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  • Articles  (34)
  • Signal Transduction
  • American Association for the Advancement of Science (AAAS)  (22)
  • Nature Publishing Group (NPG)  (12)
  • Nature Publishing Group
  • Springer Science + Business Media
  • 2010-2014  (34)
  • 1990-1994
  • 2011  (34)
Collection
  • Articles  (34)
Source
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (22)
  • Nature Publishing Group (NPG)  (12)
  • Nature Publishing Group
  • Springer Science + Business Media
Years
  • 2010-2014  (34)
  • 1990-1994
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Topic
  • 1
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    Duplications of the neuropeptide receptor gene VIPR2 confer significant risk for schizophrenia (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-02-25
    Description: Rare copy number variants (CNVs) have a prominent role in the aetiology of schizophrenia and other neuropsychiatric disorders. Substantial risk for schizophrenia is conferred by large (〉500-kilobase) CNVs at several loci, including microdeletions at 1q21.1 (ref. 2), 3q29 (ref. 3), 15q13.3 (ref. 2) and 22q11.2 (ref. 4) and microduplication at 16p11.2 (ref. 5). However, these CNVs collectively account for a small fraction (2-4%) of cases, and the relevant genes and neurobiological mechanisms are not well understood. Here we performed a large two-stage genome-wide scan of rare CNVs and report the significant association of copy number gains at chromosome 7q36.3 with schizophrenia. Microduplications with variable breakpoints occurred within a 362-kilobase region and were detected in 29 of 8,290 (0.35%) patients versus 2 of 7,431 (0.03%) controls in the combined sample. All duplications overlapped or were located within 89 kilobases upstream of the vasoactive intestinal peptide receptor gene VIPR2. VIPR2 transcription and cyclic-AMP signalling were significantly increased in cultured lymphocytes from patients with microduplications of 7q36.3. These findings implicate altered vasoactive intestinal peptide signalling in the pathogenesis of schizophrenia and indicate the VPAC2 receptor as a potential target for the development of new antipsychotic drugs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3351382/" 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/PMC3351382/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vacic, Vladimir -- McCarthy, Shane -- Malhotra, Dheeraj -- Murray, Fiona -- Chou, Hsun-Hua -- Peoples, Aine -- Makarov, Vladimir -- Yoon, Seungtai -- Bhandari, Abhishek -- Corominas, Roser -- Iakoucheva, Lilia M -- Krastoshevsky, Olga -- Krause, Verena -- Larach-Walters, Veronica -- Welsh, David K -- Craig, David -- Kelsoe, John R -- Gershon, Elliot S -- Leal, Suzanne M -- Dell Aquila, Marie -- Morris, Derek W -- Gill, Michael -- Corvin, Aiden -- Insel, Paul A -- McClellan, Jon -- King, Mary-Claire -- Karayiorgou, Maria -- Levy, Deborah L -- DeLisi, Lynn E -- Sebat, Jonathan -- 072894/Z/03/Z/Wellcome Trust/United Kingdom -- GM66232/GM/NIGMS NIH HHS/ -- HG04222/HG/NHGRI NIH HHS/ -- MH044245/MH/NIMH NIH HHS/ -- MH061399/MH/NIMH NIH HHS/ -- MH071523/MH/NIMH NIH HHS/ -- MH076431/MH/NIMH NIH HHS/ -- MH082945/MH/NIMH NIH HHS/ -- MH083989/MH/NIMH NIH HHS/ -- P41 HG004222/HG/NHGRI NIH HHS/ -- P41 HG004222-04S1/HG/NHGRI NIH HHS/ -- P41 HG004222-04S2/HG/NHGRI NIH HHS/ -- R00 HL091061/HL/NHLBI NIH HHS/ -- R01 MH061399/MH/NIMH NIH HHS/ -- R01 MH076431/MH/NIMH NIH HHS/ -- R01 MH076431-06/MH/NIMH NIH HHS/ -- R01 MH082945/MH/NIMH NIH HHS/ -- R01 MH091350/MH/NIMH NIH HHS/ -- England -- Nature. 2011 Mar 24;471(7339):499-503. doi: 10.1038/nature09884. Epub 2011 Feb 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Stanley Institute for Cognitive Genomics, Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 12824, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21346763" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Chromosomes, Human, Pair 7/genetics ; Cohort Studies ; Cyclic AMP/metabolism ; DNA Copy Number Variations/*genetics ; Female ; Gene Dosage/genetics ; Genes, Duplicate/*genetics ; Genetic Predisposition to Disease/*genetics ; Genome-Wide Association Study ; Humans ; Inheritance Patterns/genetics ; Male ; Pedigree ; Receptors, Vasoactive Intestinal Peptide, Type II/*genetics/metabolism ; Reproducibility of Results ; Schizophrenia/*genetics/metabolism ; Signal Transduction ; Transcription, Genetic/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 2
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    Phosphorylation of ULK1 (hATG1) by AMP-activated protein kinase connects energy sensing to mitophagy (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-01-06
    Description: Adenosine monophosphate-activated protein kinase (AMPK) is a conserved sensor of intracellular energy activated in response to low nutrient availability and environmental stress. In a screen for conserved substrates of AMPK, we identified ULK1 and ULK2, mammalian orthologs of the yeast protein kinase Atg1, which is required for autophagy. Genetic analysis of AMPK or ULK1 in mammalian liver and Caenorhabditis elegans revealed a requirement for these kinases in autophagy. In mammals, loss of AMPK or ULK1 resulted in aberrant accumulation of the autophagy adaptor p62 and defective mitophagy. Reconstitution of ULK1-deficient cells with a mutant ULK1 that cannot be phosphorylated by AMPK revealed that such phosphorylation is required for mitochondrial homeostasis and cell survival during starvation. These findings uncover a conserved biochemical mechanism coupling nutrient status with autophagy and cell survival.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3030664/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3030664/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Egan, Daniel F -- Shackelford, David B -- Mihaylova, Maria M -- Gelino, Sara -- Kohnz, Rebecca A -- Mair, William -- Vasquez, Debbie S -- Joshi, Aashish -- Gwinn, Dana M -- Taylor, Rebecca -- Asara, John M -- Fitzpatrick, James -- Dillin, Andrew -- Viollet, Benoit -- Kundu, Mondira -- Hansen, Malene -- Shaw, Reuben J -- 1P01CA120964/CA/NCI NIH HHS/ -- 1P01CA120964-01A/CA/NCI NIH HHS/ -- 5P30CA006516-43/CA/NCI NIH HHS/ -- P01 CA120964/CA/NCI NIH HHS/ -- P01 CA120964-05/CA/NCI NIH HHS/ -- P30 CA006516/CA/NCI NIH HHS/ -- P30 CA006516-43/CA/NCI NIH HHS/ -- P30CA014195/CA/NCI NIH HHS/ -- R01 DK080425/DK/NIDDK NIH HHS/ -- R01 DK080425-04/DK/NIDDK NIH HHS/ -- R01 DK080425-05/DK/NIDDK NIH HHS/ -- T32 CA009370/CA/NCI NIH HHS/ -- T32 CA009370-29/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Jan 28;331(6016):456-61. doi: 10.1126/science.1196371. Epub 2010 Dec 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular and Cell Biology Laboratory, Dulbecco Center for Cancer Research, Salk Institute for Biological Studies, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21205641" target="_blank"〉PubMed〈/a〉
    Keywords: AMP-Activated Protein Kinases/*metabolism ; Adaptor Proteins, Signal Transducing/metabolism ; Animals ; *Autophagy ; Caenorhabditis elegans/metabolism ; Caenorhabditis elegans Proteins/genetics/metabolism ; Cell Line ; Cell Line, Tumor ; Cell Survival ; Energy Metabolism ; Hepatocytes/metabolism ; Humans ; Insulin/metabolism ; Intracellular Signaling Peptides and Proteins/chemistry/genetics/*metabolism ; Liver/metabolism ; Metformin/pharmacology ; Mice ; Mitochondria, Liver/metabolism/ultrastructure ; Phenformin/pharmacology ; Phosphorylation ; Protein-Serine-Threonine Kinases/chemistry/genetics/*metabolism ; Signal Transduction ; Transcription Factors/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    The mutational landscape of head and neck squamous cell carcinoma (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-07-30
    Description: Head and neck squamous cell carcinoma (HNSCC) is a common, morbid, and frequently lethal malignancy. To uncover its mutational spectrum, we analyzed whole-exome sequencing data from 74 tumor-normal pairs. The majority exhibited a mutational profile consistent with tobacco exposure; human papillomavirus was detectable by sequencing DNA from infected tumors. In addition to identifying previously known HNSCC genes (TP53, CDKN2A, PTEN, PIK3CA, and HRAS), our analysis revealed many genes not previously implicated in this malignancy. At least 30% of cases harbored mutations in genes that regulate squamous differentiation (for example, NOTCH1, IRF6, and TP63), implicating its dysregulation as a major driver of HNSCC carcinogenesis. More generally, the results indicate the ability of large-scale sequencing to reveal fundamental tumorigenic mechanisms.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3415217/" 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/PMC3415217/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stransky, Nicolas -- Egloff, Ann Marie -- Tward, Aaron D -- Kostic, Aleksandar D -- Cibulskis, Kristian -- Sivachenko, Andrey -- Kryukov, Gregory V -- Lawrence, Michael S -- Sougnez, Carrie -- McKenna, Aaron -- Shefler, Erica -- Ramos, Alex H -- Stojanov, Petar -- Carter, Scott L -- Voet, Douglas -- Cortes, Maria L -- Auclair, Daniel -- Berger, Michael F -- Saksena, Gordon -- Guiducci, Candace -- Onofrio, Robert C -- Parkin, Melissa -- Romkes, Marjorie -- Weissfeld, Joel L -- Seethala, Raja R -- Wang, Lin -- Rangel-Escareno, Claudia -- Fernandez-Lopez, Juan Carlos -- Hidalgo-Miranda, Alfredo -- Melendez-Zajgla, Jorge -- Winckler, Wendy -- Ardlie, Kristin -- Gabriel, Stacey B -- Meyerson, Matthew -- Lander, Eric S -- Getz, Gad -- Golub, Todd R -- Garraway, Levi A -- Grandis, Jennifer R -- P50 CA097190/CA/NCI NIH HHS/ -- R01 CA077308/CA/NCI NIH HHS/ -- R01 CA098372/CA/NCI NIH HHS/ -- UL1 TR000005/TR/NCATS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Aug 26;333(6046):1157-60. doi: 10.1126/science.1208130. Epub 2011 Jul 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21798893" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Apoptosis ; Carcinoma/*genetics/metabolism/virology ; Carcinoma, Squamous Cell ; Cell Differentiation ; Exons ; Head and Neck Neoplasms/*genetics/metabolism/virology ; Humans ; *Mutation ; Neoplasms, Squamous Cell/*genetics/metabolism/virology ; Papillomaviridae/isolation & purification ; Papillomavirus Infections/virology ; Point Mutation ; Receptor, Notch1/*genetics/metabolism ; *Sequence Analysis, DNA ; Sequence Deletion ; Signal Transduction ; Smoking ; Tobacco
    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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    Pretreatment mitochondrial priming correlates with clinical response to cytotoxic chemotherapy (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-10-29
    Description: Cytotoxic chemotherapy targets elements common to all nucleated human cells, such as DNA and microtubules, yet it selectively kills tumor cells. Here we show that clinical response to these drugs correlates with, and may be partially governed by, the pretreatment proximity of tumor cell mitochondria to the apoptotic threshold, a property called mitochondrial priming. We used BH3 profiling to measure priming in tumor cells from patients with multiple myeloma, acute myelogenous and lymphoblastic leukemia, and ovarian cancer. This assay measures mitochondrial response to peptides derived from proapoptotic BH3 domains of proteins critical for death signaling to mitochondria. Patients with highly primed cancers exhibited superior clinical response to chemotherapy. In contrast, chemoresistant cancers and normal tissues were poorly primed. Manipulation of mitochondrial priming might enhance the efficacy of cytotoxic agents.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3280949/" 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/PMC3280949/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ni Chonghaile, Triona -- Sarosiek, Kristopher A -- Vo, Thanh-Trang -- Ryan, Jeremy A -- Tammareddi, Anupama -- Moore, Victoria Del Gaizo -- Deng, Jing -- Anderson, Kenneth C -- Richardson, Paul -- Tai, Yu-Tzu -- Mitsiades, Constantine S -- Matulonis, Ursula A -- Drapkin, Ronny -- Stone, Richard -- Deangelo, Daniel J -- McConkey, David J -- Sallan, Stephen E -- Silverman, Lewis -- Hirsch, Michelle S -- Carrasco, Daniel Ruben -- Letai, Anthony -- P01CA068484/CA/NCI NIH HHS/ -- P01CA139980/CA/NCI NIH HHS/ -- R01 CA129974/CA/NCI NIH HHS/ -- R01 CA129974-05/CA/NCI NIH HHS/ -- R01CA129974/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2011 Nov 25;334(6059):1129-33. doi: 10.1126/science.1206727. Epub 2011 Oct 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Oncology, Dana-Farber Cancer Institute, 450 Brookline Avenue, Boston, MA 02215, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22033517" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Animals ; Antineoplastic Agents/*therapeutic use ; *Apoptosis ; Cell Line, Tumor ; Cell Proliferation ; Child ; Disease-Free Survival ; Drug Resistance, Neoplasm ; Female ; Humans ; Leukemia, Myeloid, Acute/drug therapy/physiopathology ; Male ; Membrane Potential, Mitochondrial ; Mice ; Mice, Inbred C57BL ; Middle Aged ; Mitochondria/*physiology ; Multiple Myeloma/drug therapy/physiopathology ; Neoplasms/*drug therapy/*physiopathology ; Ovarian Neoplasms/drug therapy/physiopathology ; Peptide Fragments/metabolism ; Permeability ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/drug therapy/physiopathology ; Proto-Oncogene Proteins c-bcl-2/chemistry/metabolism ; Remission Induction ; 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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  • 5
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    Transplanted hypothalamic neurons restore leptin signaling and ameliorate obesity in db/db mice (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-11-26
    Description: Evolutionarily old and conserved homeostatic systems in the brain, including the hypothalamus, are organized into nuclear structures of heterogeneous and diverse neuron populations. To investigate whether such circuits can be functionally reconstituted by synaptic integration of similarly diverse populations of neurons, we generated physically chimeric hypothalami by microtransplanting small numbers of embryonic enhanced green fluorescent protein-expressing, leptin-responsive hypothalamic cells into hypothalami of postnatal leptin receptor-deficient (db/db) mice that develop morbid obesity. Donor neurons differentiated and integrated as four distinct hypothalamic neuron subtypes, formed functional excitatory and inhibitory synapses, partially restored leptin responsiveness, and ameliorated hyperglycemia and obesity in db/db mice. These experiments serve as a proof of concept that transplanted neurons can functionally reconstitute complex neuronal circuitry in the mammalian brain.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3770458/" 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/PMC3770458/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Czupryn, Artur -- Zhou, Yu-Dong -- Chen, Xi -- McNay, David -- Anderson, Matthew P -- Flier, Jeffrey S -- Macklis, Jeffrey D -- DKR37-28082/PHS HHS/ -- K02 NS054674/NS/NINDS NIH HHS/ -- NS054674/NS/NINDS NIH HHS/ -- NS057444/NS/NINDS NIH HHS/ -- NS070295/NS/NINDS NIH HHS/ -- NS41590/NS/NINDS NIH HHS/ -- NS45523/NS/NINDS NIH HHS/ -- NS49553/NS/NINDS NIH HHS/ -- R01 NS041590/NS/NINDS NIH HHS/ -- R01 NS045523/NS/NINDS NIH HHS/ -- R01 NS049553/NS/NINDS NIH HHS/ -- R01 NS057444/NS/NINDS NIH HHS/ -- R21 NS070295/NS/NINDS NIH HHS/ -- R37 DK028082/DK/NIDDK NIH HHS/ -- R37 NS041590/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2011 Nov 25;334(6059):1133-7. doi: 10.1126/science.1209870.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Stem Cell and Regenerative Biology, and Harvard Stem Cell Institute, Harvard University, Cambridge, MA 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22116886" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Glucose/analysis ; Body Weight ; Cell Shape ; Electrophysiological Phenomena ; Excitatory Postsynaptic Potentials ; Glucose/administration & dosage ; Hypothalamus/*cytology/metabolism ; Hypothalamus, Middle/*cytology/metabolism/*physiopathology ; Inhibitory Postsynaptic Potentials ; Insulin/administration & dosage/blood ; Leptin/administration & dosage/*metabolism ; Membrane Potentials ; Mice ; Mice, Obese ; Neurogenesis ; Neurons/cytology/*physiology/*transplantation ; Obesity/metabolism/*physiopathology/*therapy ; Receptors, Leptin/*metabolism ; Signal Transduction ; Synaptic Transmission
    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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    Intramembrane cleavage of AMA1 triggers Toxoplasma to switch from an invasive to a replicative mode (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-01-06
    Description: Apicomplexan parasites invade host cells and immediately initiate cell division. The extracellular parasite discharges transmembrane proteins onto its surface to mediate motility and invasion. These are shed by intramembrane cleavage, a process associated with invasion but otherwise poorly understood. Functional analysis of Toxoplasma rhomboid 4, a surface intramembrane protease, by conditional overexpression of a catalytically inactive form produced a profound block in replication. This was completely rescued by expression of the cleaved cytoplasmic tail of Toxoplasma or Plasmodium apical membrane antigen 1 (AMA1). These results reveal an unexpected function for AMA1 in parasite replication and suggest that invasion proteins help to promote parasite switch from an invasive to a replicative mode.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Santos, Joana M -- Ferguson, David J P -- Blackman, Michael J -- Soldati-Favre, Dominique -- MC_U117532063/Medical Research Council/United Kingdom -- U117532063/Medical Research Council/United Kingdom -- Howard Hughes Medical Institute/ -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2011 Jan 28;331(6016):473-7. doi: 10.1126/science.1199284. Epub 2010 Dec 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, Faculty of Medicine, 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/21205639" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, Protozoan/chemistry/genetics/*metabolism ; Cell Cycle ; Cell Division ; Cell Membrane/metabolism ; Cells, Cultured ; Fibroblasts/parasitology ; Humans ; Membrane Proteins/chemistry/genetics/*metabolism ; Movement ; Mutant Proteins/metabolism ; Plasmodium falciparum ; Protozoan Proteins/chemistry/genetics/*metabolism ; Serine Proteases/genetics/metabolism ; Signal Transduction ; Toxoplasma/cytology/growth & development/*physiology
    Print ISSN: 0036-8075
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  • 7
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    Fungal lipochitooligosaccharide symbiotic signals in arbuscular mycorrhiza (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-01-07
    Description: Arbuscular mycorrhiza (AM) is a root endosymbiosis between plants and glomeromycete fungi. It is the most widespread terrestrial plant symbiosis, improving plant uptake of water and mineral nutrients. Yet, despite its crucial role in land ecosystems, molecular mechanisms leading to its formation are just beginning to be unravelled. Recent evidence suggests that AM fungi produce diffusible symbiotic signals. Here we show that Glomus intraradices secretes symbiotic signals that are a mixture of sulphated and non-sulphated simple lipochitooligosaccharides (LCOs), which stimulate formation of AM in plant species of diverse families (Fabaceae, Asteraceae and Umbelliferae). In the legume Medicago truncatula these signals stimulate root growth and branching by the symbiotic DMI signalling pathway. These findings provide a better understanding of the evolution of signalling mechanisms involved in plant root endosymbioses and will greatly facilitate their molecular dissection. They also open the way to using these natural and very active molecules in agriculture.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maillet, Fabienne -- Poinsot, Verena -- Andre, Olivier -- Puech-Pages, Virginie -- Haouy, Alexandra -- Gueunier, Monique -- Cromer, Laurence -- Giraudet, Delphine -- Formey, Damien -- Niebel, Andreas -- Martinez, Eduardo Andres -- Driguez, Hugues -- Becard, Guillaume -- Denarie, Jean -- England -- Nature. 2011 Jan 6;469(7328):58-63. doi: 10.1038/nature09622.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire des Interactions Plantes-Microorganismes, UMR 441/2594 INRA-CNRS, B.P. 52627, F-31326 Castanet-Tolosan CEDEX, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21209659" target="_blank"〉PubMed〈/a〉
    Keywords: Carbohydrate Sequence ; Chromatography, High Pressure Liquid ; Daucus carota/chemistry/metabolism/microbiology ; Glomeromycota/metabolism ; Lipopolysaccharides/chemistry/*metabolism ; Medicago truncatula/chemistry/growth & development/metabolism/microbiology ; Molecular Sequence Data ; Mycorrhizae/*metabolism ; Plant Extracts/chemistry/metabolism ; Plant Roots/chemistry/growth & development/*metabolism/*microbiology ; Signal Transduction ; Spores, Fungal/chemistry/metabolism ; *Symbiosis
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 8
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    A Raf-induced allosteric transition of KSR stimulates phosphorylation of MEK (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-03-29
    Description: In metazoans, the Ras-Raf-MEK (mitogen-activated protein-kinase kinase)-ERK (extracellular signal-regulated kinase) signalling pathway relays extracellular stimuli to elicit changes in cellular function and gene expression. Aberrant activation of this pathway through oncogenic mutations is responsible for a large proportion of human cancer. Kinase suppressor of Ras (KSR) functions as an essential scaffolding protein to coordinate the assembly of Raf-MEK-ERK complexes. Here we integrate structural and biochemical studies to understand how KSR promotes stimulatory Raf phosphorylation of MEK (refs 6, 7). We show, from the crystal structure of the kinase domain of human KSR2 (KSR2(KD)) in complex with rabbit MEK1, that interactions between KSR2(KD) and MEK1 are mediated by their respective activation segments and C-lobe alphaG helices. Analogous to BRAF (refs 8, 9), KSR2 self-associates through a side-to-side interface involving Arg 718, a residue identified in a genetic screen as a suppressor of Ras signalling. ATP is bound to the KSR2(KD) catalytic site, and we demonstrate KSR2 kinase activity towards MEK1 by in vitro assays and chemical genetics. In the KSR2(KD)-MEK1 complex, the activation segments of both kinases are mutually constrained, and KSR2 adopts an inactive conformation. BRAF allosterically stimulates the kinase activity of KSR2, which is dependent on formation of a side-to-side KSR2-BRAF heterodimer. Furthermore, KSR2-BRAF heterodimerization results in an increase of BRAF-induced MEK phosphorylation via the KSR2-mediated relay of a signal from BRAF to release the activation segment of MEK for phosphorylation. We propose that KSR interacts with a regulatory Raf molecule in cis to induce a conformational switch of MEK, facilitating MEK's phosphorylation by a separate catalytic Raf molecule in trans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brennan, Damian F -- Dar, Arvin C -- Hertz, Nicholas T -- Chao, William C H -- Burlingame, Alma L -- Shokat, Kevan M -- Barford, David -- RR001614/RR/NCRR NIH HHS/ -- RR015804/RR/NCRR NIH HHS/ -- Cancer Research UK/United Kingdom -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 Apr 21;472(7343):366-9. doi: 10.1038/nature09860. Epub 2011 Mar 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Structural Biology, Institute of Cancer Research, Chester Beatty Laboratories, 237 Fulham Road, London SW3 6JB, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21441910" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Allosteric Regulation/physiology ; Animals ; Biocatalysis ; Catalytic Domain ; Crystallography, X-Ray ; Enzyme Activation ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Humans ; MAP Kinase Kinase 1/*chemistry/*metabolism ; Models, Molecular ; Phosphorylation ; Protein Multimerization ; Protein Structure, Quaternary ; Protein-Serine-Threonine Kinases/*chemistry/*metabolism ; Proto-Oncogene Proteins B-raf/chemistry/genetics/*metabolism ; Rabbits ; Signal Transduction
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 9
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    Cancer. New epigenetic drivers of cancers (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-03-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Elsasser, Simon J -- Allis, C David -- Lewis, Peter W -- New York, N.Y. -- Science. 2011 Mar 4;331(6021):1145-6. doi: 10.1126/science.1203280.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Chromatin Biology and Epigenetics, Rockefeller University, New York, NY 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21385704" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/*genetics/metabolism ; Chromatin/metabolism ; Chromatin Assembly and Disassembly/genetics ; DNA Helicases/*genetics/metabolism ; *Epigenesis, Genetic ; *Genes, Tumor Suppressor ; Histones/metabolism ; Humans ; Mutation ; Neuroendocrine Tumors/*genetics/metabolism ; Nuclear Proteins/*genetics/metabolism ; Nucleosomes/metabolism ; Pancreatic Neoplasms/*genetics/metabolism ; Proto-Oncogene Proteins/*genetics/metabolism ; Signal Transduction ; TOR Serine-Threonine Kinases/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 10
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    An activating mutation of AKT2 and human hypoglycemia (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-10-08
    Description: Pathological fasting hypoglycemia in humans is usually explained by excessive circulating insulin or insulin-like molecules or by inborn errors of metabolism impairing liver glucose production. We studied three unrelated children with unexplained, recurrent, and severe fasting hypoglycemia and asymmetrical growth. All were found to carry the same de novo mutation, p.Glu17Lys, in the serine/threonine kinase AKT2, in two cases as heterozygotes and in one case in mosaic form. In heterologous cells, the mutant AKT2 was constitutively recruited to the plasma membrane, leading to insulin-independent activation of downstream signaling. Thus, systemic metabolic disease can result from constitutive, cell-autonomous activation of signaling pathways normally controlled by insulin.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3204221/" 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/PMC3204221/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hussain, K -- Challis, B -- Rocha, N -- Payne, F -- Minic, M -- Thompson, A -- Daly, A -- Scott, C -- Harris, J -- Smillie, B J L -- Savage, D B -- Ramaswami, U -- De Lonlay, P -- O'Rahilly, S -- Barroso, I -- Semple, R K -- 077016/Wellcome Trust/United Kingdom -- 077016/Z/05/Z/Wellcome Trust/United Kingdom -- 078986/Wellcome Trust/United Kingdom -- 078986/Z/06/Z/Wellcome Trust/United Kingdom -- 080952/Wellcome Trust/United Kingdom -- 080952/Z/06/Z/Wellcome Trust/United Kingdom -- 091551/Wellcome Trust/United Kingdom -- 091551/Z/10/Z/Wellcome Trust/United Kingdom -- 095515/Wellcome Trust/United Kingdom -- G0502115/Medical Research Council/United Kingdom -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2011 Oct 28;334(6055):474. doi: 10.1126/science.1210878. Epub 2011 Oct 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Clinical and Molecular Genetics Unit, Developmental Endocrinology Research Group, Institute of Child Health, University College London, London WC1N 1EH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21979934" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Substitution ; Cell Membrane/metabolism ; Cell Nucleus/metabolism ; Child ; Female ; Growth ; HeLa Cells ; Heterozygote ; Humans ; Hypoglycemia/*genetics/*metabolism ; Insulin/blood/metabolism ; Male ; Mosaicism ; *Mutation ; Pedigree ; Protein Interaction Domains and Motifs ; Proto-Oncogene Proteins c-akt/chemistry/*genetics/metabolism ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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