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  • 1
    Publication Date: 2014-09-12
    Description: Activation of HIF-1α (hypoxia inducible factor-1α) prevents dry eye-induced acinar cell death in the lacrimal gland Cell Death and Disease 5, e1421 (September 2014). doi:10.1038/cddis.2014.382 Authors: Y Seo, Y W Ji, S M Lee, J Shim, H Noh, A Yeo, C Park, M S Park, E J Chang & H K Lee
    Electronic ISSN: 2041-4889
    Topics: Biology , Medicine
    Published by Springer Nature
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  • 2
    Publication Date: 2014-06-27
    Description: Activation of HIF-1α (hypoxia inducible factor-1α) prevents dry eye-induced acinar cell death in the lacrimal gland Cell Death and Disease 5, e1309 (June 2014). doi:10.1038/cddis.2014.260 Authors: Y Seo, Y W Ji, S M Lee, J Shim, H Noh, A Yeo, C Park, M S Park, E J Chang & H K Lee
    Electronic ISSN: 2041-4889
    Topics: Biology , Medicine
    Published by Springer Nature
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  • 3
    Publication Date: 2012-06-13
    Description: Movement of the plant hormone abscisic acid (ABA) within plants has been documented; however, the molecular mechanisms that regulate ABA transport are not fully understood. By using a modified yeast two-hybrid system, we screened Arabidopsis cDNAs capable of inducing interactions between the ABA receptor PYR/PYL/RCAR and PP2C protein phosphatase under low ABA concentrations. By using this approach, we identified four members of the NRT1/PTR family as candidates for ABA importers. Transport assays in yeast and insect cells demonstrated that at least one of the candidates ABA-IMPORTING TRANSPORTER (AIT) 1, which had been characterized as the low-affinity nitrate transporter NRT1.2, mediates cellular ABA uptake. Compared with WT, the ait1/nrt1.2 mutants were less sensitive to exogenously applied ABA during seed germination and/or postgermination growth, whereas overexpression of AIT1/NRT1.2 resulted in ABA hypersensitivity in the same conditions. Interestingly, the inflorescence stems of ait1/nrt1.2 had a lower surface temperature than those of the WT because of excess water loss from open stomata. We detected promoter activities of AIT1/NRT1.2 around vascular tissues in inflorescence stems, leaves, and roots. These data suggest that the function of AIT1/NRT1.2 as an ABA importer at the site of ABA biosynthesis is important for the regulation of stomatal aperture in inflorescence stems.
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
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  • 4
    Publication Date: 2019
    Description: 〈p〉Thermoregulation has substantial implications for energy consumption and human comfort and health. However, cooling technology has remained largely unchanged for more than a century and still relies on cooling the entire space regardless of the number of occupants. Personalized thermoregulation by thermoelectric devices (TEDs) can markedly reduce the cooling volume and meet individual cooling needs but has yet to be realized because of the lack of flexible TEDs with sustainable high cooling performance. Here, we demonstrate a wearable TED that can deliver more than 10°C cooling effect with a high coefficient of performance (COP 〉 1.5). Our TED is the first to achieve long-term active cooling with high flexibility, due to a novel design of double elastomer layers and high-ZT rigid TE pillars. Thermoregulation based on these devices may enable a shift from centralized cooling toward personalized cooling with the benefits of substantially lower energy consumption and improved human comfort.〈/p〉
    Electronic ISSN: 2375-2548
    Topics: Natural Sciences in General
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  • 5
    Publication Date: 2016-04-13
    Description: Stomatal movements regulate gas exchange, thus directly affecting the efficiency of photosynthesis and the sensitivity of plants to air pollutants such as ozone. The GARP family transcription factors GOLDEN 2-LIKE1 (GLK1) and GLK2 have known functions in chloroplast development. Here, we show that Arabidopsis thaliana (A. thaliana) plants expressing the...
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
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  • 6
    Publication Date: 2014-09-10
    Description: Environmentally induced alterations in the commensal microbiota have been implicated in the increasing prevalence of food allergy. We show here that sensitization to a food allergen is increased in mice that have been treated with antibiotics or are devoid of a commensal microbiota. By selectively colonizing gnotobiotic mice, we demonstrate...
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
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  • 7
    Publication Date: 2005-07-16
    Description: Mutations in mitochondrial DNA (mtDNA) accumulate in tissues of mammalian species and have been hypothesized to contribute to aging. We show that mice expressing a proofreading-deficient version of the mitochondrial DNA polymerase g (POLG) accumulate mtDNA mutations and display features of accelerated aging. Accumulation of mtDNA mutations was not associated with increased markers of oxidative stress or a defect in cellular proliferation, but was correlated with the induction of apoptotic markers, particularly in tissues characterized by rapid cellular turnover. The levels of apoptotic markers were also found to increase during aging in normal mice. Thus, accumulation of mtDNA mutations that promote apoptosis may be a central mechanism driving mammalian aging.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kujoth, G C -- Hiona, A -- Pugh, T D -- Someya, S -- Panzer, K -- Wohlgemuth, S E -- Hofer, T -- Seo, A Y -- Sullivan, R -- Jobling, W A -- Morrow, J D -- Van Remmen, H -- Sedivy, J M -- Yamasoba, T -- Tanokura, M -- Weindruch, R -- Leeuwenburgh, C -- Prolla, T A -- AG021905/AG/NIA NIH HHS/ -- AG16694/AG/NIA NIH HHS/ -- AG17994/AG/NIA NIH HHS/ -- AG18922/AG/NIA NIH HHS/ -- AG21042/AG/NIA NIH HHS/ -- DK48831/DK/NIDDK NIH HHS/ -- RR00095/RR/NCRR NIH HHS/ -- T32 AG00213/AG/NIA NIH HHS/ -- T32 GM07601/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2005 Jul 15;309(5733):481-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Genetics and Medical Genetics, University of Wisconsin, Madison, WI 53706, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16020738" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*physiology ; Amino Acid Substitution ; Animals ; *Apoptosis ; Caspase 3 ; Caspases/metabolism ; Cloning, Molecular ; DNA Damage ; DNA Fragmentation ; DNA, Mitochondrial/*genetics ; DNA-Directed DNA Polymerase/genetics ; Gene Targeting ; Humans ; Hydrogen Peroxide/metabolism ; Lipid Peroxidation ; Liver/metabolism ; Mice ; Mitochondria, Heart/metabolism ; Mitochondria, Liver/metabolism ; Muscle, Skeletal/metabolism ; *Mutation ; Myocardium/metabolism ; *Oxidative Stress ; Phenotype ; Presbycusis/etiology ; Reactive Oxygen Species/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
    Publication Date: 2011-04-30
    Description: Viperin is an interferon-inducible protein that is directly induced in cells by human cytomegalovirus (HCMV) infection. Why HCMV would induce viperin, which has antiviral activity, is unknown. We show that HCMV-induced viperin disrupts cellular metabolism to enhance the infectious process. Viperin interaction with the viral protein vMIA resulted in viperin relocalization from the endoplasmic reticulum to the mitochondria. There, viperin interacted with the mitochondrial trifunctional protein that mediates beta-oxidation of fatty acids to generate adenosine triphosphate (ATP). This interaction with viperin, but not with a mutant lacking the viperin iron-sulfur cluster-binding motif, reduced cellular ATP generation, which resulted in actin cytoskeleton disruption and enhancement of infection. This function of viperin, which was previously attributed to vMIA, suggests that HCMV has coopted viperin to facilitate the infectious process.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Seo, Jun-Young -- Yaneva, Rakina -- Hinson, Ella R -- Cresswell, Peter -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 May 27;332(6033):1093-7. doi: 10.1126/science.1202007. Epub 2011 Apr 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunobiology, Howard Hughes Medical Institute, Yale University School of Medicine, 300 Cedar Street, New Haven, CT 06520-8011, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21527675" target="_blank"〉PubMed〈/a〉
    Keywords: Actin Cytoskeleton/metabolism/ultrastructure ; Adenosine Triphosphate/metabolism ; Animals ; COS Cells ; Cell Line ; Cells, Cultured ; Cercopithecus aethiops ; Cytomegalovirus/*metabolism/*pathogenicity ; Endoplasmic Reticulum/metabolism ; Fatty Acids/metabolism ; Glycolysis ; Humans ; Hydrogen-Ion Concentration ; Immediate-Early Proteins/*metabolism ; Mice ; Mice, Knockout ; Mitochondria/metabolism ; Mitochondrial Trifunctional Protein ; Multienzyme Complexes/metabolism ; Oxidation-Reduction ; Proteins/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Stress Fibers/ultrastructure ; Transfection ; Virus Replication
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
    Publication Date: 2011-07-19
    Description: Crystalline mesoporous molecular sieves have long been sought as solid acid catalysts for organic reactions involving large molecules. We synthesized a series of mesoporous molecular sieves that possess crystalline microporous walls with zeolitelike frameworks, extending the application of zeolites to the mesoporous range of 2 to 50 nanometers. Hexagonally ordered or disordered mesopores are generated by surfactant aggregates, whereas multiple cationic moieties in the surfactant head groups direct the crystallization of microporous aluminosilicate frameworks. The wall thicknesses, framework topologies, and mesopore sizes can be controlled with different surfactants. The molecular sieves are highly active as catalysts for various acid-catalyzed reactions of bulky molecular substrates, compared with conventional zeolites and ordered mesoporous amorphous materials.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Na, Kyungsu -- Jo, Changbum -- Kim, Jeongnam -- Cho, Kanghee -- Jung, Jinhwan -- Seo, Yongbeom -- Messinger, Robert J -- Chmelka, Bradley F -- Ryoo, Ryong -- New York, N.Y. -- Science. 2011 Jul 15;333(6040):328-32. doi: 10.1126/science.1204452.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Functional Nanomaterials, Department of Chemistry, KAIST, Daejeon 305-701, Korea.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21764745" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
    Publication Date: 2010-11-26
    Description: Non-small cell lung carcinoma (NSCLC) is the leading cause of cancer-related death worldwide, with an overall 5-year survival rate of only 10-15%. Deregulation of the Ras pathway is a frequent hallmark of NSCLC, often through mutations that directly activate Kras. p53 is also frequently inactivated in NSCLC and, because oncogenic Ras can be a potent trigger of p53 (ref. 3), it seems likely that oncogenic Ras signalling has a major and persistent role in driving the selection against p53. Hence, pharmacological restoration of p53 is an appealing therapeutic strategy for treating this disease. Here we model the probable therapeutic impact of p53 restoration in a spontaneously evolving mouse model of NSCLC initiated by sporadic oncogenic activation of endogenous Kras. Surprisingly, p53 restoration failed to induce significant regression of established tumours, although it did result in a significant decrease in the relative proportion of high-grade tumours. This is due to selective activation of p53 only in the more aggressive tumour cells within each tumour. Such selective activation of p53 correlates with marked upregulation in Ras signal intensity and induction of the oncogenic signalling sensor p19(ARF)( )(ref. 6). Our data indicate that p53-mediated tumour suppression is triggered only when oncogenic Ras signal flux exceeds a critical threshold. Importantly, the failure of low-level oncogenic Kras to engage p53 reveals inherent limits in the capacity of p53 to restrain early tumour evolution and in the efficacy of therapeutic p53 restoration to eradicate cancers.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3011233/" 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/PMC3011233/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Junttila, Melissa R -- Karnezis, Anthony N -- Garcia, Daniel -- Madriles, Francesc -- Kortlever, Roderik M -- Rostker, Fanya -- Brown Swigart, Lamorna -- Pham, David M -- Seo, Youngho -- Evan, Gerard I -- Martins, Carla P -- CA100193/CA/NCI NIH HHS/ -- CA98018/CA/NCI NIH HHS/ -- R01 CA100193/CA/NCI NIH HHS/ -- R01 CA100193-09/CA/NCI NIH HHS/ -- England -- Nature. 2010 Nov 25;468(7323):567-71. doi: 10.1038/nature09526.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of California San Francisco, Department of Pathology and Helen Diller Family Comprehensive Cancer Center, San Francisco, California 94143-0502, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21107427" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carcinoma, Non-Small-Cell Lung/metabolism/*physiopathology ; Cell Proliferation ; Disease Models, Animal ; *Gene Expression Regulation, Neoplastic ; Lung Neoplasms/metabolism/*physiopathology ; Mice ; Proto-Oncogene Proteins p21(ras)/metabolism ; Tumor Suppressor Protein p53/genetics/*metabolism ; ras Proteins/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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