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  • Articles  (21)
  • Signal Transduction
  • American Association for the Advancement of Science (AAAS)  (21)
  • 2010-2014  (21)
  • 2013  (10)
  • 2012  (11)
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  • Articles  (21)
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  • 2010-2014  (21)
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  • 1
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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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  • 2
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    Minimal "Self" peptides that inhibit phagocytic clearance and enhance delivery of nanoparticles (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-02-23
    Description: Foreign particles and cells are cleared from the body by phagocytes that must also recognize and avoid clearance of "self" cells. The membrane protein CD47 is reportedly a "marker of self" in mice that impedes phagocytosis of self by signaling through the phagocyte receptor CD172a. Minimal "Self" peptides were computationally designed from human CD47 and then synthesized and attached to virus-size particles for intravenous injection into mice that express a CD172a variant compatible with hCD47. Self peptides delay macrophage-mediated clearance of nanoparticles, which promotes persistent circulation that enhances dye and drug delivery to tumors. Self-peptide affinity for CD172a is near the optimum measured for human CD172a variants, and Self peptide also potently inhibits nanoparticle uptake mediated by the contractile cytoskeleton. The reductionist approach reveals the importance of human Self peptides and their utility in enhancing drug delivery and imaging.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3966479/" 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/PMC3966479/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rodriguez, Pia L -- Harada, Takamasa -- Christian, David A -- Pantano, Diego A -- Tsai, Richard K -- Discher, Dennis E -- 8UL1TR000003/TR/NCATS NIH HHS/ -- P01-DK032094/DK/NIDDK NIH HHS/ -- P30-DK090969/DK/NIDDK NIH HHS/ -- R01 EB007049/EB/NIBIB NIH HHS/ -- R01 HL062352/HL/NHLBI NIH HHS/ -- R01-EB007049/EB/NIBIB NIH HHS/ -- R01-HL062352/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2013 Feb 22;339(6122):971-5. doi: 10.1126/science.1229568.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular and Cell Biophysics and NanoBioPolymers Laboratory, University of Pennsylvania, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23430657" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antigens, CD47/chemistry/immunology/metabolism ; Antigens, Differentiation/*metabolism ; Antineoplastic Agents/administration & dosage ; Autoantigens ; Blood Circulation ; Diagnostic Imaging/methods ; Drug Delivery Systems/*methods ; Humans ; Mice ; Mice, Inbred NOD ; Mice, SCID ; *Nanoparticles/administration & dosage/analysis ; Neoplasms/chemistry/diagnosis/drug therapy ; Paclitaxel/administration & dosage ; Particle Size ; Peptide Fragments/chemical synthesis/chemistry/immunology/*metabolism ; Phagocytes/immunology/metabolism ; *Phagocytosis ; Receptors, Immunologic/immunology/*metabolism ; 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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  • 3
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    The alarmin interleukin-33 drives protective antiviral CD8(+) T cell responses (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-02-11
    Description: Pathogen-associated molecular patterns decisively influence antiviral immune responses, whereas the contribution of endogenous signals of tissue damage, also known as damage-associated molecular patterns or alarmins, remains ill defined. We show that interleukin-33 (IL-33), an alarmin released from necrotic cells, is necessary for potent CD8(+) T cell (CTL) responses to replicating, prototypic RNA and DNA viruses in mice. IL-33 signaled through its receptor on activated CTLs, enhanced clonal expansion in a CTL-intrinsic fashion, determined plurifunctional effector cell differentiation, and was necessary for virus control. Moreover, recombinant IL-33 augmented vaccine-induced CTL responses. Radio-resistant cells of the splenic T cell zone produced IL-33, and efficient CTL responses required IL-33 from radio-resistant cells but not from hematopoietic cells. Thus, alarmin release by radio-resistant cells orchestrates protective antiviral CTL responses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bonilla, Weldy V -- Frohlich, Anja -- Senn, Karin -- Kallert, Sandra -- Fernandez, Marylise -- Johnson, Susan -- Kreutzfeldt, Mario -- Hegazy, Ahmed N -- Schrick, Christina -- Fallon, Padraic G -- Klemenz, Roman -- Nakae, Susumu -- Adler, Heiko -- Merkler, Doron -- Lohning, Max -- Pinschewer, Daniel D -- New York, N.Y. -- Science. 2012 Feb 24;335(6071):984-9. doi: 10.1126/science.1215418. Epub 2012 Feb 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Immunology, University of Geneva, 1 rue Michel Servet, 1211 Geneva 4, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22323740" target="_blank"〉PubMed〈/a〉
    Keywords: Adoptive Transfer ; Animals ; Arenaviridae Infections/*immunology/pathology ; Cell Differentiation ; Gene Expression Profiling ; Herpesviridae Infections/*immunology ; Interleukin-33 ; Interleukins/genetics/immunology/*metabolism ; Lymphocyte Activation ; Lymphocytic choriomeningitis virus/*immunology/physiology ; Mice ; Mice, Transgenic ; Necrosis ; Receptors, Interleukin/genetics/metabolism ; Recombinant Proteins/immunology ; Rhadinovirus/*immunology ; Signal Transduction ; Stromal Cells/immunology/metabolism ; T-Lymphocytes, Cytotoxic/*immunology/transplantation ; Tumor Virus Infections/immunology ; Up-Regulation ; Vaccinia virus/immunology ; Virus Replication
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Pivotal roles of cGAS-cGAMP signaling in antiviral defense and immune adjuvant effects (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-08-31
    Description: Invasion of microbial DNA into the cytoplasm of animal cells triggers a cascade of host immune reactions that help clear the infection; however, self DNA in the cytoplasm can cause autoimmune diseases. Biochemical approaches led to the identification of cyclic guanosine monophosphate-adenosine monophosphate (cGAMP) synthase (cGAS) as a cytosolic DNA sensor that triggers innate immune responses. Here, we show that cells from cGAS-deficient (cGas(-/-)) mice, including fibroblasts, macrophages, and dendritic cells, failed to produce type I interferons and other cytokines in response to DNA transfection or DNA virus infection. cGas(-/-) mice were more susceptible to lethal infection with herpes simplex virus 1 (HSV1) than wild-type mice. We also show that cGAMP is an adjuvant that boosts antigen-specific T cell activation and antibody production in mice.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3863637/" 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/PMC3863637/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Xiao-Dong -- Wu, Jiaxi -- Gao, Daxing -- Wang, Hua -- Sun, Lijun -- Chen, Zhijian J -- 5T32AI070116/AI/NIAID NIH HHS/ -- AI-093967/AI/NIAID NIH HHS/ -- R01 AI093967/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Sep 20;341(6152):1390-4. doi: 10.1126/science.1244040. Epub 2013 Aug 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390-9148, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23989956" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Viral/biosynthesis ; DNA, Viral/genetics/immunology ; Dendritic Cells/immunology ; Fibroblasts/immunology ; Herpes Simplex/*immunology ; *Herpesvirus 1, Human ; Interferon Regulatory Factor-3/genetics ; Interferon-beta/*biosynthesis/genetics ; Lymphocyte Activation ; Macrophages/immunology ; Mice ; Mice, Knockout ; Nucleotidyltransferases/genetics/*immunology ; Signal Transduction ; T-Lymphocytes/immunology ; Transfection
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Sexually dimorphic BDNF signaling directs sensory innervation of the mammary gland (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-12-12
    Description: How neural circuits associated with sexually dimorphic organs are differentially assembled during development is unclear. Here, we report a sexually dimorphic pattern of mouse mammary gland sensory innervation and the mechanism of its formation. Brain-derived neurotrophic factor (BDNF), emanating from mammary mesenchyme and signaling through its receptor TrkB on sensory axons, is required for establishing mammary gland sensory innervation of both sexes at early developmental stages. Subsequently, in males, androgens promote mammary mesenchymal expression of a truncated form of TrkB, which prevents BDNF-TrkB signaling in sensory axons and leads to a rapid loss of mammary gland innervation independent of neuronal apoptosis. Thus, sex hormone regulation of a neurotrophic factor signal directs sexually dimorphic axonal growth and maintenance, resulting in generation of a sex-specific neural circuit.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3826154/" 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/PMC3826154/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, Yin -- Rutlin, Michael -- Huang, Siyi -- Barrick, Colleen A -- Wang, Fan -- Jones, Kevin R -- Tessarollo, Lino -- Ginty, David D -- DE019440/DE/NIDCR NIH HHS/ -- EY014998/EY/NEI NIH HHS/ -- NS34814/NS/NINDS NIH HHS/ -- P30 NS050274/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Dec 7;338(6112):1357-60. doi: 10.1126/science.1228258.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Solomon H. Snyder Department of Neuroscience, Howard Hughes Medical Institute, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23224557" target="_blank"〉PubMed〈/a〉
    Keywords: Androgens/metabolism ; Animals ; Axons/*physiology ; Brain-Derived Neurotrophic Factor/genetics/*metabolism ; Female ; Male ; Mammary Glands, Animal/*embryology/*innervation ; Mice ; Mice, Inbred C57BL ; Receptor, trkB/genetics/metabolism ; *Sex Characteristics ; Signal Transduction
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Elementary Ca2+ signals through endothelial TRPV4 channels regulate vascular function (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-05-05
    Description: Major features of the transcellular signaling mechanism responsible for endothelium-dependent regulation of vascular smooth muscle tone are unresolved. We identified local calcium (Ca(2+)) signals ("sparklets") in the vascular endothelium of resistance arteries that represent Ca(2+) influx through single TRPV4 cation channels. Gating of individual TRPV4 channels within a four-channel cluster was cooperative, with activation of as few as three channels per cell causing maximal dilation through activation of endothelial cell intermediate (IK)- and small (SK)-conductance, Ca(2+)-sensitive potassium (K(+)) channels. Endothelial-dependent muscarinic receptor signaling also acted largely through TRPV4 sparklet-mediated stimulation of IK and SK channels to promote vasodilation. These results support the concept that Ca(2+) influx through single TRPV4 channels is leveraged by the amplifier effect of cooperative channel gating and the high Ca(2+) sensitivity of IK and SK channels to cause vasodilation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3715993/" 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/PMC3715993/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sonkusare, Swapnil K -- Bonev, Adrian D -- Ledoux, Jonathan -- Liedtke, Wolfgang -- Kotlikoff, Michael I -- Heppner, Thomas J -- Hill-Eubanks, David C -- Nelson, Mark T -- 1P01HL095488/HL/NHLBI NIH HHS/ -- 2-P20-RR-016435-06/RR/NCRR NIH HHS/ -- GM086736/GM/NIGMS NIH HHS/ -- HL044455/HL/NHLBI NIH HHS/ -- P01 HL095488/HL/NHLBI NIH HHS/ -- R01 HL098243/HL/NHLBI NIH HHS/ -- R01HL098243/HL/NHLBI NIH HHS/ -- R37 DK053832/DK/NIDDK NIH HHS/ -- R37DK053832/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2012 May 4;336(6081):597-601. doi: 10.1126/science.1216283.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, College of Medicine, University of Vermont, Burlington, VT 05405, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22556255" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*metabolism ; *Calcium Signaling ; Endothelial Cells/drug effects/*metabolism/physiology ; Endothelium, Vascular/drug effects/metabolism/physiology ; Intermediate-Conductance Calcium-Activated Potassium Channels/metabolism ; Ion Channel Gating ; Leucine/analogs & derivatives/pharmacology ; Mesenteric Arteries/drug effects/*metabolism/physiology ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Patch-Clamp Techniques ; Receptors, Muscarinic/metabolism ; Signal Transduction ; Small-Conductance Calcium-Activated Potassium Channels/metabolism ; Sulfonamides/pharmacology ; TRPV Cation Channels/agonists/antagonists & inhibitors/*metabolism ; *Vasodilation
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 7
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    Structural features for functional selectivity at serotonin receptors (2013)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2013-03-23
    Description: Drugs active at G protein-coupled receptors (GPCRs) can differentially modulate either canonical or noncanonical signaling pathways via a phenomenon known as functional selectivity or biased signaling. We report biochemical studies showing that the hallucinogen lysergic acid diethylamide, its precursor ergotamine (ERG), and related ergolines display strong functional selectivity for beta-arrestin signaling at the 5-HT2B 5-hydroxytryptamine (5-HT) receptor, whereas they are relatively unbiased at the 5-HT1B receptor. To investigate the structural basis for biased signaling, we determined the crystal structure of the human 5-HT2B receptor bound to ERG and compared it with the 5-HT1B/ERG structure. Given the relatively poor understanding of GPCR structure and function to date, insight into different GPCR signaling pathways is important to better understand both adverse and favorable therapeutic activities.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3644390/" 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/PMC3644390/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wacker, Daniel -- Wang, Chong -- Katritch, Vsevolod -- Han, Gye Won -- Huang, Xi-Ping -- Vardy, Eyal -- McCorvy, John D -- Jiang, Yi -- Chu, Meihua -- Siu, Fai Yiu -- Liu, Wei -- Xu, H Eric -- Cherezov, Vadim -- Roth, Bryan L -- Stevens, Raymond C -- P50 GM073197/GM/NIGMS NIH HHS/ -- R01 DK071662/DK/NIDDK NIH HHS/ -- R01 MH061887/MH/NIMH NIH HHS/ -- R01 MH61887/MH/NIMH NIH HHS/ -- U19 MH082441/MH/NIMH NIH HHS/ -- U19 MH82441/MH/NIMH NIH HHS/ -- U54 GM094618/GM/NIGMS NIH HHS/ -- Y1-CO-1020/CO/NCI NIH HHS/ -- Y1-GM-1104/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2013 May 3;340(6132):615-9. doi: 10.1126/science.1232808. Epub 2013 Mar 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Integrative Structural and Computational Biology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23519215" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Amino Acid Sequence ; Arrestin/metabolism ; Arrestins/metabolism ; Binding Sites ; Crystallography, X-Ray ; Ergolines/chemistry/metabolism ; Ergotamine/chemistry/*metabolism ; HEK293 Cells ; Humans ; Ligands ; Lysergic Acid Diethylamide/chemistry/metabolism ; Models, Molecular ; Molecular Sequence Data ; Protein Conformation ; Protein Structure, Secondary ; Receptor, Serotonin, 5-HT1B/chemistry/*metabolism ; Receptor, Serotonin, 5-HT2B/*chemistry/*metabolism ; Receptors, Serotonin/chemistry/metabolism ; Signal Transduction
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    A steroid receptor-microRNA switch regulates life span in response to signals from the gonad (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-12-15
    Description: Although the gonad primarily functions in procreation, it also affects animal life span. Here, we show that removal of the Caenorhabditis elegans germ line triggers a switch in the regulatory state of the organism to promote longevity, co-opting components involved in larval developmental timing circuits. These components include the DAF-12 steroid receptor, which is involved in the larval stage two-to-stage three (L2-L3) transition and up-regulates members of the let-7 microRNA (miRNA) family. The miRNAs target an early larval nuclear factor lin-14 and akt-1/kinase, thereby stimulating DAF-16/FOXO signaling to extend life. Our studies suggest that metazoan life span is coupled to the gonad through elements of a developmental timer.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3909774/" 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/PMC3909774/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shen, Yidong -- Wollam, Joshua -- Magner, Daniel -- Karalay, Oezlem -- Antebi, Adam -- R01 AG027498/AG/NIA NIH HHS/ -- T32 GM008231/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2012 Dec 14;338(6113):1472-6. doi: 10.1126/science.1228967.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max Planck Institute for Biology of Ageing, Joseph-Stelzmann-Strasse 9b, D-50931 Cologne, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23239738" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis elegans/genetics/growth & development/*physiology ; Caenorhabditis elegans Proteins/genetics/*physiology ; Forkhead Transcription Factors ; Gene Expression Regulation, Developmental ; Germ Cells/metabolism ; Gonads/*metabolism ; Larva/genetics/growth & development/physiology ; Longevity/genetics/*physiology ; MicroRNAs/genetics/*metabolism ; Nuclear Proteins/genetics/physiology ; Proto-Oncogene Proteins c-akt/genetics/physiology ; Receptors, Cytoplasmic and Nuclear/genetics/*physiology ; Receptors, Steroid/genetics/*physiology ; Signal Transduction ; Transcription Factors/genetics/physiology
    Print ISSN: 0036-8075
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  • 9
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    A mechanism for reorientation of cortical microtubule arrays driven by microtubule severing (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-11-10
    Description: Environmental and hormonal signals cause reorganization of microtubule arrays in higher plants, but the mechanisms driving these transitions have remained elusive. The organization of these arrays is required to direct morphogenesis. We discovered that microtubule severing by the protein katanin plays a crucial and unexpected role in the reorientation of cortical arrays, as triggered by blue light. Imaging and genetic experiments revealed that phototropin photoreceptors stimulate katanin-mediated severing specifically at microtubule intersections, leading to the generation of new microtubules at these locations. We show how this activity serves as the basis for a mechanism that amplifies microtubules orthogonal to the initial array, thereby driving array reorientation. Our observations show how severing is used constructively to build a new microtubule array.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lindeboom, Jelmer J -- Nakamura, Masayoshi -- Hibbel, Anneke -- Shundyak, Kostya -- Gutierrez, Ryan -- Ketelaar, Tijs -- Emons, Anne Mie C -- Mulder, Bela M -- Kirik, Viktor -- Ehrhardt, David W -- New York, N.Y. -- Science. 2013 Dec 6;342(6163):1245533. doi: 10.1126/science.1245533. Epub 2013 Nov 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Plant Biology, Carnegie Institution for Science, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24200811" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphatases/genetics/*metabolism ; Arabidopsis/genetics/growth & development/*metabolism/*ultrastructure ; Arabidopsis Proteins/genetics/*metabolism ; Hypocotyl/metabolism/ultrastructure ; Light ; Microtubules/*metabolism/ultrastructure ; Phosphoproteins/metabolism ; *Phototropism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction
    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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    Stimulation of de novo pyrimidine synthesis by growth signaling through mTOR and S6K1 (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-02-23
    Description: Cellular growth signals stimulate anabolic processes. The mechanistic target of rapamycin complex 1 (mTORC1) is a protein kinase that senses growth signals to regulate anabolic growth and proliferation. Activation of mTORC1 led to the acute stimulation of metabolic flux through the de novo pyrimidine synthesis pathway. mTORC1 signaling posttranslationally regulated this metabolic pathway via its downstream target ribosomal protein S6 kinase 1 (S6K1), which directly phosphorylates S1859 on CAD (carbamoyl-phosphate synthetase 2, aspartate transcarbamoylase, dihydroorotase), the enzyme that catalyzes the first three steps of de novo pyrimidine synthesis. Growth signaling through mTORC1 thus stimulates the production of new nucleotides to accommodate an increase in RNA and DNA synthesis needed for ribosome biogenesis and anabolic growth.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3753690/" 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/PMC3753690/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ben-Sahra, Issam -- Howell, Jessica J -- Asara, John M -- Manning, Brendan D -- F32 DK095508/DK/NIDDK NIH HHS/ -- F32-DK095508/DK/NIDDK NIH HHS/ -- P01 CA120964/CA/NCI NIH HHS/ -- P01-CA120964/CA/NCI NIH HHS/ -- P30 CA006516/CA/NCI NIH HHS/ -- P30-CA006516/CA/NCI NIH HHS/ -- R01 CA122617/CA/NCI NIH HHS/ -- R01-CA122617/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2013 Mar 15;339(6125):1323-8. doi: 10.1126/science.1228792. Epub 2013 Feb 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics and Complex Diseases, Harvard School of Public Health, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23429703" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3-L1 Cells ; Animals ; Aspartate Carbamoyltransferase/*metabolism ; Carbamoyl-Phosphate Synthase (Glutamine-Hydrolyzing)/*metabolism ; Dihydroorotase/*metabolism ; HeLa Cells ; Humans ; Mice ; Multiprotein Complexes/*metabolism ; Pyrimidines/*biosynthesis ; Ribosomal Protein S6 Kinases/*metabolism ; Signal Transduction ; TOR Serine-Threonine Kinases/*metabolism ; Tumor Suppressor Proteins/genetics/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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