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  • Mutation  (131)
  • Signal Transduction  (78)
  • American Association for the Advancement of Science (AAAS)  (204)
  • Cell Press
  • 2010-2014  (193)
  • 1980-1984  (11)
  • 1940-1944
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  • 1
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    The genetic landscape of the childhood cancer medulloblastoma (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-12-18
    Description: Medulloblastoma (MB) is the most common malignant brain tumor of children. To identify the genetic alterations in this tumor type, we searched for copy number alterations using high-density microarrays and sequenced all known protein-coding genes and microRNA genes using Sanger sequencing in a set of 22 MBs. We found that, on average, each tumor had 11 gene alterations, fewer by a factor of 5 to 10 than in the adult solid tumors that have been sequenced to date. In addition to alterations in the Hedgehog and Wnt pathways, our analysis led to the discovery of genes not previously known to be altered in MBs. Most notably, inactivating mutations of the histone-lysine N-methyltransferase genes MLL2 or MLL3 were identified in 16% of MB patients. These results demonstrate key differences between the genetic landscapes of adult and childhood cancers, highlight dysregulation of developmental pathways as an important mechanism underlying MBs, and identify a role for a specific type of histone methylation in human tumorigenesis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3110744/" 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/PMC3110744/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Parsons, D Williams -- Li, Meng -- Zhang, Xiaosong -- Jones, Sian -- Leary, Rebecca J -- Lin, Jimmy Cheng-Ho -- Boca, Simina M -- Carter, Hannah -- Samayoa, Josue -- Bettegowda, Chetan -- Gallia, Gary L -- Jallo, George I -- Binder, Zev A -- Nikolsky, Yuri -- Hartigan, James -- Smith, Doug R -- Gerhard, Daniela S -- Fults, Daniel W -- VandenBerg, Scott -- Berger, Mitchel S -- Marie, Suely Kazue Nagahashi -- Shinjo, Sueli Mieko Oba -- Clara, Carlos -- Phillips, Peter C -- Minturn, Jane E -- Biegel, Jaclyn A -- Judkins, Alexander R -- Resnick, Adam C -- Storm, Phillip B -- Curran, Tom -- He, Yiping -- Rasheed, B Ahmed -- Friedman, Henry S -- Keir, Stephen T -- McLendon, Roger -- Northcott, Paul A -- Taylor, Michael D -- Burger, Peter C -- Riggins, Gregory J -- Karchin, Rachel -- Parmigiani, Giovanni -- Bigner, Darell D -- Yan, Hai -- Papadopoulos, Nick -- Vogelstein, Bert -- Kinzler, Kenneth W -- Velculescu, Victor E -- CA057345/CA/NCI NIH HHS/ -- CA096832/CA/NCI NIH HHS/ -- CA118822/CA/NCI NIH HHS/ -- CA121113/CA/NCI NIH HHS/ -- CA135877/CA/NCI NIH HHS/ -- GM074906-01A1/GM/NIGMS NIH HHS/ -- HHSN261200800001E/PHS HHS/ -- P01 CA096832/CA/NCI NIH HHS/ -- P01 CA096832-03/CA/NCI NIH HHS/ -- R01 CA108622/CA/NCI NIH HHS/ -- R01 CA121113/CA/NCI NIH HHS/ -- R01 CA121113-05/CA/NCI NIH HHS/ -- R37 CA057345/CA/NCI NIH HHS/ -- R37 CA057345-20/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Jan 28;331(6016):435-9. doi: 10.1126/science.1198056. Epub 2010 Dec 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ludwig Center for Cancer Genetics and Therapeutics and Howard Hughes Medical Institute, Johns Hopkins Kimmel Cancer Center, Baltimore, MD 21231, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21163964" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Cerebellar Neoplasms/*genetics/metabolism ; Child ; DNA Copy Number Variations ; DNA-Binding Proteins/genetics/metabolism ; *Genes, Neoplasm ; Genes, Tumor Suppressor ; Histone-Lysine N-Methyltransferase/genetics/metabolism ; Histones/metabolism ; Humans ; Medulloblastoma/*genetics/metabolism ; Methylation ; MicroRNAs/genetics ; *Mutation ; Neoplasm Proteins/genetics/metabolism ; Oligonucleotide Array Sequence Analysis ; Point Mutation ; Sequence Analysis, DNA ; Signal Transduction
    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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  • 2
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    Sequence and structural convergence of broad and potent HIV antibodies that mimic CD4 binding (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-07-19
    Description: Passive transfer of broadly neutralizing HIV antibodies can prevent infection, which suggests that vaccines that elicit such antibodies would be protective. Thus far, however, few broadly neutralizing HIV antibodies that occur naturally have been characterized. To determine whether these antibodies are part of a larger group of related molecules, we cloned 576 new HIV antibodies from four unrelated individuals. All four individuals produced expanded clones of potent broadly neutralizing CD4-binding-site antibodies that mimic binding to CD4. Despite extensive hypermutation, the new antibodies shared a consensus sequence of 68 immunoglobulin H (IgH) chain amino acids and arise independently from two related IgH genes. Comparison of the crystal structure of one of the antibodies to the broadly neutralizing antibody VRC01 revealed conservation of the contacts to the HIV spike.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3351836/" 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/PMC3351836/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scheid, Johannes F -- Mouquet, Hugo -- Ueberheide, Beatrix -- Diskin, Ron -- Klein, Florian -- Oliveira, Thiago Y K -- Pietzsch, John -- Fenyo, David -- Abadir, Alexander -- Velinzon, Klara -- Hurley, Arlene -- Myung, Sunnie -- Boulad, Farid -- Poignard, Pascal -- Burton, Dennis R -- Pereyra, Florencia -- Ho, David D -- Walker, Bruce D -- Seaman, Michael S -- Bjorkman, Pamela J -- Chait, Brian T -- Nussenzweig, Michel C -- P01 AI081677/AI/NIAID NIH HHS/ -- P30 AI060354/AI/NIAID NIH HHS/ -- R01 AI033292/AI/NIAID NIH HHS/ -- RR00862/RR/NCRR NIH HHS/ -- RR022220/RR/NCRR NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Sep 16;333(6049):1633-7. doi: 10.1126/science.1207227. Epub 2011 Jul 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Immunology, The Rockefeller University, New York, NY 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21764753" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Antibodies, Neutralizing/*chemistry/*immunology/metabolism ; Antibody Affinity ; Antibody Specificity ; Antigens, CD4/immunology/*metabolism ; Binding Sites ; Binding Sites, Antibody ; Cloning, Molecular ; Consensus Sequence ; Crystallography, X-Ray ; Genes, Immunoglobulin Heavy Chain ; HIV Antibodies/*chemistry/*immunology/metabolism ; HIV Envelope Protein gp120/chemistry/*immunology/metabolism ; HIV Infections/immunology ; Humans ; Immunoglobulin Fab Fragments/chemistry ; Immunoglobulin Heavy Chains/chemistry ; Immunoglobulin Light Chains/chemistry ; Molecular Mimicry ; Molecular Sequence Data ; Mutation ; Protein Conformation
    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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  • 3
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    Rapamycin-induced insulin resistance is mediated by mTORC2 loss and uncoupled from longevity (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-03-31
    Description: Rapamycin, an inhibitor of mechanistic target of rapamycin complex 1 (mTORC1), extends the life spans of yeast, flies, and mice. Calorie restriction, which increases life span and insulin sensitivity, is proposed to function by inhibition of mTORC1, yet paradoxically, chronic administration of rapamycin substantially impairs glucose tolerance and insulin action. We demonstrate that rapamycin disrupted a second mTOR complex, mTORC2, in vivo and that mTORC2 was required for the insulin-mediated suppression of hepatic gluconeogenesis. Further, decreased mTORC1 signaling was sufficient to extend life span independently from changes in glucose homeostasis, as female mice heterozygous for both mTOR and mLST8 exhibited decreased mTORC1 activity and extended life span but had normal glucose tolerance and insulin sensitivity. Thus, mTORC2 disruption is an important mediator of the effects of rapamycin in vivo.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3324089/" 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/PMC3324089/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lamming, Dudley W -- Ye, Lan -- Katajisto, Pekka -- Goncalves, Marcus D -- Saitoh, Maki -- Stevens, Deanna M -- Davis, James G -- Salmon, Adam B -- Richardson, Arlan -- Ahima, Rexford S -- Guertin, David A -- Sabatini, David M -- Baur, Joseph A -- 1F32AG032833-01A1/AG/NIA NIH HHS/ -- CA129105/CA/NCI NIH HHS/ -- F32 AG032833/AG/NIA NIH HHS/ -- P30DK19525/DK/NIDDK NIH HHS/ -- R01 CA129105/CA/NCI NIH HHS/ -- R01 CA129105-05/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Mar 30;335(6076):1638-43. doi: 10.1126/science.1215135.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22461615" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue, White/metabolism ; Animals ; Carrier Proteins/genetics/metabolism ; Female ; Gluconeogenesis ; Glucose/metabolism ; Glucose Clamp Technique ; Homeostasis ; Insulin/administration & dosage/blood ; *Insulin Resistance ; Liver/metabolism ; *Longevity ; Male ; Mice ; Mice, Inbred C57BL ; Multiprotein Complexes ; Muscle, Skeletal/metabolism ; Phosphorylation ; Proteins/antagonists & inhibitors/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Signal Transduction ; Sirolimus/*pharmacology ; TOR Serine-Threonine Kinases/genetics/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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  • 4
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    Integrative annotation of variants from 1092 humans: application to cancer genomics (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-10-05
    Description: Interpreting variants, especially noncoding ones, in the increasing number of personal genomes is challenging. We used patterns of polymorphisms in functionally annotated regions in 1092 humans to identify deleterious variants; then we experimentally validated candidates. We analyzed both coding and noncoding regions, with the former corroborating the latter. We found regions particularly sensitive to mutations ("ultrasensitive") and variants that are disruptive because of mechanistic effects on transcription-factor binding (that is, "motif-breakers"). We also found variants in regions with higher network centrality tend to be deleterious. Insertions and deletions followed a similar pattern to single-nucleotide variants, with some notable exceptions (e.g., certain deletions and enhancers). On the basis of these patterns, we developed a computational tool (FunSeq), whose application to ~90 cancer genomes reveals nearly a hundred candidate noncoding drivers.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3947637/" 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/PMC3947637/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Khurana, Ekta -- Fu, Yao -- Colonna, Vincenza -- Mu, Xinmeng Jasmine -- Kang, Hyun Min -- Lappalainen, Tuuli -- Sboner, Andrea -- Lochovsky, Lucas -- Chen, Jieming -- Harmanci, Arif -- Das, Jishnu -- Abyzov, Alexej -- Balasubramanian, Suganthi -- Beal, Kathryn -- Chakravarty, Dimple -- Challis, Daniel -- Chen, Yuan -- Clarke, Declan -- Clarke, Laura -- Cunningham, Fiona -- Evani, Uday S -- Flicek, Paul -- Fragoza, Robert -- Garrison, Erik -- Gibbs, Richard -- Gumus, Zeynep H -- Herrero, Javier -- Kitabayashi, Naoki -- Kong, Yong -- Lage, Kasper -- Liluashvili, Vaja -- Lipkin, Steven M -- MacArthur, Daniel G -- Marth, Gabor -- Muzny, Donna -- Pers, Tune H -- Ritchie, Graham R S -- Rosenfeld, Jeffrey A -- Sisu, Cristina -- Wei, Xiaomu -- Wilson, Michael -- Xue, Yali -- Yu, Fuli -- 1000 Genomes Project Consortium -- Dermitzakis, Emmanouil T -- Yu, Haiyuan -- Rubin, Mark A -- Tyler-Smith, Chris -- Gerstein, Mark -- 085532/Wellcome Trust/United Kingdom -- 090532/Wellcome Trust/United Kingdom -- 095908/Wellcome Trust/United Kingdom -- 098051/Wellcome Trust/United Kingdom -- CA167824/CA/NCI NIH HHS/ -- G12 MD007579/MD/NIMHD NIH HHS/ -- G12 RR003050/RR/NCRR NIH HHS/ -- GM104424/GM/NIGMS NIH HHS/ -- HG005718/HG/NHGRI NIH HHS/ -- HG007000/HG/NHGRI NIH HHS/ -- P20 MD006899/MD/NIMHD NIH HHS/ -- R01 CA166661/CA/NCI NIH HHS/ -- R01 HG002898/HG/NHGRI NIH HHS/ -- R01CA152057/CA/NCI NIH HHS/ -- R01HG4719/HG/NHGRI NIH HHS/ -- U01 CA111275/CA/NCI NIH HHS/ -- U01 HG005718/HG/NHGRI NIH HHS/ -- U01HG6513/HG/NHGRI NIH HHS/ -- U41 HG007000/HG/NHGRI NIH HHS/ -- U54 HG003079/HG/NHGRI NIH HHS/ -- UL1 TR000457/TR/NCATS NIH HHS/ -- WT085532/Wellcome Trust/United Kingdom -- WT095908/Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2013 Oct 4;342(6154):1235587. doi: 10.1126/science.1235587.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Computational Biology and Bioinformatics, Yale University, New Haven, CT 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24092746" target="_blank"〉PubMed〈/a〉
    Keywords: Binding Sites/genetics ; *Genetic Variation ; Genome, Human ; Genomics ; Humans ; Kruppel-Like Transcription Factors/metabolism ; Molecular Sequence Annotation/*methods ; Mutation ; Neoplasms/*genetics ; Polymorphism, Single Nucleotide ; Population/genetics ; RNA, Untranslated/genetics ; Selection, Genetic
    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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  • 5
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    The genetic map of Artemisia annua L. identifies loci affecting yield of the antimalarial drug artemisinin (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-01-16
    Description: Artemisinin is a plant natural product produced by Artemisia annua and the active ingredient in the most effective treatment for malaria. Efforts to eradicate malaria are increasing demand for an affordable, high-quality, robust supply of artemisinin. We performed deep sequencing on the transcriptome of A. annua to identify genes and markers for fast-track breeding. Extensive genetic variation enabled us to build a detailed genetic map with nine linkage groups. Replicated field trials resulted in a quantitative trait loci (QTL) map that accounts for a significant amount of the variation in key traits controlling artemisinin yield. Enrichment for positive QTLs in parents of new high-yielding hybrids confirms that the knowledge and tools to convert A. annua into a robust crop are now available.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Graham, Ian A -- Besser, Katrin -- Blumer, Susan -- Branigan, Caroline A -- Czechowski, Tomasz -- Elias, Luisa -- Guterman, Inna -- Harvey, David -- Isaac, Peter G -- Khan, Awais M -- Larson, Tony R -- Li, Yi -- Pawson, Tanya -- Penfield, Teresa -- Rae, Anne M -- Rathbone, Deborah A -- Reid, Sonja -- Ross, Joe -- Smallwood, Margaret F -- Segura, Vincent -- Townsend, Theresa -- Vyas, Darshna -- Winzer, Thilo -- Bowles, Dianna -- New York, N.Y. -- Science. 2010 Jan 15;327(5963):328-31. doi: 10.1126/science.1182612.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Novel Agricultural Products, Department of Biology, University of York, York YO10 5YW, UK. iag1@york.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20075252" target="_blank"〉PubMed〈/a〉
    Keywords: Antimalarials/*metabolism ; Artemisia/*genetics/*metabolism ; Artemisinins/*metabolism ; *Chromosome Mapping ; Crosses, Genetic ; DNA, Complementary ; Gene Expression Profiling ; *Genes, Plant ; Genetic Association Studies ; Humans ; Malaria/drug therapy ; Mutation ; Phenotype ; Polymorphism, Single Nucleotide ; *Quantitative Trait Loci ; Sequence Analysis, DNA
    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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  • 6
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    Genotype to phenotype: a complex problem (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-04-24
    Description: We generated a high-resolution whole-genome sequence and individually deleted 5100 genes in Sigma1278b, a Saccharomyces cerevisiae strain closely related to reference strain S288c. Similar to the variation between human individuals, Sigma1278b and S288c average 3.2 single-nucleotide polymorphisms per kilobase. A genome-wide comparison of deletion mutant phenotypes identified a subset of genes that were conditionally essential by strain, including 44 essential genes unique to Sigma1278b and 13 unique to S288c. Genetic analysis indicates the conditional phenotype was most often governed by complex genetic interactions, depending on multiple background-specific modifiers. Our comprehensive analysis suggests that the presence of a complex set of modifiers will often underlie the phenotypic differences between individuals.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4412269/" 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/PMC4412269/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dowell, Robin D -- Ryan, Owen -- Jansen, An -- Cheung, Doris -- Agarwala, Sudeep -- Danford, Timothy -- Bernstein, Douglas A -- Rolfe, P Alexander -- Heisler, Lawrence E -- Chin, Brian -- Nislow, Corey -- Giaever, Guri -- Phillips, Patrick C -- Fink, Gerald R -- Gifford, David K -- Boone, Charles -- DK076284/DK/NIDDK NIH HHS/ -- GM035010/GM/NIGMS NIH HHS/ -- GM069676/GM/NIGMS NIH HHS/ -- P01 NS055923/NS/NINDS NIH HHS/ -- R01 GM035010/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Apr 23;328(5977):469. doi: 10.1126/science.1189015.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Computer Science and Artificial Intelligence Laboratory, Department of Electrical Engineering and Computer Science, Massachusetts Institute of Technology (MIT), Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20413493" target="_blank"〉PubMed〈/a〉
    Keywords: Crosses, Genetic ; Gene Deletion ; *Gene Expression Regulation, Fungal ; Gene Regulatory Networks ; *Genes, Essential ; *Genes, Fungal ; Genetic Variation ; Genome, Fungal ; Genotype ; Mutation ; Phenotype ; Saccharomyces cerevisiae/*genetics ; Sequence Analysis, DNA
    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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  • 7
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    The ancient drug salicylate directly activates AMP-activated protein kinase (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-04-21
    Description: Salicylate, a plant product, has been in medicinal use since ancient times. More recently, it has been replaced by synthetic derivatives such as aspirin and salsalate, both of which are rapidly broken down to salicylate in vivo. At concentrations reached in plasma after administration of salsalate or of aspirin at high doses, salicylate activates adenosine monophosphate-activated protein kinase (AMPK), a central regulator of cell growth and metabolism. Salicylate binds at the same site as the synthetic activator A-769662 to cause allosteric activation and inhibition of dephosphorylation of the activating phosphorylation site, threonine-172. In AMPK knockout mice, effects of salicylate to increase fat utilization and to lower plasma fatty acids in vivo were lost. Our results suggest that AMPK activation could explain some beneficial effects of salsalate and aspirin in humans.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3399766/" 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/PMC3399766/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hawley, Simon A -- Fullerton, Morgan D -- Ross, Fiona A -- Schertzer, Jonathan D -- Chevtzoff, Cyrille -- Walker, Katherine J -- Peggie, Mark W -- Zibrova, Darya -- Green, Kevin A -- Mustard, Kirsty J -- Kemp, Bruce E -- Sakamoto, Kei -- Steinberg, Gregory R -- Hardie, D Grahame -- 080982/Wellcome Trust/United Kingdom -- 097726/Wellcome Trust/United Kingdom -- MC_U127088492/Medical Research Council/United Kingdom -- Canadian Institutes of Health Research/Canada -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2012 May 18;336(6083):918-22. doi: 10.1126/science.1215327. Epub 2012 Apr 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Cell Signalling and Immunology, College of Life Sciences, University of Dundee, Dundee DD1 5EH, Scotland, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22517326" target="_blank"〉PubMed〈/a〉
    Keywords: AMP-Activated Protein Kinases/genetics/*metabolism ; Amino Acid Substitution ; Animals ; Aspirin/pharmacology ; Binding Sites ; Carbohydrate Metabolism/drug effects ; Cell Line ; Enzyme Activation ; Enzyme Activators/pharmacology ; HEK293 Cells ; Humans ; Lipid Metabolism/drug effects ; Liver/drug effects/metabolism ; Mice ; Mice, Knockout ; Mutation ; Oxygen Consumption/drug effects ; Phosphorylation ; Pyrones/pharmacology ; Rats ; Salicylates/blood/*metabolism/*pharmacology ; Thiophenes/pharmacology
    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
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    Dietary restriction: standing up for sirtuins (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-08-28
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3985480/" 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/PMC3985480/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baur, Joseph A -- Chen, Danica -- Chini, Eduardo N -- Chua, Katrin -- Cohen, Haim Y -- de Cabo, Rafael -- Deng, Chuxia -- Dimmeler, Stefanie -- Gius, David -- Guarente, Leonard P -- Helfand, Stephen L -- Imai, Shin-Ichiro -- Itoh, Hiroshi -- Kadowaki, Takashi -- Koya, Daisuke -- Leeuwenburgh, Christiaan -- McBurney, Michael -- Nabeshima, Yo-Ichi -- Neri, Christian -- Oberdoerffer, Philipp -- Pestell, Richard G -- Rogina, Blanka -- Sadoshima, Junichi -- Sartorelli, Vittorio -- Serrano, Manuel -- Sinclair, David A -- Steegborn, Clemens -- Tatar, Marc -- Tissenbaum, Heidi A -- Tong, Qiang -- Tsubota, Kazuo -- Vaquero, Alejandro -- Verdin, Eric -- P01 AG027916/AG/NIA NIH HHS/ -- R00 AG031182/AG/NIA NIH HHS/ -- R01 AG019719/AG/NIA NIH HHS/ -- R01 AG023039/AG/NIA NIH HHS/ -- R01 AG023088/AG/NIA NIH HHS/ -- R01 AG023088-08/AG/NIA NIH HHS/ -- R01 AG024360/AG/NIA NIH HHS/ -- R01 AG028730/AG/NIA NIH HHS/ -- R01 AG028730-05/AG/NIA NIH HHS/ -- R01 HL067724/HL/NHLBI NIH HHS/ -- R01 HL091469/HL/NHLBI NIH HHS/ -- R01 HL102738/HL/NHLBI NIH HHS/ -- R37 AG024360/AG/NIA NIH HHS/ -- Z99 DK999999/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2010 Aug 27;329(5995):1012-3; author reply 1013-4. doi: 10.1126/science.329.5995.1012.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20798296" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*physiology ; Animals ; *Caloric Restriction ; Humans ; *Longevity ; Signal Transduction ; Sirtuins/*physiology
    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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  • 9
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    Bacteria use type IV pili to walk upright and detach from surfaces (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-10-12
    Description: Bacterial biofilms are structured multicellular communities involved in a broad range of infections. Knowing how free-swimming bacteria adapt their motility mechanisms near surfaces is crucial for understanding the transition between planktonic and biofilm phenotypes. By translating microscopy movies into searchable databases of bacterial behavior, we identified fundamental type IV pili-driven mechanisms for Pseudomonas aeruginosa surface motility involved in distinct foraging strategies. Bacteria stood upright and "walked" with trajectories optimized for two-dimensional surface exploration. Vertical orientation facilitated surface detachment and could influence biofilm morphology.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gibiansky, Maxsim L -- Conrad, Jacinta C -- Jin, Fan -- Gordon, Vernita D -- Motto, Dominick A -- Mathewson, Margie A -- Stopka, Wiktor G -- Zelasko, Daria C -- Shrout, Joshua D -- Wong, Gerard C L -- New York, N.Y. -- Science. 2010 Oct 8;330(6001):197. doi: 10.1126/science.1194238.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Bioengineering, California Nano Systems Institute,University of California, Los Angeles, CA 90024, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20929769" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Bacterial Adhesion ; *Biofilms ; Cell Division ; Databases, Factual ; Fimbriae, Bacterial/*physiology ; Microscopy ; Motion Pictures as Topic ; Movement ; Mutation ; Pseudomonas aeruginosa/genetics/*physiology/ultrastructure
    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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  • 10
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    Phosphorylation of ULK1 (hATG1) by AMP-activated protein kinase connects energy sensing to mitophagy (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-01-06
    Description: Adenosine monophosphate-activated protein kinase (AMPK) is a conserved sensor of intracellular energy activated in response to low nutrient availability and environmental stress. In a screen for conserved substrates of AMPK, we identified ULK1 and ULK2, mammalian orthologs of the yeast protein kinase Atg1, which is required for autophagy. Genetic analysis of AMPK or ULK1 in mammalian liver and Caenorhabditis elegans revealed a requirement for these kinases in autophagy. In mammals, loss of AMPK or ULK1 resulted in aberrant accumulation of the autophagy adaptor p62 and defective mitophagy. Reconstitution of ULK1-deficient cells with a mutant ULK1 that cannot be phosphorylated by AMPK revealed that such phosphorylation is required for mitochondrial homeostasis and cell survival during starvation. These findings uncover a conserved biochemical mechanism coupling nutrient status with autophagy and cell survival.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3030664/" 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/PMC3030664/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Egan, Daniel F -- Shackelford, David B -- Mihaylova, Maria M -- Gelino, Sara -- Kohnz, Rebecca A -- Mair, William -- Vasquez, Debbie S -- Joshi, Aashish -- Gwinn, Dana M -- Taylor, Rebecca -- Asara, John M -- Fitzpatrick, James -- Dillin, Andrew -- Viollet, Benoit -- Kundu, Mondira -- Hansen, Malene -- Shaw, Reuben J -- 1P01CA120964/CA/NCI NIH HHS/ -- 1P01CA120964-01A/CA/NCI NIH HHS/ -- 5P30CA006516-43/CA/NCI NIH HHS/ -- P01 CA120964/CA/NCI NIH HHS/ -- P01 CA120964-05/CA/NCI NIH HHS/ -- P30 CA006516/CA/NCI NIH HHS/ -- P30 CA006516-43/CA/NCI NIH HHS/ -- P30CA014195/CA/NCI NIH HHS/ -- R01 DK080425/DK/NIDDK NIH HHS/ -- R01 DK080425-04/DK/NIDDK NIH HHS/ -- R01 DK080425-05/DK/NIDDK NIH HHS/ -- T32 CA009370/CA/NCI NIH HHS/ -- T32 CA009370-29/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Jan 28;331(6016):456-61. doi: 10.1126/science.1196371. Epub 2010 Dec 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular and Cell Biology Laboratory, Dulbecco Center for Cancer Research, Salk Institute for Biological Studies, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21205641" target="_blank"〉PubMed〈/a〉
    Keywords: AMP-Activated Protein Kinases/*metabolism ; Adaptor Proteins, Signal Transducing/metabolism ; Animals ; *Autophagy ; Caenorhabditis elegans/metabolism ; Caenorhabditis elegans Proteins/genetics/metabolism ; Cell Line ; Cell Line, Tumor ; Cell Survival ; Energy Metabolism ; Hepatocytes/metabolism ; Humans ; Insulin/metabolism ; Intracellular Signaling Peptides and Proteins/chemistry/genetics/*metabolism ; Liver/metabolism ; Metformin/pharmacology ; Mice ; Mitochondria, Liver/metabolism/ultrastructure ; Phenformin/pharmacology ; Phosphorylation ; Protein-Serine-Threonine Kinases/chemistry/genetics/*metabolism ; Signal Transduction ; Transcription Factors/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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