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    The alternative splicing of tau exon 10 and its regulatory proteins CLK2 and TRA2-BETA1 changes in sporadic Alzheimer's disease

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    Authors
    Glatz, Daniela C.
    Rujescu, Dan
    Tang, Yesheng
    Berendt, Frank J.
    Hartmann, Annette M.
    Faltraco, Frank
    Rosenberg, Carlyn
    Hulette, Christine
    Jellinger, Kurt
    Hampel, Harald
    Riederer, Peter
    Moller, Hans-J
    Andreadis, Athena
    Henkel, Kerstin
    Stamm, Stefan
    Show allShow less
    UMass Chan Affiliations
    Department of Cell Biology
    Document Type
    Journal Article
    Publication Date
    2005-12-24
    Keywords
    Aged
    Aged, 80 and over
    *Alternative Splicing
    Alzheimer Disease
    Antigens, CD46
    Blotting, Northern
    Brain
    Case-Control Studies
    Exons
    Female
    Gene Expression Regulation
    Humans
    Male
    Middle Aged
    Models, Biological
    Postmortem Changes
    Protein-Serine-Threonine Kinases
    Protein-Tyrosine Kinases
    RNA, Messenger
    Reverse Transcriptase Polymerase Chain Reaction
    Transfection
    tau Proteins
    Cell Biology
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    Link to Full Text
    http://dx.doi.org/10.1111/j.1471-4159.2005.03552.x
    Abstract
    Pathological inclusions containing fibrillar aggregates of hyperphosphorylated tau protein are a characteristic feature in tauopathies, which include Alzheimer's disease (AD). Tau is a microtubule-associated protein whose transcript undergoes alternative splicing in the brain. Exon 10 encodes one of four microtubule-binding repeats. Exon 10 inclusion gives rise to tau protein isoforms containing four microtubule-binding repeats (4R) whereas exclusion leads to isoforms containing only three repeats (3R). The ratio between 3R and 4R isoforms is tightly controlled via alternative splicing in the human adult nervous system and distortion of this balance results in neurodegeneration. Previous studies showed that several splicing regulators, among them hTRA2-beta1 and CLK2, regulate exon 10 alternative splicing. Like most splicing factors, htra2-beta and clk2 pre-mRNAs are regulated by alternative splicing. Here, we investigated whether human postmortem brain tissue of AD patients reveal differences in alternative splicing patterns of the tau, htra2-beta, presenilin 2 and clk2 genes when compared with age-matched controls. We found that the splicing patterns of all four genes are altered in affected brain areas of sporadic AD patients. In these affected areas, the amount of mRNAs of tau isoforms including exon 10, the htra2-beta1 isoform and an inactive form of clk2 are significantly increased. These findings suggest that a misregulation of alternative splicing seems to contribute to sporadic AD.
    Source
    J Neurochem. 2006 Feb;96(3):635-44. Epub 2005 Dec 20. Link to article on publisher's site
    DOI
    10.1111/j.1471-4159.2005.03552.x
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/25694
    PubMed ID
    16371011
    Related Resources
    Link to Article in PubMed
    ae974a485f413a2113503eed53cd6c53
    10.1111/j.1471-4159.2005.03552.x
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