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  • 1
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    Interference by huntingtin and atrophin-1 with cbp-mediated transcription leading to cellular toxicity (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-03-27
    Description: Expanded polyglutamine repeats have been proposed to cause neuronal degeneration in Huntington's disease (HD) and related disorders, through abnormal interactions with other proteins containing short polyglutamine tracts such as the transcriptional coactivator CREB binding protein, CBP. We found that CBP was depleted from its normal nuclear location and was present in polyglutamine aggregates in HD cell culture models, HD transgenic mice, and human HD postmortem brain. Expanded polyglutamine repeats specifically interfere with CBP-activated gene transcription, and overexpression of CBP rescued polyglutamine-induced neuronal toxicity. Thus, polyglutamine-mediated interference with CBP-regulated gene transcription may constitute a genetic gain of function, underlying the pathogenesis of polyglutamine disorders.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nucifora , F C Jr -- Sasaki, M -- Peters, M F -- Huang, H -- Cooper, J K -- Yamada, M -- Takahashi, H -- Tsuji, S -- Troncoso, J -- Dawson, V L -- Dawson, T M -- Ross, C A -- NS16375/NS/NINDS NIH HHS/ -- NS34172/NS/NINDS NIH HHS/ -- NS37090/NS/NINDS NIH HHS/ -- NS38144/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2001 Mar 23;291(5512):2423-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neurobiology, Department of Psychiatry, The Johns Hopkins University School of Medicine, Baltimore, MD 21205-2196, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11264541" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/metabolism ; CREB-Binding Protein ; Cell Nucleus/metabolism ; Cell Survival ; Cells, Cultured ; Humans ; Huntington Disease/genetics/*metabolism ; Mice ; Mice, Transgenic ; Mutation ; Nerve Tissue Proteins/chemistry/genetics/*metabolism ; Neurons/cytology/*metabolism ; Nuclear Proteins/chemistry/genetics/*metabolism ; Peptides/chemistry/*metabolism ; Repetitive Sequences, Amino Acid ; Trans-Activators/chemistry/*metabolism ; *Transcription, Genetic ; Transfection ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Lymphocyte apoptosis: mediation by increased type 3 inositol 1,4,5-trisphosphate receptor (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-07-26
    Description: B and T lymphocytes undergoing apoptosis in response to anti-immunoglobulin M antibodies and dexamethasone, respectively, were found to have increased amounts of messenger RNA for the inositol 1,4,5-trisphosphate receptor (IP3R) and increased amounts of IP3R protein. Immunohistochemical analysis revealed that the augmented receptor population was localized to the plasma membrane. Type 3 IP3R (IP3R3) was selectively increased during apoptosis, with no enhancement of type 1 IP3R (IP3R1). Expression of IP3R3 antisense constructs in S49 T cells blocked dexamethasone-induced apoptosis, whereas IP3R3 sense, IP3R1 sense, or IP3R1 antisense control constructs did not block cell death. Thus, the increases in IP3R3 may be causally related to apoptosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Khan, A A -- Soloski, M J -- Sharp, A H -- Schilling, G -- Sabatini, D M -- Li, S H -- Ross, C A -- Snyder, S H -- AI-20922/AI/NIAID NIH HHS/ -- AI-37934/AI/NIAID NIH HHS/ -- MH43040/MH/NIMH NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1996 Jul 26;273(5274):503-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8662540" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; *Apoptosis ; B-Lymphocytes/*cytology/metabolism ; Base Sequence ; Calcium/metabolism ; Calcium Channels/genetics/immunology/*metabolism ; Cell Line ; Cell Membrane/metabolism ; Cells, Cultured ; DNA, Antisense ; Dexamethasone/pharmacology ; Immunoblotting ; Inositol 1,4,5-Trisphosphate/*metabolism ; Inositol 1,4,5-Trisphosphate Receptors ; Mice ; Molecular Sequence Data ; Receptors, Cytoplasmic and Nuclear/genetics/immunology/*metabolism ; T-Lymphocytes/*cytology/metabolism ; Transfection ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
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