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  • Signal Transduction  (36)
  • Phosphorylation
  • American Association for the Advancement of Science (AAAS)  (54)
  • American Association of Petroleum Geologists (AAPG)
  • American Geophysical Union (AGU)
  • Elsevier
  • 2010-2014  (54)
  • 2012  (54)
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  • American Association for the Advancement of Science (AAAS)  (54)
  • American Association of Petroleum Geologists (AAPG)
  • American Geophysical Union (AGU)
  • Elsevier
  • Nature Publishing Group (NPG)  (43)
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  • 2010-2014  (54)
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  • 1
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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 More recently, it has been replaced by synthetic derivatives such as aspirin and salsalate, both of which are rapidly broken down to salicylate in vivo.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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  • 2
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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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  • 3
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    Secreted kinase phosphorylates extracellular proteins that regulate biomineralization (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-05-15
    Description: Protein phosphorylation is a fundamental mechanism regulating nearly every aspect of cellular life. Several secreted proteins are phosphorylated, but the kinases responsible are unknown. We identified a family of atypical protein kinases that localize within the Golgi apparatus and are secreted. Fam20C appears to be the Golgi casein kinase that phosphorylates secretory pathway proteins within S-x-E motifs. Fam20C phosphorylates the caseins and several secreted proteins implicated in biomineralization, including the small integrin-binding ligand, N-linked glycoproteins (SIBLINGs). Consequently, mutations in Fam20C cause an osteosclerotic bone dysplasia in humans known as Raine syndrome. Fam20C is thus a protein kinase dedicated to the phosphorylation of extracellular proteins.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3754843/" 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/PMC3754843/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tagliabracci, Vincent S -- Engel, James L -- Wen, Jianzhong -- Wiley, Sandra E -- Worby, Carolyn A -- Kinch, Lisa N -- Xiao, Junyu -- Grishin, Nick V -- Dixon, Jack E -- DK018024-37/DK/NIDDK NIH HHS/ -- DK018849-36/DK/NIDDK NIH HHS/ -- GM094575/GM/NIGMS NIH HHS/ -- R01 DK018849/DK/NIDDK NIH HHS/ -- R37 DK018024/DK/NIDDK NIH HHS/ -- T32 CA009523/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Jun 1;336(6085):1150-3. doi: 10.1126/science.1217817. Epub 2012 May 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of California, San Diego, La Jolla, CA 92093-0721, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22582013" target="_blank"〉PubMed〈/a〉
    Keywords: Abnormalities, Multiple/genetics/metabolism ; Amino Acid Motifs ; Amino Acid Sequence ; Animals ; Calcification, Physiologic ; Casein Kinase I ; Casein Kinases/metabolism ; Caseins/*metabolism ; Cattle ; Cell Line, Tumor ; Cleft Palate/genetics/metabolism ; Exophthalmos/genetics/metabolism ; Extracellular Matrix Proteins/chemistry/genetics/*metabolism/secretion ; Glycoproteins/metabolism ; Golgi Apparatus/*enzymology ; HEK293 Cells ; HeLa Cells ; Humans ; Microcephaly/genetics/metabolism ; Milk/enzymology ; Molecular Sequence Data ; Mutation ; Osteopontin ; Osteosclerosis/genetics/metabolism ; Phosphorylation ; Protein Sorting Signals ; Recombinant Fusion Proteins/chemistry/metabolism/secretion ; *Secretory Pathway ; Substrate Specificity
    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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    Kinetic responses of beta-catenin specify the sites of Wnt control (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-11-10
    Description: Despite more than 30 years of work on the Wnt signaling pathway, the basic mechanism of how the extracellular Wnt signal increases the intracellular concentration of beta-catenin is still contentious. Circumventing much of the detailed biochemistry, we used basic principles of chemical kinetics coupled with quantitative measurements to define the reactions on beta-catenin directly affected by the Wnt signal. We conclude that the core signal transduction mechanism is relatively simple, with only two regulated phosphorylation steps. Their partial inhibition gives rise to the full dynamics of the response and subsequently maintains a steady state in which the concentration of beta-catenin is increased.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hernandez, Ana R -- Klein, Allon M -- Kirschner, Marc W -- New York, N.Y. -- Science. 2012 Dec 7;338(6112):1337-40. doi: 10.1126/science.1228734. Epub 2012 Nov 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Systems Biology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23138978" target="_blank"〉PubMed〈/a〉
    Keywords: Casein Kinase I/chemistry/metabolism ; Cell Line, Tumor ; Cysteine Proteinase Inhibitors/pharmacology ; Glycogen Synthase Kinase 3/metabolism ; HEK293 Cells ; Humans ; Kinetics ; Leupeptins/pharmacology ; Phosphorylation ; *Signal Transduction ; Wnt Proteins/*metabolism ; Wnt3A Protein/metabolism ; beta Catenin/*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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  • 5
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    Hepcidin and the iron-infection axis (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-11-10
    Description: Iron lies at the center of a battle for nutritional resource between higher organisms and their microbial pathogens. The iron status of the human host affects the pathogenicity of numerous infections including malaria, HIV-1, and tuberculosis. Hepcidin, an antimicrobial-like peptide hormone, has emerged as the master regulator of iron metabolism. Hepcidin controls the absorption of dietary iron and the distribution of iron among cell types in the body, and its synthesis is regulated by both iron and innate immunity. We describe how hepcidin integrates signals from diverse physiological inputs, forming a key molecular bridge between iron trafficking and response to infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Drakesmith, Hal -- Prentice, Andrew M -- G0700844/Medical Research Council/United Kingdom -- G0901149/Medical Research Council/United Kingdom -- MC-A760-5QX00/Medical Research Council/United Kingdom -- MC_U123292699/Medical Research Council/United Kingdom -- MC_U123292700/Medical Research Council/United Kingdom -- MC_U123292701/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2012 Nov 9;338(6108):768-72. doi: 10.1126/science.1224577.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Immunology Group and Medical Research Council (MRC) Human Immunology Unit, MRC Weatherall Institute of Molecular Medicine, University of Oxford, John Radcliffe Hospital, Oxford, UK. alexander.drakesmith@ndm.ox.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23139325" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antimicrobial Cationic Peptides/*metabolism ; Bacteria/metabolism/pathogenicity ; Hepcidins ; Host-Pathogen Interactions ; Humans ; *Immunity, Innate ; Infection/*immunology/*metabolism/microbiology ; Inflammation/metabolism ; Iron/*metabolism ; Iron, Dietary/metabolism ; Leukocytes/metabolism ; Liver/metabolism ; Macrophages/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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  • 6
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    Erasure of a spinal memory trace of pain by a brief, high-dose opioid administration (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-01-17
    Description: Painful stimuli activate nociceptive C fibers and induce synaptic long-term potentiation (LTP) at their spinal terminals. LTP at C-fiber synapses represents a cellular model for pain amplification (hyperalgesia) and for a memory trace of pain. mu-Opioid receptor agonists exert a powerful but reversible depression at C-fiber synapses that renders the continuous application of low opioid doses the gold standard in pain therapy. We discovered that brief application of a high opioid dose reversed various forms of activity-dependent LTP at C-fiber synapses. Depotentiation involved Ca(2+)-dependent signaling and normalization of the phosphorylation state of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors. This also reversed hyperalgesia in behaving animals. Opioids thus not only temporarily dampen pain but may also erase a spinal memory trace of pain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Drdla-Schutting, Ruth -- Benrath, Justus -- Wunderbaldinger, Gabriele -- Sandkuhler, Jurgen -- New York, N.Y. -- Science. 2012 Jan 13;335(6065):235-8. doi: 10.1126/science.1211726.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurophysiology, Center for Brain Research, Medical University of Vienna, A-1090 Vienna, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22246779" target="_blank"〉PubMed〈/a〉
    Keywords: Analgesics, Opioid/*administration & dosage ; Animals ; Calcium Signaling ; Evoked Potentials ; Hyperalgesia/chemically induced/drug therapy ; Long-Term Potentiation/*drug effects ; Male ; Naloxone/administration & dosage ; Nerve Fibers, Unmyelinated/*drug effects/physiology ; Nociceptive Pain/*drug therapy/physiopathology ; Phosphorylation ; Piperidines/*administration & dosage ; Protein Kinase C/antagonists & inhibitors/metabolism ; Protein Phosphatase 1/antagonists & inhibitors/metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, AMPA/metabolism ; Receptors, Opioid, mu/agonists/metabolism ; Sciatic Nerve/*drug effects/physiology ; Somatostatin/administration & dosage/analogs & derivatives ; Spinal Cord/physiology ; Synapses/*drug effects/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 7
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    Cancer research. Ravenous for glucose (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-01-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Taubes, Gary -- New York, N.Y. -- Science. 2012 Jan 6;335(6064):31. doi: 10.1126/science.335.6064.31.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22223789" target="_blank"〉PubMed〈/a〉
    Keywords: Glucose/*metabolism ; *Glycolysis ; Humans ; Insulin/metabolism ; Neoplasms/*metabolism ; Signal Transduction ; Somatomedins/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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    Cancer research. Unraveling the obesity-cancer connection (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-01-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Taubes, Gary -- New York, N.Y. -- Science. 2012 Jan 6;335(6064):28, 30-2. doi: 10.1126/science.335.6064.28.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22223787" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Proliferation ; Diabetes Mellitus, Type 2/complications/*metabolism ; Diet ; Glucose/metabolism ; Humans ; Insulin/blood/*metabolism ; Mutation ; Neoplasms/*etiology/genetics/metabolism/pathology ; Obesity/complications/*metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Receptor, Insulin/metabolism ; Receptors, Somatomedin/metabolism ; Signal Transduction ; Somatomedins/*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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  • 9
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    Interleukin-22 drives endogenous thymic regeneration in mice (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-03-03
    Description: Endogenous thymic regeneration is a crucial function that allows for renewal of immune competence after stress, infection, or immunodepletion. However, the mechanisms governing this regeneration remain poorly understood. We detail such a mechanism, centered on interleukin-22 (IL-22) and triggered by the depletion of CD4(+)CD8(+) double-positive thymocytes. Intrathymic levels of IL-22 were increased after thymic insult, and thymic recovery was impaired in IL-22-deficient mice. IL-22, which signaled through thymic epithelial cells and promoted their proliferation and survival, was up-regulated by radio-resistant RORgamma(t)(+)CCR6(+)NKp46(-) lymphoid tissue inducer cells after thymic injury in an IL-23-dependent manner. Administration of IL-22 enhanced thymic recovery after total body irradiation. These studies reveal mechanisms of endogenous thymic repair and offer innovative regenerative strategies for improving immune competence.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3616391/" 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/PMC3616391/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dudakov, Jarrod A -- Hanash, Alan M -- Jenq, Robert R -- Young, Lauren F -- Ghosh, Arnab -- Singer, Natalie V -- West, Mallory L -- Smith, Odette M -- Holland, Amanda M -- Tsai, Jennifer J -- Boyd, Richard L -- van den Brink, Marcel R M -- AI080455/AI/NIAID NIH HHS/ -- CA107096/CA/NCI NIH HHS/ -- HL069929/HL/NHLBI NIH HHS/ -- HL095075/HL/NHLBI NIH HHS/ -- R01 AI080455/AI/NIAID NIH HHS/ -- R01 CA107096/CA/NCI NIH HHS/ -- R01 HL069929/HL/NHLBI NIH HHS/ -- R01 HL095075/HL/NHLBI NIH HHS/ -- T32 CA009207/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2012 Apr 6;336(6077):91-5. doi: 10.1126/science.1218004. Epub 2012 Mar 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunology Program, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA. dudakovj@mskcc.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22383805" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Count ; Cell Proliferation ; Cell Survival ; Dendritic Cells/physiology ; Epithelial Cells/cytology/physiology ; Interleukin-23/metabolism ; Interleukins/administration & dosage/deficiency/genetics/*metabolism ; Lymphocytes/cytology/physiology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Nuclear Receptor Subfamily 1, Group F, Member 3/genetics/metabolism ; Radiation Dosage ; Receptors, Interleukin/metabolism ; Recombinant Proteins/administration & dosage ; *Regeneration ; Signal Transduction ; Thymocytes/*physiology ; Thymus Gland/cytology/immunology/*physiology/radiation effects ; Up-Regulation ; Whole-Body Irradiation
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    Cell biology. FGF21 takes a fat bite (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-05-15
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3616235/" 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/PMC3616235/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Canto, Carles -- Auwerx, Johan -- 231138/European Research Council/International -- New York, N.Y. -- Science. 2012 May 11;336(6082):675-6. doi: 10.1126/science.1222646.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Nestle Institute of Health Sciences, Ecole Polytechnique Federale de Lausanne Campus, Quartier de l'Innovation, Batiment G, CH-1015 Lausanne, Switzerland. carlos.cantoalvarez@rd.nestle.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22582248" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue, Brown/metabolism ; Adipose Tissue, White/*metabolism ; Animals ; Fasting/metabolism ; Fibroblast Growth Factors/blood/*metabolism/pharmacology ; Humans ; Metabolic Syndrome X/metabolism ; Mice ; Overweight/metabolism ; PPAR gamma/metabolism ; Signal Transduction ; *Thermogenesis ; Trans-Activators/metabolism ; Transcription Factors
    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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  • 11
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    Wnt5a potentiates TGF-beta signaling to promote colonic crypt regeneration after tissue injury (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-09-08
    Description: Reestablishing homeostasis after tissue damage depends on the proper organization of stem cells and their progeny, though the repair mechanisms are unclear. The mammalian intestinal epithelium is well suited to approach this problem, as it is composed of well-delineated units called crypts of Lieberkuhn. We found that Wnt5a, a noncanonical Wnt ligand, was required for crypt regeneration after injury in mice. Unlike controls, Wnt5a-deficient mice maintained an expanded population of proliferative epithelial cells in the wound. We used an in vitro system to enrich for intestinal epithelial stem cells to discover that Wnt5a inhibited proliferation of these cells. Surprisingly, the effects of Wnt5a were mediated by activation of transforming growth factor-beta (TGF-beta) signaling. These findings suggest a Wnt5a-dependent mechanism for forming new crypt units to reestablish homeostasis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3706630/" 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/PMC3706630/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miyoshi, Hiroyuki -- Ajima, Rieko -- Luo, Christine T -- Yamaguchi, Terry P -- Stappenbeck, Thaddeus S -- 5T35DK074375/DK/NIDDK NIH HHS/ -- DK90251/DK/NIDDK NIH HHS/ -- P30-DK52574/DK/NIDDK NIH HHS/ -- R01 DK071619/DK/NIDDK NIH HHS/ -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2012 Oct 5;338(6103):108-13. doi: 10.1126/science.1223821. Epub 2012 Sep 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22956684" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Movement/drug effects/physiology ; Cell Proliferation/drug effects ; Cells, Cultured ; Colon/embryology/*injuries/*physiology ; Culture Media, Conditioned/pharmacology ; Homeostasis/drug effects/physiology ; Intestinal Mucosa/embryology/injuries/physiology ; Ligands ; Mesoderm/cytology/embryology ; Mice ; Mice, Knockout ; Receptor Tyrosine Kinase-like Orphan Receptors/metabolism ; Recombinant Proteins/pharmacology ; Signal Transduction ; Stem Cells/cytology/drug effects/physiology ; Tamoxifen/pharmacology ; Transforming Growth Factor beta/*metabolism ; Wnt Proteins/genetics/pharmacology/*physiology ; Wound Healing/drug effects/*physiology
    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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  • 12
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    GSK3-TIP60-ULK1 signaling pathway links growth factor deprivation to autophagy (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-04-28
    Description: In metazoans, cells depend on extracellular growth factors for energy homeostasis. We found that glycogen synthase kinase-3 (GSK3), when deinhibited by default in cells deprived of growth factors, activates acetyltransferase TIP60 through phosphorylating TIP60-Ser(86), which directly acetylates and stimulates the protein kinase ULK1, which is required for autophagy. Cells engineered to express TIP60(S86A) that cannot be phosphorylated by GSK3 could not undergo serum deprivation-induced autophagy. An acetylation-defective mutant of ULK1 failed to rescue autophagy in ULK1(-/-) mouse embryonic fibroblasts. Cells used signaling from GSK3 to TIP60 and ULK1 to regulate autophagy when deprived of serum but not glucose. These findings uncover an activating pathway that integrates protein phosphorylation and acetylation to connect growth factor deprivation to autophagy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lin, Shu-Yong -- Li, Terytty Yang -- Liu, Qing -- Zhang, Cixiong -- Li, Xiaotong -- Chen, Yan -- Zhang, Shi-Meng -- Lian, Guili -- Liu, Qi -- Ruan, Ka -- Wang, Zhen -- Zhang, Chen-Song -- Chien, Kun-Yi -- Wu, Jiawei -- Li, Qinxi -- Han, Jiahuai -- Lin, Sheng-Cai -- New York, N.Y. -- Science. 2012 Apr 27;336(6080):477-81. doi: 10.1126/science.1217032.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Xiamen University, Fujian, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22539723" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Autophagy ; Cell Line ; Cell Line, Tumor ; Culture Media ; Culture Media, Serum-Free ; Glucose/metabolism ; Glycogen Synthase Kinase 3/genetics/*metabolism ; HEK293 Cells ; Histone Acetyltransferases/genetics/*metabolism ; Humans ; Intercellular Signaling Peptides and Proteins/metabolism ; Intracellular Signaling Peptides and Proteins/genetics/*metabolism ; Mice ; Phosphorylation ; Protein-Serine-Threonine Kinases/genetics/*metabolism ; Rats ; *Signal Transduction ; Trans-Activators/genetics/metabolism
    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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  • 13
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    Functional supramolecular polymers (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-02-22
    Description: Supramolecular polymers can be random and entangled coils with the mechanical properties of plastics and elastomers, but with great capacity for processability, recycling, and self-healing due to their reversible monomer-to-polymer transitions. At the other extreme, supramolecular polymers can be formed by self-assembly among designed subunits to yield shape-persistent and highly ordered filaments. The use of strong and directional interactions among molecular subunits can achieve not only rich dynamic behavior but also high degrees of internal order that are not known in ordinary polymers. They can resemble, for example, the ordered and dynamic one-dimensional supramolecular assemblies of the cell cytoskeleton and possess useful biological and electronic functions.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3291483/" 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/PMC3291483/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Aida, T -- Meijer, E W -- Stupp, S I -- 2R01DE015920-06/DE/NIDCR NIH HHS/ -- 2R01EB003806-06A2/EB/NIBIB NIH HHS/ -- R01 DE015920/DE/NIDCR NIH HHS/ -- R01 DE015920-06/DE/NIDCR NIH HHS/ -- R01 EB003806/EB/NIBIB NIH HHS/ -- R01 EB003806-06A2/EB/NIBIB NIH HHS/ -- New York, N.Y. -- Science. 2012 Feb 17;335(6070):813-7. doi: 10.1126/science.1205962.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry and Biotechnology, School of Engineering, University of Tokyo, Tokyo, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22344437" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomimetic Materials/chemistry ; Forecasting ; Humans ; Molecular Structure ; Nanofibers ; Nanotubes ; *Polymers/chemistry ; Semiconductors ; Signal Transduction
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 14
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    Computational approaches to developmental patterning (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-04-14
    Description: Computational approaches are breaking new ground in understanding how embryos form. Here, we discuss recent studies that couple precise measurements in the embryo with appropriately matched modeling and computational methods to investigate classic embryonic patterning strategies. We include signaling gradients, activator-inhibitor systems, and coupled oscillators, as well as emerging paradigms such as tissue deformation. Parallel progress in theory and experiment will play an increasingly central role in deciphering developmental patterning.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morelli, Luis G -- Uriu, Koichiro -- Ares, Saul -- Oates, Andrew C -- New York, N.Y. -- Science. 2012 Apr 13;336(6078):187-91. doi: 10.1126/science.1215478.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max Planck Institute of Molecular Cell Biology and Genetics, Dresden, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22499940" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Body Patterning ; Computational Biology ; *Computer Simulation ; Drosophila/embryology ; Embryo, Nonmammalian/cytology/metabolism ; Embryonic Development ; Gene Expression Regulation, Developmental ; Gene Regulatory Networks ; *Models, Biological ; Signal Transduction ; Zebrafish/embryology
    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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  • 15
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    Host-gut microbiota metabolic interactions (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-06-08
    Description: The composition and activity of the gut microbiota codevelop with the host from birth and is subject to a complex interplay that depends on the host genome, nutrition, and life-style. The gut microbiota is involved in the regulation of multiple host metabolic pathways, giving rise to interactive host-microbiota metabolic, signaling, and immune-inflammatory axes that physiologically connect the gut, liver, muscle, and brain. A deeper understanding of these axes is a prerequisite for optimizing therapeutic strategies to manipulate the gut microbiota to combat disease and improve health.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nicholson, Jeremy K -- Holmes, Elaine -- Kinross, James -- Burcelin, Remy -- Gibson, Glenn -- Jia, Wei -- Pettersson, Sven -- R01AA020212/AA/NIAAA NIH HHS/ -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2012 Jun 8;336(6086):1262-7. doi: 10.1126/science.1223813. Epub 2012 Jun 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biomolecular Medicine, Department of Surgery and Cancer, Faculty of Medicine, Imperial College London, London, UK. j.nicholson@imperial.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22674330" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Animals ; Bacteria/*metabolism ; Diet ; Gastrointestinal Tract/*metabolism/*microbiology ; Health ; Humans ; Immune System/physiology ; Inflammation ; Liver/metabolism ; Metabolic Diseases/metabolism/*microbiology ; *Metabolic Networks and Pathways ; *Metagenome ; Signal Transduction
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 16
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    Chitin-induced dimerization activates a plant immune receptor (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-06-02
    Description: Pattern recognition receptors confer plant resistance to pathogen infection by recognizing the conserved pathogen-associated molecular patterns. The cell surface receptor chitin elicitor receptor kinase 1 of Arabidopsis (AtCERK1) directly binds chitin through its lysine motif (LysM)-containing ectodomain (AtCERK1-ECD) to activate immune responses. The crystal structure that we solved of an AtCERK1-ECD complexed with a chitin pentamer reveals that their interaction is primarily mediated by a LysM and three chitin residues. By acting as a bivalent ligand, a chitin octamer induces AtCERK1-ECD dimerization that is inhibited by shorter chitin oligomers. A mutation attenuating chitin-induced AtCERK1-ECD dimerization or formation of nonproductive AtCERK1 dimer by overexpression of AtCERK1-ECD compromises AtCERK1-mediated signaling in plant cells. Together, our data support the notion that chitin-induced AtCERK1 dimerization is critical for its activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, Tingting -- Liu, Zixu -- Song, Chuanjun -- Hu, Yunfei -- Han, Zhifu -- She, Ji -- Fan, Fangfang -- Wang, Jiawei -- Jin, Changwen -- Chang, Junbiao -- Zhou, Jian-Min -- Chai, Jijie -- New York, N.Y. -- Science. 2012 Jun 1;336(6085):1160-4. doi: 10.1126/science.1218867.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Graduate Program in Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100730, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22654057" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylglucosamine/chemistry/metabolism ; Amino Acid Motifs ; Amino Acid Sequence ; Arabidopsis/immunology/*metabolism ; Arabidopsis Proteins/*chemistry/genetics/*metabolism ; Binding Sites ; Chitin/chemistry/*metabolism ; Crystallography, X-Ray ; Hydrogen Bonding ; Ligands ; Models, Molecular ; Molecular Sequence Data ; Mutant Proteins/chemistry/metabolism ; Phosphorylation ; Plants, Genetically Modified ; Protein Multimerization ; Protein Structure, Tertiary ; Protein-Serine-Threonine Kinases/*chemistry/genetics/*metabolism ; Receptors, Pattern Recognition/*chemistry/genetics/*metabolism ; Signal Transduction
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 17
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    Akt-mediated regulation of autophagy and tumorigenesis through Beclin 1 phosphorylation (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-11-01
    Description: Aberrant signaling through the class I phosphatidylinositol 3-kinase (PI3K)-Akt axis is frequent in human cancer. Here, we show that Beclin 1, an essential autophagy and tumor suppressor protein, is a target of the protein kinase Akt. Expression of a Beclin 1 mutant resistant to Akt-mediated phosphorylation increased autophagy, reduced anchorage-independent growth, and inhibited Akt-driven tumorigenesis. Akt-mediated phosphorylation of Beclin 1 enhanced its interactions with 14-3-3 and vimentin intermediate filament proteins, and vimentin depletion increased autophagy and inhibited Akt-driven transformation. Thus, Akt-mediated phosphorylation of Beclin 1 functions in autophagy inhibition, oncogenesis, and the formation of an autophagy-inhibitory Beclin 1/14-3-3/vimentin intermediate filament complex. These findings have broad implications for understanding the role of Akt signaling and intermediate filament proteins in autophagy and cancer.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3507442/" 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/PMC3507442/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Richard C -- Wei, Yongjie -- An, Zhenyi -- Zou, Zhongju -- Xiao, Guanghua -- Bhagat, Govind -- White, Michael -- Reichelt, Julia -- Levine, Beth -- K08 CA164047/CA/NCI NIH HHS/ -- P30 CA142543/CA/NCI NIH HHS/ -- R01 CA071443/CA/NCI NIH HHS/ -- R01 CA084254/CA/NCI NIH HHS/ -- R01 CA109618/CA/NCI NIH HHS/ -- R01 CA129451/CA/NCI NIH HHS/ -- R01 CA84254-S1/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Nov 16;338(6109):956-9. doi: 10.1126/science.1225967. Epub 2012 Oct 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Dermatology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23112296" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis Regulatory Proteins/genetics/*metabolism ; *Autophagy ; Cell Line, Tumor ; Cell Transformation, Neoplastic/genetics/*metabolism ; Fibroblasts/metabolism/pathology ; HeLa Cells ; Humans ; Membrane Proteins/genetics/*metabolism ; Mice ; Phosphorylation ; Proto-Oncogene Proteins c-akt/genetics/*metabolism ; RNA, Small Interfering/genetics ; Rats ; Transduction, Genetic ; Vimentin/genetics ; Xenograft Model Antitumor Assays
    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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  • 18
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    Removal of shelterin reveals the telomere end-protection problem (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-05-05
    Description: The telomere end-protection problem is defined by the aggregate of DNA damage signaling and repair pathways that require repression at telomeres. To define the end-protection problem, we removed the whole shelterin complex from mouse telomeres through conditional deletion of TRF1 and TRF2 in nonhomologous end-joining (NHEJ) deficient cells. The data reveal two DNA damage response pathways not previously observed upon deletion of individual shelterin proteins. The shelterin-free telomeres are processed by microhomology-mediated alternative-NHEJ when Ku70/80 is absent and are attacked by nucleolytic degradation in the absence of 53BP1. The data establish that the end-protection problem is specified by six pathways [ATM (ataxia telangiectasia mutated) and ATR (ataxia telangiectasia and Rad3 related) signaling, classical-NHEJ, alt-NHEJ, homologous recombination, and resection] and show how shelterin acts with general DNA damage response factors to solve this problem.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3477646/" 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/PMC3477646/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sfeir, Agnel -- de Lange, Titia -- AG016642/AG/NIA NIH HHS/ -- GM49046/GM/NIGMS NIH HHS/ -- R01 AG016642/AG/NIA NIH HHS/ -- R01 CA076027/CA/NCI NIH HHS/ -- R37 GM049046/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2012 May 4;336(6081):593-7. doi: 10.1126/science.1218498.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Cell Biology and Genetics, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22556254" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Nuclear/genetics/metabolism ; Ataxia Telangiectasia Mutated Proteins ; Cell Cycle ; Cell Cycle Proteins/metabolism ; Cells, Cultured ; Chromosomal Proteins, Non-Histone/metabolism ; DNA Breaks, Double-Stranded ; DNA End-Joining Repair ; DNA Ligases/metabolism ; DNA Repair ; DNA-Binding Proteins/genetics/metabolism ; Homologous Recombination ; Mice ; Mice, Knockout ; Poly(ADP-ribose) Polymerases/metabolism ; Protein-Serine-Threonine Kinases/metabolism ; Signal Transduction ; Telomere/*metabolism/ultrastructure ; *Telomere Homeostasis ; Telomere-Binding Proteins/genetics/*metabolism ; Telomeric Repeat Binding Protein 1/genetics/metabolism ; Telomeric Repeat Binding Protein 2/genetics/metabolism ; Tumor Suppressor Proteins/metabolism
    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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  • 19
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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
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  • 20
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    dSarm/Sarm1 is required for activation of an injury-induced axon death pathway (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-06-09
    Description: Axonal and synaptic degeneration is a hallmark of peripheral neuropathy, brain injury, and neurodegenerative disease. Axonal degeneration has been proposed to be mediated by an active autodestruction program, akin to apoptotic cell death; however, loss-of-function mutations capable of potently blocking axon self-destruction have not been described. Here, we show that loss of the Drosophila Toll receptor adaptor dSarm (sterile alpha/Armadillo/Toll-Interleukin receptor homology domain protein) cell-autonomously suppresses Wallerian degeneration for weeks after axotomy. Severed mouse Sarm1 null axons exhibit remarkable long-term survival both in vivo and in vitro, indicating that Sarm1 prodegenerative signaling is conserved in mammals. Our results provide direct evidence that axons actively promote their own destruction after injury and identify dSarm/Sarm1 as a member of an ancient axon death signaling pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Osterloh, Jeannette M -- Yang, Jing -- Rooney, Timothy M -- Fox, A Nicole -- Adalbert, Robert -- Powell, Eric H -- Sheehan, Amy E -- Avery, Michelle A -- Hackett, Rachel -- Logan, Mary A -- MacDonald, Jennifer M -- Ziegenfuss, Jennifer S -- Milde, Stefan -- Hou, Ying-Ju -- Nathan, Carl -- Ding, Aihao -- Brown, Robert H Jr -- Conforti, Laura -- Coleman, Michael -- Tessier-Lavigne, Marc -- Zuchner, Stephan -- Freeman, Marc R -- 5R01-NS050557-05/NS/NINDS NIH HHS/ -- AI030165/AI/NIAID NIH HHS/ -- R01NS059991/NS/NINDS NIH HHS/ -- R01NS072248/NS/NINDS NIH HHS/ -- RC2-NS070-342/NS/NINDS NIH HHS/ -- U54NS065712/NS/NINDS NIH HHS/ -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Jul 27;337(6093):481-4. doi: 10.1126/science.1223899. Epub 2012 Jun 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, University of Massachusetts Medical School, Worcester, MA 01605, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22678360" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Genetically Modified ; Apoptosis ; Armadillo Domain Proteins/analysis/*genetics/*physiology ; Axons/*physiology/ultrastructure ; Axotomy ; Cell Survival ; Cells, Cultured ; Cytoskeletal Proteins/analysis/*genetics/*physiology ; Denervation ; Drosophila/embryology/genetics/physiology ; Drosophila Proteins/analysis/*genetics/*physiology ; Mice ; Mutation ; Neurons/*physiology ; Sciatic Nerve/injuries/physiology ; Signal Transduction ; Superior Cervical Ganglion/cytology ; Tissue Culture Techniques ; *Wallerian Degeneration
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Vasopressin/oxytocin-related signaling regulates gustatory associative learning in C. elegans (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-11-01
    Description: Vasopressin- and oxytocin-related neuropeptides are key regulators of animal physiology, including water balance and reproduction. Although these neuropeptides also modulate social behavior and cognition in mammals, the mechanism for influencing behavioral plasticity and the evolutionary origin of these effects are not well understood. Here, we present a functional vasopressin- and oxytocin-like signaling system in the nematode Caenorhabditis elegans. Through activation of its receptor NTR-1, a vasopressin/oxytocin-related neuropeptide, designated nematocin, facilitates the experience-driven modulation of salt chemotaxis, a type of gustatory associative learning in C. elegans. Our study suggests that vasopressin and oxytocin neuropeptides have ancient roles in modulating sensory processing in neural circuits that underlie behavioral plasticity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Beets, Isabel -- Janssen, Tom -- Meelkop, Ellen -- Temmerman, Liesbet -- Suetens, Nick -- Rademakers, Suzanne -- Jansen, Gert -- Schoofs, Liliane -- New York, N.Y. -- Science. 2012 Oct 26;338(6106):543-5. doi: 10.1126/science.1226860.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Functional Genomics and Proteomics Unit, KU Leuven, 3000 Leuven, Belgium.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23112336" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Biological Evolution ; Caenorhabditis elegans/genetics/*physiology ; Caenorhabditis elegans ; Proteins/agonists/chemistry/genetics/metabolism/pharmacology/*physiology ; Learning/drug effects/*physiology ; Male ; Molecular Sequence Data ; Neuropeptides/chemistry/genetics/pharmacology/*physiology ; Oxytocin/chemistry/genetics/pharmacology/*physiology ; Receptors, G-Protein-Coupled/agonists/genetics/metabolism/*physiology ; Signal Transduction ; Taste/drug effects/*physiology ; Vasopressins/chemistry/genetics/pharmacology/*physiology
    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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    Joint Congress on Evolutionary Biology. Insulin may guarantee the honesty of beetle's massive horn (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-07-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, Elizabeth -- New York, N.Y. -- Science. 2012 Jul 27;337(6093):408. doi: 10.1126/science.337.6093.408-a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22837505" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Beetles/*anatomy & histology/growth & development/*physiology ; Female ; Flight, Animal ; Horns/*anatomy & histology/growth & development ; Insulin/*metabolism ; Male ; *Mating Preference, Animal ; Signal Transduction ; Wings, Animal/anatomy & histology
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  • 23
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    Conformational control of the Ste5 scaffold protein insulates against MAP kinase misactivation (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-08-11
    Description: Cells reuse signaling proteins in multiple pathways, raising the potential for improper cross talk. Scaffold proteins are thought to insulate against such miscommunication by sequestering proteins into distinct physical complexes. We show that the scaffold protein Ste5, which organizes the yeast mating mitogen-activated protein kinase (MAPK) pathway, does not use sequestration to prevent misactivation of the mating response. Instead, Ste5 appears to use a conformation mechanism: Under basal conditions, an intramolecular interaction of the pleckstrin homology (PH) domain with the von Willebrand type A (VWA) domain blocks the ability to coactivate the mating-specific MAPK Fus3. Pheromone-induced membrane binding of Ste5 triggers release of this autoinhibition. Thus, in addition to serving as a conduit guiding kinase communication, Ste5 directly receives input information to decide if and when signal can be transmitted to mating output.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3631425/" 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/PMC3631425/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zalatan, Jesse G -- Coyle, Scott M -- Rajan, Saravanan -- Sidhu, Sachdev S -- Lim, Wendell A -- MOPS-93725/Canadian Institutes of Health Research/Canada -- P41 RR001614/RR/NCRR NIH HHS/ -- P50 GM081879/GM/NIGMS NIH HHS/ -- PN2 EY016546/EY/NEI NIH HHS/ -- R01 GM055040/GM/NIGMS NIH HHS/ -- R01 GM55040/GM/NIGMS NIH HHS/ -- R01 GM62583/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Sep 7;337(6099):1218-22. doi: 10.1126/science.1220683. Epub 2012 Aug 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular and Molecular Pharmacology, University of California, San Francisco, 600 16th Street, San Francisco, CA 94158, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22878499" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/antagonists & ; inhibitors/*chemistry/*metabolism ; Enzyme Activation ; MAP Kinase Kinase Kinases/metabolism ; MAP Kinase Signaling System ; Mitogen-Activated Protein Kinase Kinases/metabolism ; Mitogen-Activated Protein Kinases/*metabolism ; Models, Biological ; Phosphorylation ; Protein Conformation ; Protein Interaction Domains and Motifs ; Protein Kinases/metabolism ; Protein Precursors/metabolism ; Saccharomyces cerevisiae/*metabolism/physiology ; Saccharomyces cerevisiae Proteins/antagonists & inhibitors/*chemistry/*metabolism
    Print ISSN: 0036-8075
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    Bacterial quorum sensing and metabolic incentives to cooperate (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-10-16
    Description: The opportunistic pathogen Pseudomonas aeruginosa uses a cell-cell communication system termed "quorum sensing" to control production of public goods, extracellular products that can be used by any community member. Not all individuals respond to quorum-sensing signals and synthesize public goods. Such social cheaters enjoy the benefits of the products secreted by cooperators. There are some P. aeruginosa cellular enzymes controlled by quorum sensing, and we show that quorum sensing-controlled expression of such private goods can put a metabolic constraint on social cheating and prevent a tragedy of the commons. Metabolic constraint of social cheating provides an explanation for private-goods regulation by a cooperative system and has general implications for population biology, infection control, and stabilization of quorum-sensing circuits in synthetic biology.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3587168/" 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/PMC3587168/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dandekar, Ajai A -- Chugani, Sudha -- Greenberg, E Peter -- GM-59026/GM/NIGMS NIH HHS/ -- P30 DK 89507/DK/NIDDK NIH HHS/ -- P30 DK089507/DK/NIDDK NIH HHS/ -- R01 GM059026/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2012 Oct 12;338(6104):264-6. doi: 10.1126/science.1227289.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Pulmonary and Critical Care Medicine, University of Washington School of Medicine, Seattle, WA 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23066081" target="_blank"〉PubMed〈/a〉
    Keywords: Acyl-Butyrolactones/metabolism ; Adenosine/*metabolism ; Bacterial Proteins/genetics/metabolism ; Caseins/metabolism ; Culture Media/metabolism ; Microarray Analysis ; Mutation ; Pseudomonas aeruginosa/genetics/*growth & development/*metabolism ; Quorum Sensing/genetics/*physiology ; Signal Transduction ; Social Behavior ; Trans-Activators/genetics/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    CTD tyrosine phosphorylation impairs termination factor recruitment to RNA polymerase II (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-06-30
    Description: In different phases of the transcription cycle, RNA polymerase (Pol) II recruits various factors via its C-terminal domain (CTD), which consists of conserved heptapeptide repeats with the sequence Tyr(1)-Ser(2)-Pro(3)-Thr(4)-Ser(5)-Pro(6)-Ser(7). We show that the CTD of transcribing yeast Pol II is phosphorylated at Tyr(1), in addition to Ser(2), Thr(4), Ser(5), and Ser(7). Tyr(1) phosphorylation stimulates binding of elongation factor Spt6 and impairs recruitment of termination factors Nrd1, Pcf11, and Rtt103. Tyr(1) phosphorylation levels rise downstream of the transcription start site and decrease before the polyadenylation site, largely excluding termination factors from gene bodies. These results show that CTD modifications trigger and block factor recruitment and lead to an extended CTD code that explains transcription cycle coordination on the basis of differential phosphorylation of Tyr(1), Ser(2), and Ser(5).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mayer, Andreas -- Heidemann, Martin -- Lidschreiber, Michael -- Schreieck, Amelie -- Sun, Mai -- Hintermair, Corinna -- Kremmer, Elisabeth -- Eick, Dirk -- Cramer, Patrick -- New York, N.Y. -- Science. 2012 Jun 29;336(6089):1723-5. doi: 10.1126/science.1219651.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gene Center and Department of Biochemistry, Center for Integrated Protein Science Munich, Ludwig-Maximilians-Universitat Munchen, Feodor-Lynen-Strasse 25, 81377 Munich, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22745433" target="_blank"〉PubMed〈/a〉
    Keywords: Catalytic Domain ; Chromatin Immunoprecipitation ; HeLa Cells ; Humans ; Peptide Termination Factors/metabolism ; Phosphorylation ; Protein Kinases/metabolism ; RNA Polymerase II/*metabolism ; Saccharomyces cerevisiae ; Saccharomyces cerevisiae Proteins/metabolism ; Transcriptional Elongation Factors/metabolism ; Tyrosine/*metabolism
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    Evolutionary dynamics of gene and isoform regulation in Mammalian tissues (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-12-22
    Description: Most mammalian genes produce multiple distinct messenger RNAs through alternative splicing, but the extent of splicing conservation is not clear. To assess tissue-specific transcriptome variation across mammals, we sequenced complementary DNA from nine tissues from four mammals and one bird in biological triplicate, at unprecedented depth. We find that while tissue-specific gene expression programs are largely conserved, alternative splicing is well conserved in only a subset of tissues and is frequently lineage-specific. Thousands of previously unknown, lineage-specific, and conserved alternative exons were identified; widely conserved alternative exons had signatures of binding by MBNL, PTB, RBFOX, STAR, and TIA family splicing factors, implicating them as ancestral mammalian splicing regulators. Our data also indicate that alternative splicing often alters protein phosphorylatability, delimiting the scope of kinase signaling.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3568499/" 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/PMC3568499/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Merkin, Jason -- Russell, Caitlin -- Chen, Ping -- Burge, Christopher B -- OD011092/OD/NIH HHS/ -- R01 HG002439/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2012 Dec 21;338(6114):1593-9. doi: 10.1126/science.1228186.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23258891" target="_blank"〉PubMed〈/a〉
    Keywords: *Alternative Splicing ; Animals ; Biological Evolution ; Cattle ; Chickens ; Conserved Sequence ; DNA, Complementary ; DNA-Binding Proteins/metabolism ; *Evolution, Molecular ; Exons ; Gene Expression Profiling ; *Gene Expression Regulation ; Introns ; Macaca mulatta ; Male ; Mammals/*genetics ; Mice ; Models, Genetic ; Phosphorylation ; Phylogeny ; Protein Isoforms/chemistry/*genetics/metabolism ; Protein Kinases/genetics/metabolism ; RNA Splice Sites ; RNA Splicing ; RNA-Binding Proteins/metabolism ; Rats ; Sequence Analysis, DNA ; *Transcriptome
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    Molecular mechanics of cardiac myosin-binding protein C in native thick filaments (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-08-28
    Description: The heart's pumping capacity results from highly regulated interactions of actomyosin molecular motors. Mutations in the gene for a potential regulator of these motors, cardiac myosin-binding protein C (cMyBP-C), cause hypertrophic cardiomyopathy. However, cMyBP-C's ability to modulate cardiac contractility is not well understood. Using single-particle fluorescence imaging techniques, transgenic protein expression, proteomics, and modeling, we found that cMyBP-C slowed actomyosin motion generation in native cardiac thick filaments. This mechanical effect was localized to where cMyBP-C resides within the thick filament (i.e., the C-zones) and was modulated by phosphorylation and site-specific proteolytic degradation. These results provide molecular insight into why cMyBP-C should be considered a member of a tripartite complex with actin and myosin that allows fine tuning of cardiac muscle contraction.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3561468/" 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/PMC3561468/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Previs, M J -- Beck Previs, S -- Gulick, J -- Robbins, J -- Warshaw, D M -- 8P20GM103449/GM/NIGMS NIH HHS/ -- HL007647/HL/NHLBI NIH HHS/ -- HL059408/HL/NHLBI NIH HHS/ -- P01 HL059408/HL/NHLBI NIH HHS/ -- P20 GM103449/GM/NIGMS NIH HHS/ -- R01 HL086728/HL/NHLBI NIH HHS/ -- T32 HL007647/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2012 Sep 7;337(6099):1215-8. doi: 10.1126/science.1223602. Epub 2012 Aug 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Physiology and Biophysics, University of Vermont, Burlington, VT 05405, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22923435" target="_blank"〉PubMed〈/a〉
    Keywords: Actin Cytoskeleton/*physiology ; Actomyosin/metabolism ; Amino Acid Motifs ; Animals ; Carrier Proteins/chemistry/*metabolism ; Mice ; Mice, Transgenic ; *Myocardial Contraction ; Myocardium/*metabolism/ultrastructure ; Myofibrils/*metabolism ; Myosins/*metabolism ; Phosphorylation ; Proteolysis ; Sarcomeres/metabolism
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    Systems biology for enhanced plant nitrogen nutrition (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-06-30
    Description: Nitrogen (N)-based fertilizers increase agricultural productivity but have detrimental effects on the environment and human health. Research is generating improved understanding of the signaling components plants use to sense N and regulate metabolism, physiology, and growth and development. However, we still need to integrate these regulatory factors into signal transduction pathways and connect them to downstream response pathways. Systems biology approaches facilitate identification of new components and N-regulatory networks linked to other plant processes. A holistic view of plant N nutrition should open avenues to translate this knowledge into effective strategies to improve N-use efficiency and enhance crop production systems for more sustainable agricultural practices.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gutierrez, Rodrigo A -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Jun 29;336(6089):1673-5. doi: 10.1126/science.1217620.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉FONDAP Center for Genome Regulation, Millennium Nucleus Center for Plant Functional Genomics, Departamento de Genetica Molecular y Microbiologia, Pontificia Universidad Catolica de Chile, Avenida Libertador Bernardo O'Higgins 340, Santiago, Chile. rgutierrez@bio.puc.cl〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22745422" target="_blank"〉PubMed〈/a〉
    Keywords: Agriculture ; Fertilizers ; Forecasting ; Nitrogen/*metabolism ; Plants/*metabolism ; Signal Transduction ; *Systems Biology
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  • 29
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    Processing and subcellular trafficking of ER-tethered EIN2 control response to ethylene gas (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-09-01
    Description: Ethylene gas is essential for many developmental processes and stress responses in plants. ETHYLENE INSENSITIVE2 (EIN2), an NRAMP-like integral membrane protein, plays an essential role in ethylene signaling, but its function remains enigmatic. Here we report that phosphorylation-regulated proteolytic processing of EIN2 triggers its endoplasmic reticulum (ER)-to-nucleus translocation. ER-tethered EIN2 shows CONSTITUTIVE TRIPLE RESPONSE1 (CTR1) kinase-dependent phosphorylation. Ethylene triggers dephosphorylation at several sites and proteolytic cleavage at one of these sites, resulting in nuclear translocation of a carboxyl-terminal EIN2 fragment (EIN2-C'). Mutations that mimic EIN2 dephosphorylation, or inactivate CTR1, show constitutive cleavage and nuclear localization of EIN2-C' and EIN3 and EIN3-LIKE1-dependent activation of ethylene responses. These findings uncover a mechanism of subcellular communication whereby ethylene stimulates phosphorylation-dependent cleavage and nuclear movement of the EIN2-C' peptide, linking hormone perception and signaling components in the ER with nuclear-localized transcriptional regulators.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3523706/" 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/PMC3523706/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Qiao, Hong -- Shen, Zhouxin -- Huang, Shao-shan Carol -- Schmitz, Robert J -- Urich, Mark A -- Briggs, Steven P -- Ecker, Joseph R -- F32 HG004830/HG/NHGRI NIH HHS/ -- F32-HG004830/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Oct 19;338(6105):390-3. doi: 10.1126/science.1225974. Epub 2012 Aug 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Plant Biology Laboratory, 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/22936567" target="_blank"〉PubMed〈/a〉
    Keywords: Active Transport, Cell Nucleus ; Arabidopsis/drug effects/*metabolism ; Arabidopsis Proteins/genetics/*metabolism ; Cell Nucleus/*metabolism ; Endoplasmic Reticulum/*metabolism ; Ethylenes/*metabolism/pharmacology ; Gases/metabolism/pharmacology ; Mutation ; Nuclear Localization Signals/genetics/metabolism ; Phosphorylation ; Protein Kinases/metabolism ; Proteolysis ; Receptors, Cell Surface/genetics/*metabolism
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    Acute inflammation initiates the regenerative response in the adult zebrafish brain (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-11-10
    Description: The zebrafish regenerates its brain after injury and hence is a useful model organism to study the mechanisms enabling regenerative neurogenesis, which is poorly manifested in mammals. Yet the signaling mechanisms initiating such a regenerative response in fish are unknown. Using cerebroventricular microinjection of immunogenic particles and immunosuppression assays, we showed that inflammation is required and sufficient for enhancing the proliferation of neural progenitors and subsequent neurogenesis by activating injury-induced molecular programs that can be observed after traumatic brain injury. We also identified cysteinyl leukotriene signaling as an essential component of inflammation in the regenerative process of the adult zebrafish brain. Thus, our results demonstrate that in zebrafish, in contrast to mammals, inflammation is a positive regulator of neuronal regeneration in the central nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kyritsis, Nikos -- Kizil, Caghan -- Zocher, Sara -- Kroehne, Volker -- Kaslin, Jan -- Freudenreich, Dorian -- Iltzsche, Anne -- Brand, Michael -- New York, N.Y. -- Science. 2012 Dec 7;338(6112):1353-6. doi: 10.1126/science.1228773. Epub 2012 Nov 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Deutsche Forshungsgemeinschaft-Center for Regenerative Therapies Dresden-Cluster of Excellence, Technische Universitat Dresden, Fetscherstrasse 105, 01307 Dresden, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23138980" target="_blank"〉PubMed〈/a〉
    Keywords: Acute Disease ; Animals ; Brain Injuries/*physiopathology ; Encephalitis/*physiopathology ; Leukotrienes/metabolism ; Neural Stem Cells/*physiology ; *Neurogenesis ; Receptors, Leukotriene/metabolism ; *Regeneration ; Signal Transduction ; Zebrafish/*physiology
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    Coagulation factor X activates innate immunity to human species C adenovirus (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-09-29
    Description: Although coagulation factors play a role in host defense for "living fossils" such as horseshoe crabs, the role of the coagulation system in immunity in higher organisms remains unclear. We modeled the interface of human species C adenovirus (HAdv) interaction with coagulation factor X (FX) and introduced a mutation that abrogated formation of the HAdv-FX complex. In vivo genome-wide transcriptional profiling revealed that FX-binding-ablated virus failed to activate a distinct network of nuclear factor kappaB-dependent early-response genes that are activated by HAdv-FX complex downstream of TLR4/MyD88/TRIF/TRAF6 signaling. Our study implicates host factor "decoration" of the virus as a mechanism to trigger an innate immune sensor that responds to a misplacement of coagulation FX from the blood into intracellular macrophage compartments upon virus entry into the cell.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4762479/" 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/PMC4762479/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Doronin, Konstantin -- Flatt, Justin W -- Di Paolo, Nelson C -- Khare, Reeti -- Kalyuzhniy, Oleksandr -- Acchione, Mauro -- Sumida, John P -- Ohto, Umeharu -- Shimizu, Toshiyuki -- Akashi-Takamura, Sachiko -- Miyake, Kensuke -- MacDonald, James W -- Bammler, Theo K -- Beyer, Richard P -- Farin, Frederico M -- Stewart, Phoebe L -- Shayakhmetov, Dmitry M -- AI065429/AI/NIAID NIH HHS/ -- CA141439/CA/NCI NIH HHS/ -- P30ES07033/ES/NIEHS NIH HHS/ -- R01 AI065429/AI/NIAID NIH HHS/ -- R01 CA141439/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2012 Nov 9;338(6108):795-8. doi: 10.1126/science.1226625. Epub 2012 Sep 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Washington, Seattle, WA 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23019612" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviridae Infections/*immunology/metabolism/virology ; Adenoviruses, Human/genetics/*immunology/*metabolism ; Animals ; CHO Cells ; Capsid Proteins/chemistry/genetics/metabolism ; Cell Line, Tumor ; Cricetinae ; Cricetulus ; Cryoelectron Microscopy ; Cytokines/metabolism ; Factor X/chemistry/*metabolism ; Gene Expression Profiling ; Gene Expression Regulation ; Hepatocytes/virology ; Humans ; *Immunity, Innate ; Macrophages/metabolism/virology ; Mice ; Mice, Inbred C57BL ; Molecular Dynamics Simulation ; Mutation ; NF-kappa B/metabolism ; Signal Transduction ; Virus Internalization
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    GFAJ-1 is an arsenate-resistant, phosphate-dependent organism (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-07-10
    Description: The bacterial isolate GFAJ-1 has been proposed to substitute arsenic for phosphorus to sustain growth. We have shown that GFAJ-1 is able to grow at low phosphate concentrations (1.7 muM), even in the presence of high concentrations of arsenate (40 mM), but lacks the ability to grow in phosphorus-depleted (〈0.3 muM), arsenate-containing medium. High-resolution mass spectrometry analyses revealed that phosphorylated central metabolites and phosphorylated nucleic acids predominated. A few arsenylated compounds, including C6 sugar arsenates, were detected in extracts of GFAJ-1, when GFAJ-1 was incubated with arsenate, but further experiments showed they formed abiotically. Inductively coupled plasma mass spectrometry confirmed the presence of phosphorus in nucleic acid extracts, while arsenic could not be detected and was below 1 per mil relative to phosphorus. Taken together, we conclude that GFAJ-1 is an arsenate-resistant, but still a phosphate-dependent, bacterium.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Erb, Tobias J -- Kiefer, Patrick -- Hattendorf, Bodo -- Gunther, Detlef -- Vorholt, Julia A -- New York, N.Y. -- Science. 2012 Jul 27;337(6093):467-70. doi: 10.1126/science.1218455. Epub 2012 Jul 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Microbiology, Eidgenossische Technische Hochschule Zurich, Wolfgang-Pauli-Strasse 10, 8093 Zurich, Switzerland. toerb@ethz.ch〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22773139" target="_blank"〉PubMed〈/a〉
    Keywords: Arsenates/metabolism/*pharmacology ; Arsenic/*analysis ; Culture Media/chemistry ; DNA, Bacterial/chemistry ; Drug Resistance, Bacterial ; Glycolysis ; Halomonadaceae/drug effects/*growth & development/*metabolism ; Hexosephosphates/metabolism ; Hexoses/metabolism ; Mass Spectrometry/methods ; Metabolome ; Nucleotides/metabolism ; Phosphates/analysis/*metabolism ; Phosphorus/analysis ; Phosphorylation ; RNA, Bacterial/chemistry
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    Cis-acting transcriptional repression establishes a sharp boundary in chordate embryos (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-08-28
    Description: The function of bone morphogenetic protein (BMP) signaling in dorsoventral (DV) patterning of animal embryos is conserved among Bilateria. In vertebrates, the BMP ligand antidorsalizing morphogenetic protein (Admp) is expressed dorsally and moves to the opposite side to specify the ventral fate. Here, we show that Pinhead is an antagonist specific for Admp with a role in establishing the DV axis of the trunk epidermis in embryos of the ascidian Ciona intestinalis. Pinhead and Admp exist in tandem in the genomes of various animals from arthropods to vertebrates. This genomic configuration is important for mutually exclusive expression of these genes, because Pinhead transcription directly disturbs the action of the Admp enhancer. Our data suggest that this dual negative regulatory mechanism is widely conserved in animals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Imai, Kaoru S -- Daido, Yutaka -- Kusakabe, Takehiro G -- Satou, Yutaka -- New York, N.Y. -- Science. 2012 Aug 24;337(6097):964-7. doi: 10.1126/science.1222488.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biodiversity, Graduate School of Science, Kyoto University, Sakyo-ku, Kyoto 606-8502, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22923581" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; *Body Patterning ; Bone Morphogenetic Protein 2/genetics/metabolism ; Bone Morphogenetic Protein 4/genetics/metabolism ; Bone Morphogenetic Proteins/chemistry/*genetics/metabolism ; Ciona intestinalis/*embryology/genetics/metabolism ; Embryo, Nonmammalian/*metabolism ; Embryonic Development ; Enhancer Elements, Genetic ; Epidermis/embryology ; Gastrula/metabolism ; *Gene Expression Regulation, Developmental ; Molecular Sequence Data ; Oligodeoxyribonucleotides, Antisense ; Oryzias/embryology/genetics/metabolism ; Promoter Regions, Genetic ; Signal Transduction ; *Transcription, Genetic
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    ESCRT-III governs the Aurora B-mediated abscission checkpoint through CHMP4C (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-03-17
    Description: The endosomal sorting complex required for transport (ESCRT) machinery plays an evolutionarily conserved role in cytokinetic abscission, the final step of cell division where daughter cells are physically separated. Here, we show that charged multivesicular body (MVB) protein 4C (CHMP4C), a human ESCRT-III subunit, is involved in abscission timing. This function correlated with its differential spatiotemporal distribution during late stages of cytokinesis. Accordingly, CHMP4C functioned in the Aurora B-dependent abscission checkpoint to prevent both premature resolution of intercellular chromosome bridges and accumulation of DNA damage. CHMP4C engaged the chromosomal passenger complex (CPC) via interaction with Borealin, which suggested a model whereby CHMP4C inhibits abscission upon phosphorylation by Aurora B. Thus, the ESCRT machinery may protect against genetic damage by coordinating midbody resolution with the abscission checkpoint.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3998087/" 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/PMC3998087/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carlton, Jeremy G -- Caballe, Anna -- Agromayor, Monica -- Kloc, Magdalena -- Martin-Serrano, Juan -- 092429/Z/10/Z/Wellcome Trust/United Kingdom -- 093056/Wellcome Trust/United Kingdom -- G0802777/Medical Research Council/United Kingdom -- WT093056MA/Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2012 Apr 13;336(6078):220-5. doi: 10.1126/science.1217180. Epub 2012 Mar 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Infectious Diseases, King's College London School of Medicine, London, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22422861" target="_blank"〉PubMed〈/a〉
    Keywords: Aurora Kinase B ; Aurora Kinases ; Cell Cycle Checkpoints ; Cell Cycle Proteins/metabolism ; Cell Line ; Chromosomes, Human/metabolism ; *Cytokinesis ; DNA Damage ; Endosomal Sorting Complexes Required for Transport/*metabolism ; Endosomes/metabolism ; HeLa Cells ; Histocompatibility Antigens Class I/metabolism ; Humans ; Mitosis ; Phosphorylation ; Protein Transport ; Protein-Serine-Threonine Kinases/*metabolism ; Recombinant Fusion Proteins/metabolism
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    The APC/C inhibitor XErp1/Emi2 is essential for Xenopus early embryonic divisions (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-09-29
    Description: Mitotic divisions result from the oscillating activity of cyclin-dependent kinase 1 (Cdk1). Cdk1 activity is terminated by the anaphase-promoting complex/cyclosome (APC/C), a ubiquitin ligase that targets cyclin B for destruction. In somatic divisions, the early mitotic inhibitor 1 (Emi1) and the spindle assembly checkpoint (SAC) regulate cell cycle progression by inhibiting the APC/C. Early embryonic divisions lack these APC/C-inhibitory components, which raises the question of how those cycles are controlled. We found that the APC/C-inhibitory activity of XErp1 (also known as Emi2) was essential for early divisions in Xenopus embryos. Loss of XErp1 resulted in untimely destruction of APC/C substrates and embryonic lethality. XErp1's APC/C-inhibitory function was negatively regulated by Cdk1 and positively by protein phosphatase 2A (PP2A). Thus, Cdk1 and PP2A operate at the core of early mitotic cell cycles by antagonistically controlling XErp1 activity, which results in oscillating APC/C activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tischer, Thomas -- Hormanseder, Eva -- Mayer, Thomas U -- New York, N.Y. -- Science. 2012 Oct 26;338(6106):520-4. doi: 10.1126/science.1228394. Epub 2012 Sep 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology and Konstanz Research School Chemical Biology, University of Konstanz, Universitatsstr. 10, 78457 Konstanz, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23019610" target="_blank"〉PubMed〈/a〉
    Keywords: Anaphase-Promoting Complex-Cyclosome ; Animals ; CDC2 Protein Kinase/metabolism ; Embryo, Nonmammalian/*cytology/enzymology ; F-Box Proteins/antagonists & inhibitors/genetics/*metabolism ; Mitosis/genetics/*physiology ; Phosphorylation ; Protein Phosphatase 2/metabolism ; Ubiquitin-Protein Ligase Complexes/antagonists & inhibitors/*metabolism ; Xenopus Proteins/antagonists & inhibitors/genetics/*metabolism ; Xenopus laevis/*embryology/genetics
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    Physiology. De-meaning of metabolism (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-06-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lazar, Mitchell A -- Birnbaum, Morris J -- P01 CA093615/CA/NCI NIH HHS/ -- P01 DK49210/DK/NIDDK NIH HHS/ -- R01 DK056886/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2012 Jun 29;336(6089):1651-2. doi: 10.1126/science.1221834.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, and The Institute for Diabetes, Obesity, and Metabolism, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA 19104, USA. lazar@mail.med.upenn.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22745413" target="_blank"〉PubMed〈/a〉
    Keywords: Humans ; Metabolic Diseases/metabolism ; *Metabolism ; Neoplasms/metabolism ; Signal Transduction ; Terminology as Topic
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    C/EBP transcription factors mediate epicardial activation during heart development and injury (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-11-20
    Description: The epicardium encapsulates the heart and functions as a source of multipotent progenitor cells and paracrine factors essential for cardiac development and repair. Injury of the adult heart results in reactivation of a developmental gene program in the epicardium, but the transcriptional basis of epicardial gene expression has not been delineated. We established a mouse embryonic heart organ culture and gene expression system that facilitated the identification of epicardial enhancers activated during heart development and injury. Epicardial activation of these enhancers depends on a combinatorial transcriptional code centered on CCAAT/enhancer binding protein (C/EBP) transcription factors. Disruption of C/EBP signaling in the adult epicardium reduced injury-induced neutrophil infiltration and improved cardiac function. These findings reveal a transcriptional basis for epicardial activation and heart injury, providing a platform for enhancing cardiac regeneration.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3613149/" 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/PMC3613149/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, Guo N -- Thatcher, Jeffrey E -- McAnally, John -- Kong, Yongli -- Qi, Xiaoxia -- Tan, Wei -- DiMaio, J Michael -- Amatruda, James F -- Gerard, Robert D -- Hill, Joseph A -- Bassel-Duby, Rhonda -- Olson, Eric N -- 1K99HL114738/HL/NHLBI NIH HHS/ -- HL100401-01/HL/NHLBI NIH HHS/ -- K99 HL114738/HL/NHLBI NIH HHS/ -- R01 HL077439/HL/NHLBI NIH HHS/ -- R01 HL093039/HL/NHLBI NIH HHS/ -- R01 HL111665/HL/NHLBI NIH HHS/ -- U01 HL100401/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2012 Dec 21;338(6114):1599-603. doi: 10.1126/science.1229765. Epub 2012 Nov 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23160954" target="_blank"〉PubMed〈/a〉
    Keywords: Aldehyde Oxidoreductases/genetics/metabolism ; Animals ; Binding Sites ; CCAAT-Enhancer-Binding Protein-beta/genetics/metabolism ; CCAAT-Enhancer-Binding Protein-delta/genetics/metabolism ; CCAAT-Enhancer-Binding Proteins/genetics/*metabolism ; Enhancer Elements, Genetic ; Female ; *Gene Expression Regulation ; Gene Expression Regulation, Developmental ; Heart/embryology/*physiopathology ; Male ; Mice ; Mice, Transgenic ; Models, Genetic ; Myocardial Contraction ; Myocardial Infarction/*genetics/metabolism ; Myocardial Reperfusion Injury/*genetics/metabolism ; Neutrophil Infiltration ; Oligonucleotide Array Sequence Analysis ; Organ Culture Techniques ; Pericardium/cytology/*embryology/*metabolism ; Signal Transduction ; Uroplakin III/genetics/metabolism ; Ventricular Remodeling ; WT1 Proteins/genetics/metabolism
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    Stem cells. Immune reactions help reprogram cells (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-11-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, Gretchen -- New York, N.Y. -- Science. 2012 Nov 2;338(6107):590. doi: 10.1126/science.338.6107.590.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23118158" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cellular Reprogramming ; Gene Expression Regulation ; *Immunity, Innate ; Induced Pluripotent Stem Cells/*physiology ; Retroviridae/genetics/immunology/*physiology ; Signal Transduction ; Toll-Like Receptor 3/*metabolism
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  • 39
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    Atg7 modulates p53 activity to regulate cell cycle and survival during metabolic stress (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-04-14
    Description: Withdrawal of nutrients triggers an exit from the cell division cycle, the induction of autophagy, and eventually the activation of cell death pathways. The relation, if any, among these events is not well characterized. We found that starved mouse embryonic fibroblasts lacking the essential autophagy gene product Atg7 failed to undergo cell cycle arrest. Independent of its E1-like enzymatic activity, Atg7 could bind to the tumor suppressor p53 to regulate the transcription of the gene encoding the cell cycle inhibitor p21(CDKN1A). With prolonged metabolic stress, the absence of Atg7 resulted in augmented DNA damage with increased p53-dependent apoptosis. Inhibition of the DNA damage response by deletion of the protein kinase Chk2 partially rescued postnatal lethality in Atg7(-/-) mice. Thus, when nutrients are limited, Atg7 regulates p53-dependent cell cycle and cell death pathways.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4721513/" 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/PMC4721513/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, In Hye -- Kawai, Yoshichika -- Fergusson, Maria M -- Rovira, Ilsa I -- Bishop, Alexander J R -- Motoyama, Noboru -- Cao, Liu -- Finkel, Toren -- Z01 HL005012-12/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2012 Apr 13;336(6078):225-8. doi: 10.1126/science.1218395.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Molecular Medicine, National Heart, Lung, and Blood Institute, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22499945" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Autophagy ; Cell Cycle ; Cell Cycle Checkpoints ; Cell Line, Tumor ; Cells, Cultured ; Checkpoint Kinase 2 ; Cyclin-Dependent Kinase Inhibitor p21/genetics ; DNA Damage ; Gene Expression Regulation ; Humans ; Mice ; Microtubule-Associated Proteins/genetics/*metabolism ; Phosphorylation ; Promoter Regions, Genetic ; Protein Binding ; Protein Multimerization ; Protein-Serine-Threonine Kinases/genetics ; *Stress, Physiological ; Transcription, Genetic ; Tumor Suppressor Protein p53/*metabolism ; Ubiquitin-Activating Enzymes/genetics/*metabolism
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  • 40
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    Rescued tolerant CD8 T cells are preprogrammed to reestablish the tolerant state (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-01-24
    Description: Tolerant self-antigen-specific CD8 T cells fail to proliferate in response to antigen, thereby preventing autoimmune disease. By using an in vivo mouse model, we show that tolerant T cells proliferate and become functional under lymphopenic conditions, even in a tolerogenic environment. However, T cell rescue is only transient, with tolerance reimposed upon lymphorepletion even in the absence of tolerogen (self-antigen), challenging the prevailing paradigm that continuous antigen exposure is critical to maintain tolerance. Genome-wide messenger RNA and microRNA profiling revealed that tolerant T cells have a tolerance-specific gene profile that can be temporarily overridden under lymphopenic conditions but is inevitably reimposed, which suggests epigenetic regulation. These insights into the regulatory mechanisms that maintain or break self-tolerance may lead to new strategies for the treatment of cancer and autoimmunity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3754789/" 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/PMC3754789/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schietinger, Andrea -- Delrow, Jeffrey J -- Basom, Ryan S -- Blattman, Joseph N -- Greenberg, Philip D -- K01 CA117985/CA/NCI NIH HHS/ -- P30 CA015704/CA/NCI NIH HHS/ -- P30 CA015704-35/CA/NCI NIH HHS/ -- P30 DK 56465/DK/NIDDK NIH HHS/ -- P30 DK056465/DK/NIDDK NIH HHS/ -- R01 CA033084/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2012 Feb 10;335(6069):723-7. doi: 10.1126/science.1214277. Epub 2012 Jan 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, University of Washington (UW), Seattle, WA 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22267581" target="_blank"〉PubMed〈/a〉
    Keywords: Adoptive Transfer ; Animals ; Autoantigens/immunology ; CD8-Positive T-Lymphocytes/*immunology/physiology/transplantation ; Cell Proliferation ; Epigenesis, Genetic ; Gene Expression Profiling ; Gene Expression Regulation ; Homeostasis ; Immunologic Memory ; Lymphocyte Activation ; Lymphocyte Count ; Lymphopenia/*immunology ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; MicroRNAs/genetics/metabolism ; Oligonucleotide Array Sequence Analysis ; *Self Tolerance/genetics ; Signal Transduction ; T-Lymphocyte Subsets/immunology
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    Bergmann glial AMPA receptors are required for fine motor coordination (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-07-07
    Description: The impact of glial neurotransmitter receptors in vivo is still elusive. In the cerebellum, Bergmann glial (BG) cells express alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-type glutamate receptors (AMPARs) composed exclusively of GluA1 and/or GluA4 subunits. With the use of conditional gene inactivation, we found that the majority of cerebellar GluA1/A4-type AMPARs are expressed in BG cells. In young mice, deletion of BG AMPARs resulted in retraction of glial appendages from Purkinje cell (PC) synapses, increased amplitude and duration of evoked PC currents, and a delayed formation of glutamatergic synapses. In adult mice, AMPAR inactivation also caused retraction of glial processes. The physiological and structural changes were accompanied by behavioral impairments in fine motor coordination. Thus, BG AMPARs are essential to optimize synaptic integration and cerebellar output function throughout life.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Saab, Aiman S -- Neumeyer, Alexander -- Jahn, Hannah M -- Cupido, Alexander -- Simek, Antonia A M -- Boele, Henk-Jan -- Scheller, Anja -- Le Meur, Karim -- Gotz, Magdalena -- Monyer, Hannah -- Sprengel, Rolf -- Rubio, Maria E -- Deitmer, Joachim W -- De Zeeuw, Chris I -- Kirchhoff, Frank -- R01-DC006881/DC/NIDCD NIH HHS/ -- New York, N.Y. -- Science. 2012 Aug 10;337(6095):749-53. doi: 10.1126/science.1221140. Epub 2012 Jul 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Physiology, University of Saarland, Homburg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22767895" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/*metabolism/ultrastructure ; Cerebellar Cortex/*cytology/growth & development/physiology ; Conditioning, Eyelid ; Excitatory Postsynaptic Potentials ; Locomotion ; Mice ; Mice, Knockout ; *Motor Activity ; Neurites/physiology/ultrastructure ; Patch-Clamp Techniques ; Psychomotor Performance ; Purkinje Cells/cytology/physiology ; Receptors, AMPA/*metabolism ; Signal Transduction ; Synapses/physiology/ultrastructure ; Synaptic Transmission
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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
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    The dorsal aorta initiates a molecular cascade that instructs sympatho-adrenal specification (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-06-23
    Description: The autonomic nervous system, which includes the sympathetic neurons and adrenal medulla, originates from the neural crest. Combining avian blood vessel-specific gene manipulation and mouse genetics, we addressed a long-standing question of how neural crest cells (NCCs) generate sympathetic and medullary lineages during embryogenesis. We found that the dorsal aorta acts as a morphogenetic signaling center that coordinates NCC migration and cell lineage segregation. Bone morphogenetic proteins (BMPs) produced by the dorsal aorta are critical for the production of the chemokine stromal cell-derived factor-1 (SDF -1) and Neuregulin 1 in the para-aortic region, which act as chemoattractants for early migration. Later, BMP signaling is directly involved in the sympatho-medullary segregation. This study provides insights into the complex developmental signaling cascade that instructs one of the earliest events of neurovascular interactions guiding embryonic development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Saito, Daisuke -- Takase, Yuta -- Murai, Hidetaka -- Takahashi, Yoshiko -- New York, N.Y. -- Science. 2012 Jun 22;336(6088):1578-81. doi: 10.1126/science.1222369.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Graduate School of Biological Sciences, Nara Institute of Science and Technology, Ikoma, Nara, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22723422" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Cortex/embryology/metabolism ; Adrenal Medulla/*cytology/embryology ; Animals ; Aorta/*embryology/*metabolism ; Avian Proteins/metabolism ; Bone Morphogenetic Proteins/*metabolism ; Cell Line ; Cell Lineage ; Cell Movement ; Chemokine CXCL12/metabolism ; Chemotactic Factors/metabolism ; Chick Embryo ; Coculture Techniques ; Embryonic Development ; Ganglia, Sympathetic/*cytology ; Mice ; Mice, Knockout ; Morphogenesis ; Neural Crest/*cytology/physiology ; Neuregulin-1/metabolism ; Signal Transduction ; Stem Cells/cytology/physiology
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    Mutations in BCKD-kinase lead to a potentially treatable form of autism with epilepsy (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-09-08
    Description: Autism spectrum disorders are a genetically heterogeneous constellation of syndromes characterized by impairments in reciprocal social interaction. Available somatic treatments have limited efficacy. We have identified inactivating mutations in the gene BCKDK (Branched Chain Ketoacid Dehydrogenase Kinase) in consanguineous families with autism, epilepsy, and intellectual disability. The encoded protein is responsible for phosphorylation-mediated inactivation of the E1alpha subunit of branched-chain ketoacid dehydrogenase (BCKDH). Patients with homozygous BCKDK mutations display reductions in BCKDK messenger RNA and protein, E1alpha phosphorylation, and plasma branched-chain amino acids. Bckdk knockout mice show abnormal brain amino acid profiles and neurobehavioral deficits that respond to dietary supplementation. Thus, autism presenting with intellectual disability and epilepsy caused by BCKDK mutations represents a potentially treatable syndrome.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3704165/" 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/PMC3704165/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Novarino, Gaia -- El-Fishawy, Paul -- Kayserili, Hulya -- Meguid, Nagwa A -- Scott, Eric M -- Schroth, Jana -- Silhavy, Jennifer L -- Kara, Majdi -- Khalil, Rehab O -- Ben-Omran, Tawfeg -- Ercan-Sencicek, A Gulhan -- Hashish, Adel F -- Sanders, Stephan J -- Gupta, Abha R -- Hashem, Hebatalla S -- Matern, Dietrich -- Gabriel, Stacey -- Sweetman, Larry -- Rahimi, Yasmeen -- Harris, Robert A -- State, Matthew W -- Gleeson, Joseph G -- K08 MH087639/MH/NIMH NIH HHS/ -- K08MH087639/MH/NIMH NIH HHS/ -- P01 HD070494/HD/NICHD NIH HHS/ -- P01HD070494/HD/NICHD NIH HHS/ -- P30 NS047101/NS/NINDS NIH HHS/ -- P30NS047101/NS/NINDS NIH HHS/ -- R01 NS041537/NS/NINDS NIH HHS/ -- R01 NS048453/NS/NINDS NIH HHS/ -- R01NS048453/NS/NINDS NIH HHS/ -- R25 MH077823/MH/NIMH NIH HHS/ -- RC2 MH089956/MH/NIMH NIH HHS/ -- RC2MH089956/MH/NIMH NIH HHS/ -- T32MH018268/MH/NIMH NIH HHS/ -- U54HG003067/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Oct 19;338(6105):394-7. doi: 10.1126/science.1224631. Epub 2012 Sep 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neurogenetics Laboratory, Howard Hughes Medical Institute, Department of Neurosciences, University of California, San Diego, La Jolla, CA 92093, USA. gnovarino@ucsd.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22956686" target="_blank"〉PubMed〈/a〉
    Keywords: 3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide)/*administration & ; dosage/deficiency/*genetics ; Adolescent ; Amino Acids, Branched-Chain/administration & dosage/blood/deficiency ; Animals ; Arginine/genetics ; Autistic Disorder/*diet therapy/enzymology/*genetics ; Base Sequence ; Brain/metabolism ; Child ; Child, Preschool ; Diet ; Epilepsy/*diet therapy/enzymology/*genetics ; Female ; Homozygote ; Humans ; Intellectual Disability/diet therapy/enzymology/genetics ; Male ; Mice ; Mice, Knockout ; Molecular Sequence Data ; Mutation ; Pedigree ; Phosphorylation ; Protein Folding ; Protein Structure, Tertiary ; RNA, Messenger/metabolism ; Young Adult
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    Immunology. Orchestrating inflammasomes (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-09-18
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4340476/" 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/PMC4340476/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Franchi, Luigi -- Nunez, Gabriel -- R01 DK091191/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2012 Sep 14;337(6100):1299-300. doi: 10.1126/science.1229010.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Comprehensive Cancer Center, University of Michigan Medical School, Ann Arbor, MI 48109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22984056" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CARD Signaling Adaptor Proteins/genetics/*metabolism ; Calcium-Binding Proteins/genetics/*metabolism ; Enzyme Activation ; Gram-Negative Bacteria/*immunology ; Gram-Negative Bacterial Infections/enzymology/*immunology ; Humans ; Inflammasomes/*metabolism ; Mice ; Mice, Mutant Strains ; Mutation ; Phosphorylation ; Protein Kinase C-delta/*metabolism ; Serine/genetics/metabolism
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    An immunosurveillance mechanism controls cancer cell ploidy (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-09-29
    Description: Cancer cells accommodate multiple genetic and epigenetic alterations that initially activate intrinsic (cell-autonomous) and extrinsic (immune-mediated) oncosuppressive mechanisms. Only once these barriers to oncogenesis have been overcome can malignant growth proceed unrestrained. Tetraploidization can contribute to oncogenesis because hyperploid cells are genomically unstable. We report that hyperploid cancer cells become immunogenic because of a constitutive endoplasmic reticulum stress response resulting in the aberrant cell surface exposure of calreticulin. Hyperploid, calreticulin-exposing cancer cells readily proliferated in immunodeficient mice and conserved their increased DNA content. In contrast, hyperploid cells injected into immunocompetent mice generated tumors only after a delay, and such tumors exhibited reduced DNA content, endoplasmic reticulum stress, and calreticulin exposure. Our results unveil an immunosurveillance system that imposes immunoselection against hyperploidy in carcinogen- and oncogene-induced cancers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Senovilla, Laura -- Vitale, Ilio -- Martins, Isabelle -- Tailler, Maximilien -- Pailleret, Claire -- Michaud, Mickael -- Galluzzi, Lorenzo -- Adjemian, Sandy -- Kepp, Oliver -- Niso-Santano, Mireia -- Shen, Shensi -- Marino, Guillermo -- Criollo, Alfredo -- Boileve, Alice -- Job, Bastien -- Ladoire, Sylvain -- Ghiringhelli, Francois -- Sistigu, Antonella -- Yamazaki, Takahiro -- Rello-Varona, Santiago -- Locher, Clara -- Poirier-Colame, Vichnou -- Talbot, Monique -- Valent, Alexander -- Berardinelli, Francesco -- Antoccia, Antonio -- Ciccosanti, Fabiola -- Fimia, Gian Maria -- Piacentini, Mauro -- Fueyo, Antonio -- Messina, Nicole L -- Li, Ming -- Chan, Christopher J -- Sigl, Verena -- Pourcher, Guillaume -- Ruckenstuhl, Christoph -- Carmona-Gutierrez, Didac -- Lazar, Vladimir -- Penninger, Josef M -- Madeo, Frank -- Lopez-Otin, Carlos -- Smyth, Mark J -- Zitvogel, Laurence -- Castedo, Maria -- Kroemer, Guido -- New York, N.Y. -- Science. 2012 Sep 28;337(6102):1678-84.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉INSERM, U848, Villejuif, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23019653" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calreticulin/immunology ; Cell Line, Tumor ; Common Variable Immunodeficiency/genetics ; DNA, Neoplasm/analysis/genetics ; Endoplasmic Reticulum Stress/*immunology ; Eukaryotic Initiation Factor-2/metabolism ; Humans ; Immunocompetence ; *Immunologic Surveillance ; Mice ; Mice, Inbred BALB C ; Neoplasms/chemically induced/*genetics/*immunology ; Phosphorylation ; *Ploidies
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    A critical period for social experience-dependent oligodendrocyte maturation and myelination (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-09-18
    Description: Early social isolation results in adult behavioral and cognitive dysfunction that correlates with white matter alterations. However, how social deprivation influences myelination and the significance of these myelin defects in the adult remained undefined. We show that mice isolated for 2 weeks immediately after weaning have alterations in prefrontal cortex function and myelination that do not recover with reintroduction into a social environment. These alterations, which occur only during this critical period, are phenocopied by loss of oligodendrocyte ErbB3 receptors, and social isolation leads to reduced expression of the ErbB3 ligand neuregulin-1. These findings indicate that social experience regulates prefrontal cortex myelination through neuregulin-1/ErbB3 signaling and that this is essential for normal cognitive function, thus providing a cellular and molecular context to understand the consequences of social isolation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4165613/" 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/PMC4165613/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Makinodan, Manabu -- Rosen, Kenneth M -- Ito, Susumu -- Corfas, Gabriel -- P30 HD018655/HD/NICHD NIH HHS/ -- P30-HD 18655/HD/NICHD NIH HHS/ -- R01 NS035884/NS/NINDS NIH HHS/ -- R01 NS35884/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2012 Sep 14;337(6100):1357-60. doi: 10.1126/science.1220845.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉F. M. Kirby Neurobiology Center, Children's Hospital, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22984073" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Behavior, Animal ; Female ; Green Fluorescent Proteins/genetics/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Myelin Sheath/*metabolism ; Neuregulin-1/genetics/metabolism ; Oligodendroglia/cytology/*metabolism ; Prefrontal Cortex/cytology/*metabolism ; Receptor, ErbB-3/genetics/metabolism ; Signal Transduction ; *Social Isolation
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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
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    B cell receptor signal transduction in the GC is short-circuited by high phosphatase activity (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-05-05
    Description: Germinal centers (GCs) generate memory B and plasma cells, which are essential for long-lived humoral immunity. GC B cells with high-affinity B cell receptors (BCRs) are selectively expanded. To enable this selection, BCRs of such cells are thought to signal differently from those with lower affinity. We show that, surprisingly, most proliferating GC B cells did not demonstrate active BCR signaling. Rather, spontaneous and induced signaling was limited by increased phosphatase activity. Accordingly, both SH2 domain-containing phosphatase-1 (SHP-1) and SH2 domain-containing inositol 5 phosphatase were hyperphosphorylated in GC cells and remained colocalized with BCRs after ligation. Furthermore, SHP-1 was required for GC maintenance. Intriguingly, GC B cells in the cell-cycle G(2) period regained responsiveness to BCR stimulation. These data have implications for how higher-affinity B cells are selected in the GC.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3777391/" 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/PMC3777391/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Khalil, Ashraf M -- Cambier, John C -- Shlomchik, Mark J -- AI43603/AI/NIAID NIH HHS/ -- AR44077/AR/NIAMS NIH HHS/ -- R01 AI043603/AI/NIAID NIH HHS/ -- R01 AR044077/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 2012 Jun 1;336(6085):1178-81. doi: 10.1126/science.1213368. Epub 2012 May 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Laboratory Medicine, 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/22555432" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibody Affinity ; Antigen Presentation ; Antigens/immunology ; Antigens, CD79/metabolism ; B-Lymphocytes/enzymology/*immunology/metabolism ; Calcium/metabolism ; Cell Cycle ; Down-Regulation ; Germinal Center/cytology/*immunology ; Intracellular Signaling Peptides and Proteins/metabolism ; Lymphocyte Activation ; Mice ; Mice, Inbred BALB C ; Mice, Transgenic ; Models, Immunological ; Phosphoric Monoester Hydrolases/metabolism ; Phosphorylation ; Protein Tyrosine Phosphatase, Non-Receptor Type 6/*metabolism ; Protein-Tyrosine Kinases/metabolism ; Receptors, Antigen, B-Cell/*immunology/*metabolism ; Signal Transduction
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    Cilia at the node of mouse embryos sense fluid flow for left-right determination via Pkd2 (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-09-18
    Description: Unidirectional fluid flow plays an essential role in the breaking of left-right (L-R) symmetry in mouse embryos, but it has remained unclear how the flow is sensed by the embryo. We report that the Ca(2+) channel Polycystin-2 (Pkd2) is required specifically in the perinodal crown cells for sensing the nodal flow. Examination of mutant forms of Pkd2 shows that the ciliary localization of Pkd2 is essential for correct L-R patterning. Whereas Kif3a mutant embryos, which lack all cilia, failed to respond to an artificial flow, restoration of primary cilia in crown cells rescued the response to the flow. Our results thus suggest that nodal flow is sensed in a manner dependent on Pkd2 by the cilia of crown cells located at the edge of the node.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3711115/" 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/PMC3711115/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yoshiba, Satoko -- Shiratori, Hidetaka -- Kuo, Ivana Y -- Kawasumi, Aiko -- Shinohara, Kyosuke -- Nonaka, Shigenori -- Asai, Yasuko -- Sasaki, Genta -- Belo, Jose Antonio -- Sasaki, Hiroshi -- Nakai, Junichi -- Dworniczak, Bernd -- Ehrlich, Barbara E -- Pennekamp, Petra -- Hamada, Hiroshi -- P30 DK090744/DK/NIDDK NIH HHS/ -- P50 DK057328/DK/NIDDK NIH HHS/ -- R01 DK087844/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2012 Oct 12;338(6104):226-31. doi: 10.1126/science.1222538. Epub 2012 Sep 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Developmental Genetics Group, Graduate School of Frontier Biosciences, Osaka University, 1-3 Yamada-oka, Suita, 565-0871 Osaka, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22983710" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Body Fluids/physiology ; *Body Patterning ; Calcium/metabolism ; Cilia/metabolism/physiology ; Embryo, Mammalian/anatomy & histology/cytology/*physiology ; Gene Expression Regulation, Developmental ; Intercellular Signaling Peptides and Proteins/metabolism ; Kinesin/genetics ; Left-Right Determination Factors/genetics/*metabolism ; Mice ; Mice, Mutant Strains ; Mutation ; Organizers, Embryonic/cytology/*physiology ; Signal Transduction ; TRPP Cation Channels/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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  • 51
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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
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 52
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    Mechanical control of morphogenesis by Fat/Dachsous/Four-jointed planar cell polarity pathway (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-04-14
    Description: During animal development, several planar cell polarity (PCP) pathways control tissue shape by coordinating collective cell behavior. Here, we characterize by means of multiscale imaging epithelium morphogenesis in the Drosophila dorsal thorax and show how the Fat/Dachsous/Four-jointed PCP pathway controls morphogenesis. We found that the proto-cadherin Dachsous is polarized within a domain of its tissue-wide expression gradient. Furthermore, Dachsous polarizes the myosin Dachs, which in turn promotes anisotropy of junction tension. By combining physical modeling with quantitative image analyses, we determined that this tension anisotropy defines the pattern of local tissue contraction that contributes to shaping the epithelium mainly via oriented cell rearrangements. Our results establish how tissue planar polarization coordinates the local changes of cell mechanical properties to control tissue morphogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bosveld, Floris -- Bonnet, Isabelle -- Guirao, Boris -- Tlili, Sham -- Wang, Zhimin -- Petitalot, Ambre -- Marchand, Raphael -- Bardet, Pierre-Luc -- Marcq, Philippe -- Graner, Francois -- Bellaiche, Yohanns -- New York, N.Y. -- Science. 2012 May 11;336(6082):724-7. doi: 10.1126/science.1221071. Epub 2012 Apr 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Polarity, Division and Morphogenesis Team, Institut Curie, CNRS UMR 3215, INSERM U934, 26 Rue d'Ulm, 75248 Paris Cedex 05, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22499807" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anisotropy ; Cadherins/genetics/*metabolism ; Cell Adhesion Molecules/genetics/*metabolism ; *Cell Polarity ; Cell Shape ; Drosophila Proteins/genetics/*metabolism ; Drosophila melanogaster/cytology/genetics/*growth & development/metabolism ; Epithelial Cells/cytology/metabolism ; Intercellular Junctions/metabolism/physiology ; Membrane Glycoproteins/genetics/*metabolism ; Metamorphosis, Biological ; Models, Biological ; *Morphogenesis ; Myosins/metabolism ; Pupa/growth & development/metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Thorax/cytology/growth & development/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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  • 53
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    PI4P and PI(4,5)P2 are essential but independent lipid determinants of membrane identity (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-06-23
    Description: The quantitatively minor phospholipid phosphatidylinositol (4,5)-bisphosphate [PI(4,5)P(2)] fulfills many cellular functions in the plasma membrane (PM), whereas its synthetic precursor, phosphatidylinositol 4-phosphate (PI4P), has no assigned PM roles apart from PI(4,5)P(2) synthesis. We used a combination of pharmacological and chemical genetic approaches to probe the function of PM PI4P, most of which was not required for the synthesis or functions of PI(4,5)P(2). However, depletion of both lipids was required to prevent PM targeting of proteins that interact with acidic lipids or activation of the transient receptor potential vanilloid 1 cation channel. Therefore, PI4P contributes to the pool of polyanionic lipids that define plasma membrane identity and to some functions previously attributed specifically to PI(4,5)P(2), which may be fulfilled by a more general polyanionic lipid requirement.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3646512/" 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/PMC3646512/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hammond, Gerald R V -- Fischer, Michael J -- Anderson, Karen E -- Holdich, Jon -- Koteci, Ardita -- Balla, Tamas -- Irvine, Robin F -- ZIA HD000196-12/Intramural NIH HHS/ -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2012 Aug 10;337(6095):727-30. doi: 10.1126/science.1222483. Epub 2012 Jun 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of Cambridge, Tennis Court Road, Cambridge, CB2 1PD, UK. gerald.hammond@nih.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22722250" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; COS Cells ; Cell Membrane/*metabolism ; Cercopithecus aethiops ; Endocytosis ; HEK293 Cells ; Humans ; Membrane Proteins/metabolism ; Peptide Fragments/metabolism ; Phosphatidylinositol 4,5-Diphosphate/antagonists & ; inhibitors/biosynthesis/*metabolism ; Phosphatidylinositol Phosphates/*metabolism ; Phosphoric Monoester Hydrolases/genetics/metabolism ; Polymers ; Receptor, Muscarinic M1/metabolism ; Recombinant Fusion Proteins/metabolism ; Saccharomyces cerevisiae Proteins/genetics/metabolism ; Signal Transduction ; Static Electricity ; TRPV Cation Channels/antagonists & inhibitors/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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  • 54
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    New paradigms in type 2 immunity (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-07-28
    Description: Nearly half of the world's population harbors helminth infections or suffers from allergic disorders. A common feature of this population is the so-called "type 2 immune response," which confers protection against helminths, but also promotes pathologic responses associated with allergic inflammation. However, the mechanisms that initiate and control type 2 responses remain enigmatic. Recent advances have revealed a role for the innate immune system in orchestrating type 2 responses against a bewildering array of stimuli, from nanometer-sized allergens to 20-meter-long helminth parasites. Here, we review these advances and suggest that the human immune system has evolved multiple mechanisms of sensing such stimuli, from recognition of molecular patterns via innate immune receptors to detecting metabolic changes and tissue damage caused by these stimuli.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4078898/" 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/PMC4078898/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pulendran, Bali -- Artis, David -- AI061570/AI/NIAID NIH HHS/ -- AI074878/AI/NIAID NIH HHS/ -- AI083480/AI/NIAID NIH HHS/ -- AI087990/AI/NIAID NIH HHS/ -- AI095466/AI/NIAID NIH HHS/ -- AI095608/AI/NIAID NIH HHS/ -- HHSN266200700006C/PHS HHS/ -- N01 AI50025/AI/NIAID NIH HHS/ -- R37 AI048638/AI/NIAID NIH HHS/ -- R37 DK057665/DK/NIDDK NIH HHS/ -- R37AI48638/AI/NIAID NIH HHS/ -- R37DK057665/DK/NIDDK NIH HHS/ -- U19 AI057266/AI/NIAID NIH HHS/ -- U19 AI090023/AI/NIAID NIH HHS/ -- U19AI057266/AI/NIAID NIH HHS/ -- U19AI090023/AI/NIAID NIH HHS/ -- U54 AI057157/AI/NIAID NIH HHS/ -- U54AI057157/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2012 Jul 27;337(6093):431-5. doi: 10.1126/science.1221064.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Emory Vaccine Center, Yerkes National Primate Research Center, 954 Gatewood Road, Atlanta, GA 30329, USA. bpulend@emory.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22837519" target="_blank"〉PubMed〈/a〉
    Keywords: Allergens/*immunology ; Animals ; Basophils/immunology ; Biological Evolution ; Cell Communication ; Cellular Microenvironment ; Dendritic Cells/immunology ; Helminthiasis/*immunology ; Helminths/*immunology ; Humans ; Hypersensitivity/*immunology ; *Immunity, Innate ; Inflammation/immunology ; Receptors, Pattern Recognition/immunology/metabolism ; Signal Transduction ; Th2 Cells/*immunology/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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