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  • 1
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    Vitamin D receptor as an intestinal bile acid sensor (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-05-23
    Description: The vitamin D receptor (VDR) mediates the effects of the calcemic hormone 1alpha,25-dihydroxyvitamin D3 [1,25(OH)2D3]. We show that VDR also functions as a receptor for the secondary bile acid lithocholic acid (LCA), which is hepatotoxic and a potential enteric carcinogen. VDR is an order of magnitude more sensitive to LCA and its metabolites than are other nuclear receptors. Activation of VDR by LCA or vitamin D induced expression in vivo of CYP3A, a cytochrome P450 enzyme that detoxifies LCA in the liver and intestine. These studies offer a mechanism that may explain the proposed protective effects of vitamin D and its receptor against colon cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Makishima, Makoto -- Lu, Timothy T -- Xie, Wen -- Whitfield, G Kerr -- Domoto, Hideharu -- Evans, Ronald M -- Haussler, Mark R -- Mangelsdorf, David J -- New York, N.Y. -- Science. 2002 May 17;296(5571):1313-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Pharmacology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-9050, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12016314" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Aryl Hydrocarbon Hydroxylases ; Binding, Competitive ; COS Cells ; Cell Line ; Colonic Neoplasms/prevention & control ; Cytochrome P-450 CYP3A ; Cytochrome P-450 Enzyme System/genetics/metabolism ; DNA-Binding Proteins/metabolism ; Dimerization ; Gene Expression Regulation, Enzymologic ; Histone Acetyltransferases ; Humans ; Intestine, Small/*metabolism ; Ligands ; Lithocholic Acid/analogs & derivatives/*metabolism/pharmacology ; Male ; Mice ; Nuclear Receptor Coactivator 1 ; Oxidoreductases, N-Demethylating/genetics/metabolism ; Promoter Regions, Genetic ; Rats ; Receptors, Calcitriol/agonists/genetics/*metabolism ; Receptors, Cytoplasmic and Nuclear/metabolism ; Receptors, Steroid/metabolism ; Transcription Factors/metabolism ; Transfection
    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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    Neural mechanisms of ageing and cognitive decline (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-03-26
    Description: During the past century, treatments for the diseases of youth and middle age have helped raise life expectancy significantly. However, cognitive decline has emerged as one of the greatest health threats of old age, with nearly 50% of adults over the age of 85 afflicted with Alzheimer's disease. Developing therapeutic interventions for such conditions demands a greater understanding of the processes underlying normal and pathological brain ageing. Recent advances in the biology of ageing in model organisms, together with molecular and systems-level studies of the brain, are beginning to shed light on these mechanisms and their potential roles in cognitive decline.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2927852/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2927852/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bishop, Nicholas A -- Lu, Tao -- Yankner, Bruce A -- DP1 AG044161/AG/NIA NIH HHS/ -- P01 AG027916/AG/NIA NIH HHS/ -- P01 AG027916-05/AG/NIA NIH HHS/ -- R01 AG026651/AG/NIA NIH HHS/ -- R01 AG026651-05/AG/NIA NIH HHS/ -- R01 AG027040/AG/NIA NIH HHS/ -- R01 AG027040-04/AG/NIA NIH HHS/ -- RC1 AG036106/AG/NIA NIH HHS/ -- RC1 AG036106-02/AG/NIA NIH HHS/ -- England -- Nature. 2010 Mar 25;464(7288):529-35. doi: 10.1038/nature08983.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20336135" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*pathology ; Animals ; Autophagy ; Brain/physiology/*physiopathology ; Cognition Disorders/*physiopathology ; Epigenesis, Genetic/physiology ; Humans ; Insulin/metabolism ; Insulin-Like Growth Factor I/metabolism ; Mitochondria/pathology ; Oxidative Stress/physiology ; Signal Transduction
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 3
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    Sustained axon regeneration induced by co-deletion of PTEN and SOCS3 (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-11-08
    Description: A formidable challenge in neural repair in the adult central nervous system (CNS) is the long distances that regenerating axons often need to travel in order to reconnect with their targets. Thus, a sustained capacity for axon regeneration is critical for achieving functional restoration. Although deletion of either phosphatase and tensin homologue (PTEN), a negative regulator of mammalian target of rapamycin (mTOR), or suppressor of cytokine signalling 3 (SOCS3), a negative regulator of Janus kinase/signal transducers and activators of transcription (JAK/STAT) pathway, in adult retinal ganglion cells (RGCs) individually promoted significant optic nerve regeneration, such regrowth tapered off around 2 weeks after the crush injury. Here we show that, remarkably, simultaneous deletion of both PTEN and SOCS3 enables robust and sustained axon regeneration. We further show that PTEN and SOCS3 regulate two independent pathways that act synergistically to promote enhanced axon regeneration. Gene expression analyses suggest that double deletion not only results in the induction of many growth-related genes, but also allows RGCs to maintain the expression of a repertoire of genes at the physiological level after injury. Our results reveal concurrent activation of mTOR and STAT3 pathways as key for sustaining long-distance axon regeneration in adult CNS, a crucial step towards functional recovery.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3240702/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3240702/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sun, Fang -- Park, Kevin K -- Belin, Stephane -- Wang, Dongqing -- Lu, Tao -- Chen, Gang -- Zhang, Kang -- Yeung, Cecil -- Feng, Guoping -- Yankner, Bruce A -- He, Zhigang -- DP1 AG044161/AG/NIA NIH HHS/ -- R01 EY018660/EY/NEI NIH HHS/ -- R01 EY021342/EY/NEI NIH HHS/ -- R01 EY021342-01A1/EY/NEI NIH HHS/ -- R01 EY021374/EY/NEI NIH HHS/ -- R01 EY021526/EY/NEI NIH HHS/ -- R01 EY021526-01/EY/NEI NIH HHS/ -- England -- Nature. 2011 Nov 6;480(7377):372-5. doi: 10.1038/nature10594.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉F.M. Kirby Neurobiology Center, Children's Hospital, Department of Neurology, Harvard Medical School, 300 Longwood Avenue, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22056987" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/pathology/*physiology ; Cell Growth Processes/genetics ; Gene Expression Regulation ; Mice ; Mice, Inbred C57BL ; Nerve Crush ; Nerve Regeneration/*physiology ; Optic Nerve/cytology/growth & development/pathology ; Optic Nerve Injuries/genetics/metabolism/pathology ; PTEN Phosphohydrolase/*deficiency/genetics ; Retinal Ganglion Cells/metabolism ; STAT3 Transcription Factor/metabolism ; Signal Transduction ; Suppressor of Cytokine Signaling Proteins/*deficiency/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 4
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    The DNA damage response induces inflammation and senescence by inhibiting autophagy of GATA4 (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-09-26
    Description: Cellular senescence is a terminal stress-activated program controlled by the p53 and p16(INK4a) tumor suppressor proteins. A striking feature of senescence is the senescence-associated secretory phenotype (SASP), a pro-inflammatory response linked to tumor promotion and aging. We have identified the transcription factor GATA4 as a senescence and SASP regulator. GATA4 is stabilized in cells undergoing senescence and is required for the SASP. Normally, GATA4 is degraded by p62-mediated selective autophagy, but this regulation is suppressed during senescence, thereby stabilizing GATA4. GATA4 in turn activates the transcription factor NF-kappaB to initiate the SASP and facilitate senescence. GATA4 activation depends on the DNA damage response regulators ATM and ATR, but not on p53 or p16(INK4a). GATA4 accumulates in multiple tissues, including the aging brain, and could contribute to aging and its associated inflammation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kang, Chanhee -- Xu, Qikai -- Martin, Timothy D -- Li, Mamie Z -- Demaria, Marco -- Aron, Liviu -- Lu, Tao -- Yankner, Bruce A -- Campisi, Judith -- Elledge, Stephen J -- AG009909/AG/NIA NIH HHS/ -- AG017242/AG/NIA NIH HHS/ -- AG046174/AG/NIA NIH HHS/ -- DP1 OD006849/OD/NIH HHS/ -- DP1OD006849/OD/NIH HHS/ -- GM44664/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2015 Sep 25;349(6255):aaa5612. doi: 10.1126/science.aaa5612.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Harvard Medical School, Division of Genetics, Brigham and Women's Hospital, Howard Hughes Medical Institute, Boston, MA 02115, USA. ; Buck Institute for Research on Aging, Novato, CA 94945, USA. ; Department of Genetics, Harvard Medical School, Boston, MA 02115, USA. ; Department of Genetics, Harvard Medical School, Division of Genetics, Brigham and Women's Hospital, Howard Hughes Medical Institute, Boston, MA 02115, USA. selledge@genetics.med.harvard.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26404840" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*genetics/metabolism ; Animals ; Ataxia Telangiectasia Mutated Proteins/metabolism ; Autophagy/*genetics ; Brain/metabolism ; Cell Aging/*genetics ; Cell Cycle/genetics ; Cells, Cultured ; Cyclin-Dependent Kinase Inhibitor p16 ; *DNA Damage ; Fibroblasts ; GATA4 Transcription Factor/genetics/*metabolism ; Gene Expression Profiling ; Humans ; Inflammation/*genetics ; Interleukin-1alpha/genetics/metabolism ; Mice ; Mice, Inbred C57BL ; MicroRNAs/genetics/metabolism ; NF-kappa B/metabolism ; Phenotype ; Promoter Regions, Genetic ; Tumor Necrosis Factor Receptor-Associated Peptides and ; Proteins/genetics/metabolism ; Tumor Suppressor Protein p53/metabolism
    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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  • 5
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    Microwaves: effect on thermoregulatory behavior in rats (1979)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1979-12-07
    Description: Rats, with their fur clipped, pressed a lever to turn on an infrared lamp while in a cold chamber. When they were exposed to continuous-wave microwaves at 2450 megahertz for 15-minute periods, the rate at which they turned on the infrared lamp decreased as a function of the microwave power density, which ranged between 5 and 20 milliwatts per square centimeter. This result indicates that behaviorally significant levels of heating may occur at an exposure duration and intensities that do not produce measurable changes in many other behavioral measures or in colonic temperature. Further study of how microwaves affect thermoregulatory behavior may help us understand such phenomena as the reported "nonthermal" behavioral effects of microwaves.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stern, S -- Margolin, L -- Weiss, B -- Lu, S T -- Michaelson, S M -- New York, N.Y. -- Science. 1979 Dec 7;206(4423):1198-201.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/505008" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Behavior, Animal/*radiation effects ; Body Temperature Regulation/*radiation effects ; Male ; *Microwaves ; Rats
    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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