{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,2]],"date-time":"2026-10-02T11:00:54Z","timestamp":1790938854127,"version":"4.1.0"},"reference-count":67,"publisher":"Rockefeller University Press","issue":"2","content-domain":{"domain":["rupress.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2011,7,25]]},"abstract":"<jats:p>Adenosine monophosphate\u2013activated protein kinase (AMPK) is a major energy sensor that maintains cellular energy homeostasis. Huntington\u2019s disease (HD) is a neurodegenerative disorder caused by the expansion of CAG repeats in the huntingtin (Htt) gene. In this paper, we report that activation of the \u03b11 isoform of AMPK (AMPK-\u03b11) occurred in striatal neurons of humans and mice with HD. Overactivation of AMPK in the striatum caused brain atrophy, facilitated neuronal loss, and increased formation of Htt aggregates in a transgenic mouse model (R6\/2) of HD. Such nuclear accumulation of AMPK-\u03b11 was activity dependent. Prevention of nuclear translocation or inactivation of AMPK-\u03b11 ameliorated cell death and down-regulation of Bcl2 caused by mutant Htt (mHtt). Conversely, enhanced expression of Bcl2 protected striatal cells from the toxicity evoked by mHtt and AMPK overactivation. These data demonstrate that aberrant activation of AMPK-\u03b11 in the nuclei of striatal cells represents a new toxic pathway induced by mHtt.<\/jats:p>","DOI":"10.1083\/jcb.201105010","type":"journal-article","created":{"date-parts":[[2011,7,18]],"date-time":"2011-07-18T20:35:11Z","timestamp":1311021311000},"page":"209-227","update-policy":"https:\/\/doi.org\/10.1083\/jcb.crossmarkpolicy","source":"Crossref","is-referenced-by-count":182,"title":["Nuclear translocation of AMPK-\u03b11 potentiates striatal neurodegeneration in Huntington\u2019s disease"],"prefix":"10.1083","volume":"194","author":[{"given":"Tz-Chuen","family":"Ju","sequence":"first","affiliation":[{"name":"Institute of Neuroscience 1 and 2"},{"name":"Institute of Biochemistry and Molecular Biology, School of Life Sciences, National Yang Ming University, Taipei 112, Taiwan 1 and 2"},{"name":"Division of Neuroscience, Institute of Biomedical Sciences, Academia Sinica, Taipei 11529, Taiwan 3"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hui-Mei","family":"Chen","sequence":"additional","affiliation":[{"name":"Division of Neuroscience, Institute of Biomedical Sciences, Academia Sinica, Taipei 11529, Taiwan 3"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jiun-Tsai","family":"Lin","sequence":"additional","affiliation":[{"name":"Division of Neuroscience, Institute of Biomedical Sciences, Academia Sinica, Taipei 11529, Taiwan 3"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ching-Pang","family":"Chang","sequence":"additional","affiliation":[{"name":"Division of Neuroscience, Institute of Biomedical Sciences, Academia Sinica, Taipei 11529, Taiwan 3"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wei-Cheng","family":"Chang","sequence":"additional","affiliation":[{"name":"Institute of Neuroscience 1 and 2"},{"name":"Institute of Biochemistry and Molecular Biology, School of Life Sciences, National Yang Ming University, Taipei 112, Taiwan 1 and 2"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jheng-Jie","family":"Kang","sequence":"additional","affiliation":[{"name":"Institute of Neuroscience 1 and 2"},{"name":"Institute of Biochemistry and Molecular Biology, School of Life Sciences, National Yang Ming University, Taipei 112, Taiwan 1 and 2"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cheng-Pu","family":"Sun","sequence":"additional","affiliation":[{"name":"Institute of Neuroscience 1 and 2"},{"name":"Institute of Biochemistry and Molecular Biology, School of Life Sciences, National Yang Ming University, Taipei 112, Taiwan 1 and 2"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mi-Hua","family":"Tao","sequence":"additional","affiliation":[{"name":"Division of Neuroscience, Institute of Biomedical Sciences, Academia Sinica, Taipei 11529, Taiwan 3"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pang-Hsien","family":"Tu","sequence":"additional","affiliation":[{"name":"Division of Neuroscience, Institute of Biomedical Sciences, Academia Sinica, Taipei 11529, Taiwan 3"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chen","family":"Chang","sequence":"additional","affiliation":[{"name":"Division of Neuroscience, Institute of Biomedical Sciences, Academia Sinica, Taipei 11529, Taiwan 3"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dennis W.","family":"Dickson","sequence":"additional","affiliation":[{"name":"Department of Neuroscience, Mayo Clinic College of Medicine, Jacksonville, FL 32224 4"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yijuang","family":"Chern","sequence":"additional","affiliation":[{"name":"Institute of Neuroscience 1 and 2"},{"name":"Institute of Biochemistry and Molecular Biology, School of Life Sciences, National Yang Ming University, Taipei 112, Taiwan 1 and 2"},{"name":"Division of Neuroscience, Institute of Biomedical Sciences, Academia Sinica, Taipei 11529, Taiwan 3"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"291","published-online":{"date-parts":[[2011,7,18]]},"reference":[{"key":"2023072916334588800_bib1","doi-asserted-by":"publisher","first-page":"377","DOI":"10.1016\/j.cmet.2008.02.011","article-title":"Hypothalamic CaMKK2 contributes to the regulation of energy balance","volume":"7","author":"Anderson","year":"2008","journal-title":"Cell Metab."},{"key":"2023072916334588800_bib2","doi-asserted-by":"publisher","first-page":"28","DOI":"10.1016\/j.nbd.2010.02.003","article-title":"The role of REST in transcriptional and epigenetic dysregulation in Huntington\u2019s disease","volume":"39","author":"Buckley","year":"2010","journal-title":"Neurobiol. 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