetic screen, typically performed in invertebrates or mammalian cell lines, has been instrumental in discovering genes essential for neural function. In this issue of Neuron, Wertz et al. (2020) demonstrate the first viral-mediated, genome-wide screen to identify neuroprotective genes in wild-type and Huntington's disease (HD) mouse brains.
    MeSH term(s) Animals ; Cell Death ; Cell Survival ; Huntington Disease ; Mice ; Neurons ; Neuroprotection
    Language English
    Publishing date 2020-04-09
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 808167-0
    ISSN 1097-4199 ; 0896-6273
    ISSN (online) 1097-4199
    ISSN 0896-6273
    DOI 10.1016/j.neuron.2020.03.020
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  6. Article ; Online: Genetically-directed Sparse Neuronal Labeling in BAC Transgenic Mice through Mononucleotide Repeat Frameshift.

    Lu, Xiao-Hong / Yang, X William

    Scientific reports

    2017  Volume 7, Page(s) 43915

    Abstract: Mosaicism with Repeat Frameshift (MORF) allows a single Bacterial Artificial Chromosome (BAC) transgene to direct sparse labeling of genetically-defined neuronal populations in mice. The BAC transgene drives cell-type-specific transcription of an out-of- ... ...

    Abstract Mosaicism with Repeat Frameshift (MORF) allows a single Bacterial Artificial Chromosome (BAC) transgene to direct sparse labeling of genetically-defined neuronal populations in mice. The BAC transgene drives cell-type-specific transcription of an out-of-frame mononucleotide repeat that is placed between a translational start codon and a membrane-bound fluorescent protein lacking its start codon. The stochastic frameshift of the unstable repeat DNA in a subset of BAC-expressing neurons results in the in-frame translation of the reporter protein hence the sparse neuronal labeling. As a proof-of-concept, we generated D1-dopamine receptor (D1) BAC MORF mice that label about 1% striatal D1-expressing medium spiny neurons and allow visualization of their dendrites. These mice enable the study of D1-MSN dendrite development in wildtype mice, and its degeneration in a mouse model of Huntington's disease.
    MeSH term(s) Animals ; Chromosomes, Artificial, Bacterial/genetics ; Frameshift Mutation ; Huntington Disease/metabolism ; Huntington Disease/pathology ; Huntington Disease/veterinary ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Microscopy, Fluorescence ; Neurons/metabolism ; Receptors, Dopamine D1/genetics ; Spine/metabolism ; Spine/pathology
    Chemical Substances Receptors, Dopamine D1
    Language English
    Publishing date 2017-03-08
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/srep43915
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Molecular insights into cortico-striatal miscommunications in Huntington's disease.

    Veldman, Matthew B / Yang, X William

    Current opinion in neurobiology

    2017  Volume 48, Page(s) 79–89

    Abstract: Huntington's disease (HD), a dominantly inherited neurodegenerative disease, is defined by its genetic cause, a CAG-repeat expansion in the HTT gene, its motor and psychiatric symptomology and primary loss of striatal medium spiny neurons (MSNs). However, ...

    Abstract Huntington's disease (HD), a dominantly inherited neurodegenerative disease, is defined by its genetic cause, a CAG-repeat expansion in the HTT gene, its motor and psychiatric symptomology and primary loss of striatal medium spiny neurons (MSNs). However, the molecular mechanisms from genetic lesion to disease phenotype remain largely unclear. Mouse models of HD have been created that exhibit phenotypes partially recapitulating those in the patient, and specifically, cortico-striatal disconnectivity appears to be a shared pathogenic event shared by HD mouse models and patients. Molecular studies have begun to unveil converging molecular and cellular pathogenic mechanisms that may account for cortico-striatal miscommunication in various HD mouse models. Systems biological approaches help to illuminate synaptic molecular networks as a nexus for HD cortio-striatal pathogenesis, and may offer new candidate targets to modify the disease.
    MeSH term(s) Animals ; Cerebral Cortex/pathology ; Corpus Striatum/pathology ; Humans ; Huntington Disease/genetics ; Huntington Disease/pathology ; Synapses/genetics ; Synapses/pathology
    Language English
    Publishing date 2017-11-07
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1078046-4
    ISSN 1873-6882 ; 0959-4388
    ISSN (online) 1873-6882
    ISSN 0959-4388
    DOI 10.1016/j.conb.2017.10.019
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  8. Article ; Online: Huntington's Disease: Nuclear Gatekeepers Under Attack.

    Veldman, Matthew B / Yang, X William

    Neuron

    2017  Volume 94, Issue 1, Page(s) 1–4

    Abstract: In this issue of Neuron, Gasset-Rosa et al. (2017) and Grima et al. (2017) describe defects in the nuclear pore complex and impaired nucleocytoplasmic transport in Huntington's disease (HD). The findings suggest that erosion of nuclear gatekeeping ... ...

    Abstract In this issue of Neuron, Gasset-Rosa et al. (2017) and Grima et al. (2017) describe defects in the nuclear pore complex and impaired nucleocytoplasmic transport in Huntington's disease (HD). The findings suggest that erosion of nuclear gatekeeping function, which is found in normal brain aging, may play an important role in the pathogenesis of multiple neurodegenerative disorders, including HD.
    MeSH term(s) Aging ; Brain ; Humans ; Huntington Disease ; Neurons ; Nuclear Proteins
    Chemical Substances Nuclear Proteins
    Language English
    Publishing date 2017-04-05
    Publishing country United States
    Document type Journal Article
    ZDB-ID 808167-0
    ISSN 1097-4199 ; 0896-6273
    ISSN (online) 1097-4199
    ISSN 0896-6273
    DOI 10.1016/j.neuron.2017.03.032
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  9. Article ; Online: Novel circuitry and molecular pathogenic mechanisms in Huntington's disease

    Yang X William

    Molecular Neurodegeneration, Vol 7, Iss Suppl 1, p L

    2012  Volume 18

    Keywords Neurology. Diseases of the nervous system ; RC346-429 ; Neurosciences. Biological psychiatry. Neuropsychiatry ; RC321-571 ; Internal medicine ; RC31-1245 ; Medicine ; R ; DOAJ:Neurology ; DOAJ:Medicine (General) ; DOAJ:Health Sciences
    Language English
    Publishing date 2012-02-01T00:00:00Z
    Publisher BioMed Central
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  10. Article ; Online: Publisher Correction: m

    Sun, Yuxiang / Dai, Hui / Dai, Xiaoxia / Yin, Jiekai / Cui, Yuxiang / Liu, Xiaochuan / Gonzalez, Gwendolyn / Yuan, Jun / Tang, Feng / Wang, Nan / Perlegos, Alexandra E / Bonini, Nancy M / Yang, X William / Gu, Weifeng / Wang, Yinsheng

    Nature

    2024  Volume 625, Issue 7995, Page(s) E16

    Language English
    Publishing date 2024-01-01
    Publishing country England
    Document type Published Erratum
    ZDB-ID 120714-3
    ISSN 1476-4687 ; 0028-0836
    ISSN (online) 1476-4687
    ISSN 0028-0836
    DOI 10.1038/s41586-023-06994-6
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