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  • Animals  (10)
  • Cell Line, Tumor  (3)
  • Nature Publishing Group (NPG)  (8)
  • American Association for the Advancement of Science (AAAS)  (5)
  • American Chemical Society (ACS)
  • Oxford University Press
  • 2010-2014  (6)
  • 2005-2009  (7)
  • 1940-1944
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Keywords
Publisher
  • Nature Publishing Group (NPG)  (8)
  • American Association for the Advancement of Science (AAAS)  (5)
  • American Chemical Society (ACS)
  • Oxford University Press
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  • 1
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    The landscape of somatic copy-number alteration across human cancers (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-02-19
    Description: A powerful way to discover key genes with causal roles in oncogenesis is to identify genomic regions that undergo frequent alteration in human cancers. Here we present high-resolution analyses of somatic copy-number alterations (SCNAs) from 3,131 cancer specimens, belonging largely to 26 histological types. We identify 158 regions of focal SCNA that are altered at significant frequency across several cancer types, of which 122 cannot be explained by the presence of a known cancer target gene located within these regions. Several gene families are enriched among these regions of focal SCNA, including the BCL2 family of apoptosis regulators and the NF-kappaBeta pathway. We show that cancer cells containing amplifications surrounding the MCL1 and BCL2L1 anti-apoptotic genes depend on the expression of these genes for survival. Finally, we demonstrate that a large majority of SCNAs identified in individual cancer types are present in several cancer types.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2826709/" 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/PMC2826709/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Beroukhim, Rameen -- Mermel, Craig H -- Porter, Dale -- Wei, Guo -- Raychaudhuri, Soumya -- Donovan, Jerry -- Barretina, Jordi -- Boehm, Jesse S -- Dobson, Jennifer -- Urashima, Mitsuyoshi -- Mc Henry, Kevin T -- Pinchback, Reid M -- Ligon, Azra H -- Cho, Yoon-Jae -- Haery, Leila -- Greulich, Heidi -- Reich, Michael -- Winckler, Wendy -- Lawrence, Michael S -- Weir, Barbara A -- Tanaka, Kumiko E -- Chiang, Derek Y -- Bass, Adam J -- Loo, Alice -- Hoffman, Carter -- Prensner, John -- Liefeld, Ted -- Gao, Qing -- Yecies, Derek -- Signoretti, Sabina -- Maher, Elizabeth -- Kaye, Frederic J -- Sasaki, Hidefumi -- Tepper, Joel E -- Fletcher, Jonathan A -- Tabernero, Josep -- Baselga, Jose -- Tsao, Ming-Sound -- Demichelis, Francesca -- Rubin, Mark A -- Janne, Pasi A -- Daly, Mark J -- Nucera, Carmelo -- Levine, Ross L -- Ebert, Benjamin L -- Gabriel, Stacey -- Rustgi, Anil K -- Antonescu, Cristina R -- Ladanyi, Marc -- Letai, Anthony -- Garraway, Levi A -- Loda, Massimo -- Beer, David G -- True, Lawrence D -- Okamoto, Aikou -- Pomeroy, Scott L -- Singer, Samuel -- Golub, Todd R -- Lander, Eric S -- Getz, Gad -- Sellers, William R -- Meyerson, Matthew -- K08 AR055688/AR/NIAMS NIH HHS/ -- K08 AR055688-03/AR/NIAMS NIH HHS/ -- K08 AR055688-04/AR/NIAMS NIH HHS/ -- K08 CA122833/CA/NCI NIH HHS/ -- K08 CA122833-01A1/CA/NCI NIH HHS/ -- K08 CA122833-02/CA/NCI NIH HHS/ -- K08 CA122833-03/CA/NCI NIH HHS/ -- K08 CA134931/CA/NCI NIH HHS/ -- K08CA122833/CA/NCI NIH HHS/ -- P01CA 098101/CA/NCI NIH HHS/ -- P01CA085859/CA/NCI NIH HHS/ -- P50CA90578/CA/NCI NIH HHS/ -- R01 CA109038/CA/NCI NIH HHS/ -- R01 GM074024/GM/NIGMS NIH HHS/ -- R01CA109038/CA/NCI NIH HHS/ -- R01CA109467/CA/NCI NIH HHS/ -- T32 GM007753/GM/NIGMS NIH HHS/ -- U24 CA126546/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Feb 18;463(7283):899-905. doi: 10.1038/nature08822.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Program and Medical and Population Genetics Group, The Broad Institute of M.I.T. and Harvard, 7 Cambridge Center.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20164920" target="_blank"〉PubMed〈/a〉
    Keywords: Apoptosis/genetics ; Cell Line, Tumor ; Cell Survival/genetics ; DNA Copy Number Variations/*genetics ; Gene Amplification/genetics ; Gene Dosage/*genetics ; Genomics ; Humans ; Multigene Family/genetics ; Myeloid Cell Leukemia Sequence 1 Protein ; Neoplasms/classification/*genetics/pathology ; Proto-Oncogene Proteins c-bcl-2/genetics ; Signal Transduction ; bcl-X Protein/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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  • 2
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    TRPC channel activation by extracellular thioredoxin (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-01-04
    Description: Mammalian homologues of Drosophila melanogaster transient receptor potential (TRP) are a large family of multimeric cation channels that act, or putatively act, as sensors of one or more chemical factor. Major research objectives are the identification of endogenous activators and the determination of cellular and tissue functions of these channels. Here we show the activation of TRPC5 (canonical TRP 5) homomultimeric and TRPC5-TRPC1 heteromultimeric channels by extracellular reduced thioredoxin, which acts by breaking a disulphide bridge in the predicted extracellular loop adjacent to the ion-selectivity filter of TRPC5. Thioredoxin is an endogenous redox protein with established intracellular functions, but it is also secreted and its extracellular targets are largely unknown. Particularly high extracellular concentrations of thioredoxin are apparent in rheumatoid arthritis, an inflammatory joint disease that disables millions of people worldwide. We show that TRPC5 and TRPC1 are expressed in secretory fibroblast-like synoviocytes from patients with rheumatoid arthritis, that endogenous TRPC5-TRPC1 channels of the cells are activated by reduced thioredoxin, and that blockade of the channels enhances secretory activity and prevents the suppression of secretion by thioredoxin. The data indicate the presence of a previously unrecognized ion-channel activation mechanism that couples extracellular thioredoxin to cell function.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2645077/" 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/PMC2645077/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xu, Shang-Zhong -- Sukumar, Piruthivi -- Zeng, Fanning -- Li, Jing -- Jairaman, Amit -- English, Anne -- Naylor, Jacqueline -- Ciurtin, Coziana -- Majeed, Yasser -- Milligan, Carol J -- Bahnasi, Yahya M -- Al-Shawaf, Eman -- Porter, Karen E -- Jiang, Lin-Hua -- Emery, Paul -- Sivaprasadarao, Asipu -- Beech, David J -- 077424/Wellcome Trust/United Kingdom -- 083857/Wellcome Trust/United Kingdom -- 18475/Arthritis Research UK/United Kingdom -- BB/D524875/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- England -- Nature. 2008 Jan 3;451(7174):69-72. doi: 10.1038/nature06414.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Membrane and Systems Biology, Garstang Building, Faculty of Biological Sciences, University of Leeds, Leeds LS2 9JT, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18172497" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arthritis, Rheumatoid/metabolism/pathology ; Cell Line ; Disulfides/chemistry/metabolism ; Electric Conductivity ; Humans ; Oxidation-Reduction/drug effects ; Patch-Clamp Techniques ; Rabbits ; TRPC Cation Channels/*agonists/chemistry/*metabolism ; Thioredoxins/chemistry/*pharmacology
    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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    Tankyrase inhibition stabilizes axin and antagonizes Wnt signalling (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-09-18
    Description: The stability of the Wnt pathway transcription factor beta-catenin is tightly regulated by the multi-subunit destruction complex. Deregulated Wnt pathway activity has been implicated in many cancers, making this pathway an attractive target for anticancer therapies. However, the development of targeted Wnt pathway inhibitors has been hampered by the limited number of pathway components that are amenable to small molecule inhibition. Here, we used a chemical genetic screen to identify a small molecule, XAV939, which selectively inhibits beta-catenin-mediated transcription. XAV939 stimulates beta-catenin degradation by stabilizing axin, the concentration-limiting component of the destruction complex. Using a quantitative chemical proteomic approach, we discovered that XAV939 stabilizes axin by inhibiting the poly-ADP-ribosylating enzymes tankyrase 1 and tankyrase 2. Both tankyrase isoforms interact with a highly conserved domain of axin and stimulate its degradation through the ubiquitin-proteasome pathway. Thus, our study provides new mechanistic insights into the regulation of axin protein homeostasis and presents new avenues for targeted Wnt pathway therapies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, Shih-Min A -- Mishina, Yuji M -- Liu, Shanming -- Cheung, Atwood -- Stegmeier, Frank -- Michaud, Gregory A -- Charlat, Olga -- Wiellette, Elizabeth -- Zhang, Yue -- Wiessner, Stephanie -- Hild, Marc -- Shi, Xiaoying -- Wilson, Christopher J -- Mickanin, Craig -- Myer, Vic -- Fazal, Aleem -- Tomlinson, Ronald -- Serluca, Fabrizio -- Shao, Wenlin -- Cheng, Hong -- Shultz, Michael -- Rau, Christina -- Schirle, Markus -- Schlegl, Judith -- Ghidelli, Sonja -- Fawell, Stephen -- Lu, Chris -- Curtis, Daniel -- Kirschner, Marc W -- Lengauer, Christoph -- Finan, Peter M -- Tallarico, John A -- Bouwmeester, Tewis -- Porter, Jeffery A -- Bauer, Andreas -- Cong, Feng -- England -- Nature. 2009 Oct 1;461(7264):614-20. doi: 10.1038/nature08356. Epub 2009 Sep 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Novartis Institutes for Biomedical Research, 250 Massachusetts Avenue, Cambridge, Massachusetts 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19759537" target="_blank"〉PubMed〈/a〉
    Keywords: Axin Protein ; Cell Division/drug effects ; Cell Line ; Cell Line, Tumor ; Colorectal Neoplasms/drug therapy/metabolism ; Heterocyclic Compounds, 3-Ring/pharmacology ; Humans ; Proteasome Endopeptidase Complex/metabolism ; Protein Binding ; Proteomics ; Repressor Proteins/chemistry/*metabolism ; Signal Transduction/*drug effects ; Tankyrases/*antagonists & inhibitors/metabolism ; Transcription, Genetic/drug effects ; Ubiquitin/metabolism ; Ubiquitination ; Wnt Proteins/*antagonists & inhibitors/metabolism ; beta Catenin/antagonists & inhibitors/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
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    The molecular architecture of axonemes revealed by cryoelectron tomography (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-08-19
    Description: Eukaryotic flagella and cilia are built on a 9 + 2 array of microtubules plus 〉250 accessory proteins, forming a biological machine called the axoneme. Here we describe the three-dimensional structure of rapidly frozen axonemes from Chlamydomonas and sea urchin sperm, using cryoelectron tomography and image processing to focus on the motor enzyme dynein. Our images suggest a model for the way dynein generates force to slide microtubules. They also reveal two dynein linkers that may provide "hard-wiring" to coordinate motor enzyme action, both circumferentially and along the axoneme. Periodic densities were also observed inside doublet microtubules; these may contribute to doublet stability.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nicastro, Daniela -- Schwartz, Cindi -- Pierson, Jason -- Gaudette, Richard -- Porter, Mary E -- McIntosh, J Richard -- 2R37-GM55667/GM/NIGMS NIH HHS/ -- RR 000592/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2006 Aug 18;313(5789):944-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for 3D Electron Microscopy of Cells, Department of Molecular, Cellular, and Developmental Biology, CB 347, University of Colorado, Boulder, CO 80309-0347, USA. nicastro@colorado.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16917055" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carrier Proteins/chemistry/ultrastructure ; Chlamydomonas reinhardtii/ultrastructure ; Cryoelectron Microscopy ; Dyneins/*chemistry/physiology/*ultrastructure ; Flagella/chemistry/physiology/*ultrastructure ; Freezing ; Image Processing, Computer-Assisted ; Imaging, Three-Dimensional ; Male ; Microtubule-Associated Proteins ; Microtubules/chemistry/physiology/*ultrastructure ; Models, Biological ; Molecular Motor Proteins/chemistry/ultrastructure ; Protein Structure, Tertiary ; Sea Urchins ; Sperm Tail/chemistry/physiology/*ultrastructure ; Tomography
    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 Chlamydomonas genome reveals the evolution of key animal and plant functions (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-10-13
    Description: Chlamydomonas reinhardtii is a unicellular green alga whose lineage diverged from land plants over 1 billion years ago. It is a model system for studying chloroplast-based photosynthesis, as well as the structure, assembly, and function of eukaryotic flagella (cilia), which were inherited from the common ancestor of plants and animals, but lost in land plants. We sequenced the approximately 120-megabase nuclear genome of Chlamydomonas and performed comparative phylogenomic analyses, identifying genes encoding uncharacterized proteins that are likely associated with the function and biogenesis of chloroplasts or eukaryotic flagella. Analyses of the Chlamydomonas genome advance our understanding of the ancestral eukaryotic cell, reveal previously unknown genes associated with photosynthetic and flagellar functions, and establish links between ciliopathy and the composition and function of flagella.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2875087/" 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/PMC2875087/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Merchant, Sabeeha S -- Prochnik, Simon E -- Vallon, Olivier -- Harris, Elizabeth H -- Karpowicz, Steven J -- Witman, George B -- Terry, Astrid -- Salamov, Asaf -- Fritz-Laylin, Lillian K -- Marechal-Drouard, Laurence -- Marshall, Wallace F -- Qu, Liang-Hu -- Nelson, David R -- Sanderfoot, Anton A -- Spalding, Martin H -- Kapitonov, Vladimir V -- Ren, Qinghu -- Ferris, Patrick -- Lindquist, Erika -- Shapiro, Harris -- Lucas, Susan M -- Grimwood, Jane -- Schmutz, Jeremy -- Cardol, Pierre -- Cerutti, Heriberto -- Chanfreau, Guillaume -- Chen, Chun-Long -- Cognat, Valerie -- Croft, Martin T -- Dent, Rachel -- Dutcher, Susan -- Fernandez, Emilio -- Fukuzawa, Hideya -- Gonzalez-Ballester, David -- Gonzalez-Halphen, Diego -- Hallmann, Armin -- Hanikenne, Marc -- Hippler, Michael -- Inwood, William -- Jabbari, Kamel -- Kalanon, Ming -- Kuras, Richard -- Lefebvre, Paul A -- Lemaire, Stephane D -- Lobanov, Alexey V -- Lohr, Martin -- Manuell, Andrea -- Meier, Iris -- Mets, Laurens -- Mittag, Maria -- Mittelmeier, Telsa -- Moroney, James V -- Moseley, Jeffrey -- Napoli, Carolyn -- Nedelcu, Aurora M -- Niyogi, Krishna -- Novoselov, Sergey V -- Paulsen, Ian T -- Pazour, Greg -- Purton, Saul -- Ral, Jean-Philippe -- Riano-Pachon, Diego Mauricio -- Riekhof, Wayne -- Rymarquis, Linda -- Schroda, Michael -- Stern, David -- Umen, James -- Willows, Robert -- Wilson, Nedra -- Zimmer, Sara Lana -- Allmer, Jens -- Balk, Janneke -- Bisova, Katerina -- Chen, Chong-Jian -- Elias, Marek -- Gendler, Karla -- Hauser, Charles -- Lamb, Mary Rose -- Ledford, Heidi -- Long, Joanne C -- Minagawa, Jun -- Page, M Dudley -- Pan, Junmin -- Pootakham, Wirulda -- Roje, Sanja -- Rose, Annkatrin -- Stahlberg, Eric -- Terauchi, Aimee M -- Yang, Pinfen -- Ball, Steven -- Bowler, Chris -- Dieckmann, Carol L -- Gladyshev, Vadim N -- Green, Pamela -- Jorgensen, Richard -- Mayfield, Stephen -- Mueller-Roeber, Bernd -- Rajamani, Sathish -- Sayre, Richard T -- Brokstein, Peter -- Dubchak, Inna -- Goodstein, David -- Hornick, Leila -- Huang, Y Wayne -- Jhaveri, Jinal -- Luo, Yigong -- Martinez, Diego -- Ngau, Wing Chi Abby -- Otillar, Bobby -- Poliakov, Alexander -- Porter, Aaron -- Szajkowski, Lukasz -- Werner, Gregory -- Zhou, Kemin -- Grigoriev, Igor V -- Rokhsar, Daniel S -- Grossman, Arthur R -- GM07185/GM/NIGMS NIH HHS/ -- GM42143/GM/NIGMS NIH HHS/ -- R01 GM032843/GM/NIGMS NIH HHS/ -- R01 GM042143/GM/NIGMS NIH HHS/ -- R01 GM042143-09/GM/NIGMS NIH HHS/ -- R01 GM060992/GM/NIGMS NIH HHS/ -- R01 GM062915-06/GM/NIGMS NIH HHS/ -- R37 GM030626/GM/NIGMS NIH HHS/ -- R37 GM042143/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2007 Oct 12;318(5848):245-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry and Biochemistry, University of California at Los Angeles, Los Angeles, CA 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17932292" target="_blank"〉PubMed〈/a〉
    Keywords: Algal Proteins/*genetics/*physiology ; Animals ; *Biological Evolution ; Chlamydomonas reinhardtii/*genetics/physiology ; Chloroplasts/metabolism ; Computational Biology ; DNA, Algal/genetics ; Flagella/metabolism ; Genes ; *Genome ; Genomics ; Membrane Transport Proteins/genetics/physiology ; Molecular Sequence Data ; Multigene Family ; Photosynthesis/genetics ; Phylogeny ; Plants/genetics ; Proteome ; 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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    Seawater chemistry and early carbonate biomineralization (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-06-02
    Description: The first appearances of aragonite and calcite skeletons in 18 animal clades that independently evolved mineralization during the late Ediacaran through the Ordovician (approximately 550 to 444 million years ago) correspond to intervals when seawater chemistry favored aragonite and calcite precipitation, respectively. Skeletal mineralogies rarely changed once skeletons evolved, despite subsequent changes in seawater chemistry. Thus, the selection of carbonate skeletal minerals appears to have been dictated by seawater chemistry at the time a clade first acquired its mineralized skeleton.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Porter, Susannah M -- New York, N.Y. -- Science. 2007 Jun 1;316(5829):1302.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Earth Science, University of California at Santa Barbara, Santa Barbara, CA 93106, USA. porter@geol.ucsb.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17540895" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; *Calcification, Physiologic ; Calcium/analysis ; Calcium Carbonate/*analysis ; Chemical Precipitation ; Crystallization ; *Fossils ; Invertebrates/*chemistry ; Magnesium/analysis ; Seawater/*chemistry
    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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    Caspases 3 and 7: key mediators of mitochondrial events of apoptosis (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-02-14
    Description: The current model of apoptosis holds that upstream signals lead to activation of downstream effector caspases. We generated mice deficient in the two effectors, caspase 3 and caspase 7, which died immediately after birth with defects in cardiac development. Fibroblasts lacking both enzymes were highly resistant to both mitochondrial and death receptor-mediated apoptosis, displayed preservation of mitochondrial membrane potential, and had defective nuclear translocation of apoptosis-inducing factor (AIF). Furthermore, the early apoptotic events of Bax translocation and cytochrome c release were also delayed. We conclude that caspases 3 and 7 are critical mediators of mitochondrial events of apoptosis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3738210/" 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/PMC3738210/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lakhani, Saquib A -- Masud, Ali -- Kuida, Keisuke -- Porter, George A Jr -- Booth, Carmen J -- Mehal, Wajahat Z -- Inayat, Irteza -- Flavell, Richard A -- 1 K08 HD044580/HD/NICHD NIH HHS/ -- 5 K12 HD01401/HD/NICHD NIH HHS/ -- K08 DK002965/DK/NIDDK NIH HHS/ -- K08 DK002965-04/DK/NIDDK NIH HHS/ -- K12 HD00850/HD/NICHD NIH HHS/ -- NIDDK P30-34989/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2006 Feb 10;311(5762):847-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16469926" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Apoptosis Inducing Factor/metabolism ; Caspase 3 ; Caspase 7 ; Caspases/deficiency/*metabolism ; Cell Nucleus/metabolism ; Cell Shape ; Cell Survival ; Cells, Cultured ; Cytochromes c/metabolism ; DNA Fragmentation ; Female ; Fibroblasts/cytology ; Heart/embryology ; Heart Defects, Congenital/etiology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mitochondria/metabolism/*physiology ; Mitochondrial Membranes/physiology ; Permeability ; T-Lymphocytes/cytology ; bcl-2-Associated X Protein/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
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    Dauer-independent insulin/IGF-1-signalling implicates collagen remodelling in longevity (2014)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2014-12-18
    Description: Interventions that delay ageing mobilize mechanisms that protect and repair cellular components, but it is unknown how these interventions might slow the functional decline of extracellular matrices, which are also damaged during ageing. Reduced insulin/IGF-1 signalling (rIIS) extends lifespan across the evolutionary spectrum, and in juvenile Caenorhabditis elegans also allows the transcription factor DAF-16/FOXO to induce development into dauer, a diapause that withstands harsh conditions. It has been suggested that rIIS delays C. elegans ageing through activation of dauer-related processes during adulthood, but some rIIS conditions confer robust lifespan extension unaccompanied by any dauer-like traits. Here we show that rIIS can promote C. elegans longevity through a program that is genetically distinct from the dauer pathway, and requires the Nrf (NF-E2-related factor) orthologue SKN-1 acting in parallel to DAF-16. SKN-1 is inhibited by IIS and has been broadly implicated in longevity, but is rendered dispensable for rIIS lifespan extension by even mild activity of dauer-related processes. When IIS is decreased under conditions that do not induce dauer traits, SKN-1 most prominently increases expression of collagens and other extracellular matrix genes. Diverse genetic, nutritional, and pharmacological pro-longevity interventions delay an age-related decline in collagen expression. These collagens mediate adulthood extracellular matrix remodelling, and are needed for ageing to be delayed by interventions that do not involve dauer traits. By genetically delineating a dauer-independent rIIS ageing pathway, our results show that IIS controls a broad set of protective mechanisms during C. elegans adulthood, and may facilitate elucidation of processes of general importance for longevity. The importance of collagen production in diverse anti-ageing interventions implies that extracellular matrix remodelling is a generally essential signature of longevity assurance, and that agents promoting extracellular matrix youthfulness may have systemic benefit.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4352135/" 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/PMC4352135/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ewald, Collin Y -- Landis, Jess N -- Porter Abate, Jess -- Murphy, Coleen T -- Blackwell, T Keith -- 5T32DK007260/DK/NIDDK NIH HHS/ -- GM062891/GM/NIGMS NIH HHS/ -- P30 DK036836/DK/NIDDK NIH HHS/ -- P30DK036836/DK/NIDDK NIH HHS/ -- R01 GM062891/GM/NIGMS NIH HHS/ -- England -- Nature. 2015 Mar 5;519(7541):97-101. doi: 10.1038/nature14021. Epub 2014 Dec 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Joslin Diabetes Center, One Joslin Place, Boston, Massachusetts 02215, USA [2] Harvard Stem Cell Institute, 7 Divinity Avenue, Cambridge, Massachusetts 02138, USA [3] Department of Genetics, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, Massachusetts 02215, USA. ; Department of Molecular Biology, Lewis-Sigler Institute for Integrative Genomics, Princeton University, 148 Carl Icahn Laboratory, Washington Road, Princeton, New Jersey 08544, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25517099" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/physiology ; Animals ; Caenorhabditis elegans/growth & development/*metabolism ; Caenorhabditis elegans Proteins/*metabolism ; Collagen/biosynthesis/genetics/*metabolism ; DNA-Binding Proteins/*metabolism ; Extracellular Matrix/metabolism ; Forkhead Transcription Factors ; Insulin/*metabolism ; Insulin-Like Growth Factor I/*metabolism ; Larva/growth & development ; Longevity/*physiology ; *Signal Transduction ; Transcription Factors/*metabolism
    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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    A call for transparent reporting to optimize the predictive value of preclinical research (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-10-13
    Description: The US National Institute of Neurological Disorders and Stroke convened major stakeholders in June 2012 to discuss how to improve the methodological reporting of animal studies in grant applications and publications. The main workshop recommendation is that at a minimum studies should report on sample-size estimation, whether and how animals were randomized, whether investigators were blind to the treatment, and the handling of data. We recognize that achieving a meaningful improvement in the quality of reporting will require a concerted effort by investigators, reviewers, funding agencies and journal editors. Requiring better reporting of animal studies will raise awareness of the importance of rigorous study design to accelerate scientific progress.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3511845/" 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/PMC3511845/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Landis, Story C -- Amara, Susan G -- Asadullah, Khusru -- Austin, Chris P -- Blumenstein, Robi -- Bradley, Eileen W -- Crystal, Ronald G -- Darnell, Robert B -- Ferrante, Robert J -- Fillit, Howard -- Finkelstein, Robert -- Fisher, Marc -- Gendelman, Howard E -- Golub, Robert M -- Goudreau, John L -- Gross, Robert A -- Gubitz, Amelie K -- Hesterlee, Sharon E -- Howells, David W -- Huguenard, John -- Kelner, Katrina -- Koroshetz, Walter -- Krainc, Dimitri -- Lazic, Stanley E -- Levine, Michael S -- Macleod, Malcolm R -- McCall, John M -- Moxley, Richard T 3rd -- Narasimhan, Kalyani -- Noble, Linda J -- Perrin, Steve -- Porter, John D -- Steward, Oswald -- Unger, Ellis -- Utz, Ursula -- Silberberg, Shai D -- P01 NS012151/NS/NINDS NIH HHS/ -- P30 MH062261/MH/NIMH NIH HHS/ -- R01 NS006477/NS/NINDS NIH HHS/ -- R01 NS034774/NS/NINDS NIH HHS/ -- R01 NS041574/NS/NINDS NIH HHS/ -- T32 MH020016/MH/NIMH NIH HHS/ -- T32 NS007280/NS/NINDS NIH HHS/ -- UL1 RR024160/RR/NCRR NIH HHS/ -- Z99 NS999999/Intramural NIH HHS/ -- England -- Nature. 2012 Oct 11;490(7419):187-91. doi: 10.1038/nature11556.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Institute of Neurological Disorders and Stroke, NIH, Bethesda, Maryland 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23060188" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Publishing/*standards/trends ; Random Allocation ; Research Design/*standards ; Sample Size ; Statistics as Topic
    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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    The Cancer Cell Line Encyclopedia enables predictive modelling of anticancer drug sensitivity (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-03-31
    Description: The systematic translation of cancer genomic data into knowledge of tumour biology and therapeutic possibilities remains challenging. Such efforts should be greatly aided by robust preclinical model systems that reflect the genomic diversity of human cancers and for which detailed genetic and pharmacological annotation is available. Here we describe the Cancer Cell Line Encyclopedia (CCLE): a compilation of gene expression, chromosomal copy number and massively parallel sequencing data from 947 human cancer cell lines. When coupled with pharmacological profiles for 24 anticancer drugs across 479 of the cell lines, this collection allowed identification of genetic, lineage, and gene-expression-based predictors of drug sensitivity. In addition to known predictors, we found that plasma cell lineage correlated with sensitivity to IGF1 receptor inhibitors; AHR expression was associated with MEK inhibitor efficacy in NRAS-mutant lines; and SLFN11 expression predicted sensitivity to topoisomerase inhibitors. Together, our results indicate that large, annotated cell-line collections may help to enable preclinical stratification schemata for anticancer agents. The generation of genetic predictions of drug response in the preclinical setting and their incorporation into cancer clinical trial design could speed the emergence of 'personalized' therapeutic regimens.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3320027/" 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/PMC3320027/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barretina, Jordi -- Caponigro, Giordano -- Stransky, Nicolas -- Venkatesan, Kavitha -- Margolin, Adam A -- Kim, Sungjoon -- Wilson, Christopher J -- Lehar, Joseph -- Kryukov, Gregory V -- Sonkin, Dmitriy -- Reddy, Anupama -- Liu, Manway -- Murray, Lauren -- Berger, Michael F -- Monahan, John E -- Morais, Paula -- Meltzer, Jodi -- Korejwa, Adam -- Jane-Valbuena, Judit -- Mapa, Felipa A -- Thibault, Joseph -- Bric-Furlong, Eva -- Raman, Pichai -- Shipway, Aaron -- Engels, Ingo H -- Cheng, Jill -- Yu, Guoying K -- Yu, Jianjun -- Aspesi, Peter Jr -- de Silva, Melanie -- Jagtap, Kalpana -- Jones, Michael D -- Wang, Li -- Hatton, Charles -- Palescandolo, Emanuele -- Gupta, Supriya -- Mahan, Scott -- Sougnez, Carrie -- Onofrio, Robert C -- Liefeld, Ted -- MacConaill, Laura -- Winckler, Wendy -- Reich, Michael -- Li, Nanxin -- Mesirov, Jill P -- Gabriel, Stacey B -- Getz, Gad -- Ardlie, Kristin -- Chan, Vivien -- Myer, Vic E -- Weber, Barbara L -- Porter, Jeff -- Warmuth, Markus -- Finan, Peter -- Harris, Jennifer L -- Meyerson, Matthew -- Golub, Todd R -- Morrissey, Michael P -- Sellers, William R -- Schlegel, Robert -- Garraway, Levi A -- DP2 OD002750/OD/NIH HHS/ -- DP2 OD002750-01/OD/NIH HHS/ -- R33 CA126674/CA/NCI NIH HHS/ -- R33 CA126674-04/CA/NCI NIH HHS/ -- R33 CA155554/CA/NCI NIH HHS/ -- R33 CA155554-02/CA/NCI NIH HHS/ -- England -- Nature. 2012 Mar 28;483(7391):603-7. doi: 10.1038/nature11003.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Broad Institute of Harvard and MIT, Cambridge, Massachusetts 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22460905" target="_blank"〉PubMed〈/a〉
    Keywords: Antineoplastic Agents/pharmacology ; Cell Line, Tumor ; Cell Lineage ; Chromosomes, Human/genetics ; Clinical Trials as Topic/methods ; *Databases, Factual ; Drug Screening Assays, Antitumor/*methods ; *Encyclopedias as Topic ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Genes, ras/genetics ; Genome, Human/genetics ; Genomics ; Humans ; Mitogen-Activated Protein Kinase Kinases/antagonists & inhibitors/metabolism ; *Models, Biological ; Neoplasms/*drug therapy/genetics/metabolism/*pathology ; Pharmacogenetics ; Plasma Cells/cytology/drug effects/metabolism ; Precision Medicine/methods ; Receptor, IGF Type 1/antagonists & inhibitors/metabolism ; Receptors, Aryl Hydrocarbon/genetics/metabolism ; Sequence Analysis, DNA ; Topoisomerase Inhibitors/pharmacology
    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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