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  • *Signal Transduction  (18)
  • American Association for the Advancement of Science (AAAS)  (18)
  • American Physical Society
  • Copernicus
  • 2010-2014
  • 2005-2009  (18)
  • 2005  (18)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (18)
  • American Physical Society
  • Copernicus
Years
  • 2010-2014
  • 2005-2009  (18)
Year
  • 1
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    DISC1 and PDE4B are interacting genetic factors in schizophrenia that regulate cAMP signaling (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-11-19
    Description: The disrupted in schizophrenia 1 (DISC1) gene is a candidate susceptibility factor for schizophrenia, but its mechanistic role in the disorder is unknown. Here we report that the gene encoding phosphodiesterase 4B (PDE4B) is disrupted by a balanced translocation in a subject diagnosed with schizophrenia and a relative with chronic psychiatric illness. The PDEs inactivate adenosine 3',5'-monophosphate (cAMP), a second messenger implicated in learning, memory, and mood. We show that DISC1 interacts with the UCR2 domain of PDE4B and that elevation of cellular cAMP leads to dissociation of PDE4B from DISC1 and an increase in PDE4B activity. We propose a mechanistic model whereby DISC1 sequesters PDE4B in resting cells and releases it in an activated state in response to elevated cAMP.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Millar, J Kirsty -- Pickard, Benjamin S -- Mackie, Shaun -- James, Rachel -- Christie, Sheila -- Buchanan, Sebastienne R -- Malloy, M Pat -- Chubb, Jennifer E -- Huston, Elaine -- Baillie, George S -- Thomson, Pippa A -- Hill, Elaine V -- Brandon, Nicholas J -- Rain, Jean-Christophe -- Camargo, L Miguel -- Whiting, Paul J -- Houslay, Miles D -- Blackwood, Douglas H R -- Muir, Walter J -- Porteous, David J -- G8604010/Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2005 Nov 18;310(5751):1187-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Genetics Section, Molecular Medicine Centre, University of Edinburgh, Edinburgh EH4 2XU, UK. Kirsty.Millar@ed.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16293762" target="_blank"〉PubMed〈/a〉
    Keywords: 3',5'-Cyclic-AMP Phosphodiesterases/*genetics/metabolism ; Adult ; Affective Disorders, Psychotic/genetics/metabolism ; Animals ; Cadherins/genetics ; Cell Line ; Chromosomes, Human, Pair 1 ; Chromosomes, Human, Pair 16 ; Cyclic AMP/*metabolism ; Cyclic Nucleotide Phosphodiesterases, Type 4 ; Enzyme Activation ; Genetic Predisposition to Disease ; Humans ; Male ; Nerve Tissue Proteins/*genetics/metabolism ; Protein Binding ; Rats ; Schizophrenia/enzymology/*genetics/metabolism ; *Signal Transduction ; Translocation, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    Causal protein-signaling networks derived from multiparameter single-cell data (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-04-23
    Description: Machine learning was applied for the automated derivation of causal influences in cellular signaling networks. This derivation relied on the simultaneous measurement of multiple phosphorylated protein and phospholipid components in thousands of individual primary human immune system cells. Perturbing these cells with molecular interventions drove the ordering of connections between pathway components, wherein Bayesian network computational methods automatically elucidated most of the traditionally reported signaling relationships and predicted novel interpathway network causalities, which we verified experimentally. Reconstruction of network models from physiologically relevant primary single cells might be applied to understanding native-state tissue signaling biology, complex drug actions, and dysfunctional signaling in diseased cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sachs, Karen -- Perez, Omar -- Pe'er, Dana -- Lauffenburger, Douglas A -- Nolan, Garry P -- AI35304/AI/NIAID NIH HHS/ -- P01-AI39646/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2005 Apr 22;308(5721):523-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biological Engineering Division, Massachusetts Institute of Technology (MIT), Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15845847" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Artificial Intelligence ; *Bayes Theorem ; CD4-Positive T-Lymphocytes/*metabolism ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Flow Cytometry ; Humans ; Intracellular Signaling Peptides and Proteins/*metabolism ; Mathematics ; *Models, Biological ; Phospholipids/metabolism ; Phosphoproteins/metabolism ; Phosphorylation ; Protein Kinase C/metabolism ; Protein-Serine-Threonine Kinases/metabolism ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-akt ; RNA, Small Interfering ; *Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Mathematical modeling of planar cell polarity to understand domineering nonautonomy (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-01-22
    Description: Planar cell polarity (PCP) signaling generates subcellular asymmetry along an axis orthogonal to the epithelial apical-basal axis. Through a poorly understood mechanism, cell clones that have mutations in some PCP signaling components, including some, but not all, alleles of the receptor frizzled, cause polarity disruptions of neighboring wild-type cells, a phenomenon referred to as domineering nonautonomy. Here, a contact-dependent signaling hypothesis, derived from experimental results, is shown by reaction-diffusion, partial differential equation modeling and simulation to fully reproduce PCP phenotypes, including domineering nonautonomy, in the Drosophila wing. The sufficiency of this model and the experimental validation of model predictions reveal how specific protein-protein interactions produce autonomy or domineering nonautonomy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Amonlirdviman, Keith -- Khare, Narmada A -- Tree, David R P -- Chen, Wei-Shen -- Axelrod, Jeffrey D -- Tomlin, Claire J -- R01-GM59823/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2005 Jan 21;307(5708):423-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Aeronautics and Astronautics, Stanford University, Stanford, CA 94305-4035, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15662015" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Alleles ; Animals ; Cell Membrane/metabolism ; *Cell Polarity ; Diffusion ; Drosophila/*cytology/genetics/metabolism ; Drosophila Proteins/genetics/metabolism ; Feedback, Physiological ; Frizzled Receptors ; Mathematics ; Membrane Proteins/genetics/metabolism ; *Models, Biological ; Mutation ; Phenotype ; Phosphoproteins/genetics/metabolism ; Protein Binding ; Receptors, G-Protein-Coupled ; *Signal Transduction ; Wings, Animal/*cytology/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Connected to death: the (unexpurgated) mitochondrial pathway of apoptosis (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-10-08
    Description: The mitochondrial pathway of apoptosis in vertebrates is dependent on the process of mitochondrial outer membrane permeabilization (MOMP), which leads to the release of proteins from the mitochondrial intermembrane space into the cytosol. "Upstairs" of this event are the Bcl-2 family proteins that regulate and mediate MOMP; "downstairs" is the activation of caspases that orchestrate the dismantling of the cell. In the Connections Map database at Science's Signal Transduction Knowledge Environment (STKE), the pathways that define the mitochondrial pathway of apotosis are illustrated, with the bulk of control occurring "upstairs" of MOMP.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Spierings, Diana -- McStay, Gavin -- Saleh, Maya -- Bender, Cheryl -- Chipuk, Jerry -- Maurer, Uli -- Green, Douglas R -- New York, N.Y. -- Science. 2005 Oct 7;310(5745):66-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉La Jolla Institute for Allergy and Immunology, 10355 Science Center Drive, San Diego, CA 92121, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16210526" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Apoptotic Protease-Activating Factor 1 ; Caspases/metabolism ; Cytochromes c/metabolism ; Cytosol/metabolism ; Inhibitor of Apoptosis Proteins ; Intracellular Membranes/*metabolism ; Mitochondria/*metabolism ; Models, Biological ; Permeability ; Proteins/*metabolism ; Proto-Oncogene Proteins c-bcl-2/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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  • 5
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    Toll-like receptor 8-mediated reversal of CD4+ regulatory T cell function (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-08-27
    Description: CD4+ regulatory T (Treg) cells have a profound ability to suppress host immune responses, yet little is understood about how these cells are regulated. We describe a mechanism linking Toll-like receptor (TLR) 8 signaling to the control of Treg cell function, in which synthetic and natural ligands for human TLR8 can reverse Treg cell function. This effect was independent of dendritic cells but required functional TLR8-MyD88-IRAK4 signaling in Treg cells. Adoptive transfer of TLR8 ligand-stimulated Treg cells into tumor-bearing mice enhanced anti-tumor immunity. These results suggest that TLR8 signaling could play a critical role in controlling immune responses to cancer and other diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peng, Guangyong -- Guo, Zhong -- Kiniwa, Yukiko -- Voo, Kui Shin -- Peng, Weiyi -- Fu, Tihui -- Wang, Daniel Y -- Li, Yanchun -- Wang, Helen Y -- Wang, Rong-Fu -- P01CA94237/CA/NCI NIH HHS/ -- P50 CA093459/CA/NCI NIH HHS/ -- P50CA58204/CA/NCI NIH HHS/ -- R01CA101795/CA/NCI NIH HHS/ -- R01CA90327/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2005 Aug 26;309(5739):1380-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Cell and Gene Therapy and Department of Immunology, Baylor College of Medicine, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16123302" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Adoptive Transfer ; Animals ; Antigens, Differentiation/genetics/physiology ; CD4-Positive T-Lymphocytes/*immunology ; Cell Line ; Cell Line, Tumor ; Humans ; Immune Tolerance ; Interleukin-1 Receptor-Associated Kinases ; Killer Cells, Natural/immunology ; Ligands ; Lymphocyte Activation ; Membrane Glycoproteins/genetics/*physiology ; Mice ; Myeloid Differentiation Factor 88 ; Neoplasm Transplantation ; Neoplasms, Experimental/immunology/pathology ; Oligodeoxyribonucleotides/immunology ; Phosphotransferases (Alcohol Group Acceptor)/genetics/physiology ; Poly G/immunology ; RNA Interference ; Receptors, Cell Surface/genetics/*physiology ; Receptors, Immunologic/genetics/physiology ; *Signal Transduction ; T-Lymphocyte Subsets/*immunology ; Toll-Like Receptor 8 ; Toll-Like Receptors
    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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    Direct control of germline stem cell division and cyst growth by neural insulin in Drosophila (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-08-16
    Description: Stem cells reside in specialized niches that provide signals required for their maintenance and division. Tissue-extrinsic signals can also modify stem cell activity, although this is poorly understood. Here, we report that neural-derived Drosophila insulin-like peptides (DILPs) directly regulate germline stem cell division rate, demonstrating that signals mediating the ovarian response to nutritional input can modify stem cell activity in a niche-independent manner. We also reveal a crucial direct role of DILPs in controlling germline cyst growth and vitellogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉LaFever, Leesa -- Drummond-Barbosa, Daniela -- GM 069875/GM/NIGMS NIH HHS/ -- R01 GM069875/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2005 Aug 12;309(5737):1071-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell and Developmental Biology, Vanderbilt University Medical Center, 4120B Medical Research Building III, 465 21st Avenue South, Nashville, TN 37232-8240, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16099985" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Division ; Cell Proliferation ; Drosophila/cytology/genetics/*physiology ; Drosophila Proteins/genetics/*physiology ; Female ; Food ; Germ Cells/*cytology ; Insulin/*physiology ; Mutation ; Ovarian Follicle/cytology/physiology ; Ovary/cytology/physiology ; Peptides/physiology ; Receptor Protein-Tyrosine Kinases/genetics/physiology ; *Signal Transduction ; Stem Cells/*cytology ; Vitellogenesis
    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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  • 7
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    Retinoic acid signaling restricts the cardiac progenitor pool (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-01-18
    Description: Organogenesis begins with specification of a progenitor cell population, the size of which provides a foundation for the organ's final dimensions. Here, we present a new mechanism for regulating the number of progenitor cells by limiting their density within a competent region. We demonstrate that retinoic acid signaling restricts cardiac specification in the zebrafish embryo. Reduction of retinoic acid signaling causes formation of an excess of cardiomyocytes, via fate transformations that increase cardiac progenitor density within a multipotential zone. Thus, retinoic acid signaling creates a balance between cardiac and noncardiac identities, thereby refining the dimensions of the cardiac progenitor pool.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Keegan, Brian R -- Feldman, Jessica L -- Begemann, Gerrit -- Ingham, Philip W -- Yelon, Deborah -- New York, N.Y. -- Science. 2005 Jan 14;307(5707):247-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Developmental Genetics Program, Skirball Institute of Biomolecular Medicine, and Department of Cell Biology, New York University School of Medicine, New York, NY 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15653502" target="_blank"〉PubMed〈/a〉
    Keywords: Aldehyde Oxidoreductases/genetics/metabolism ; Animals ; Blastomeres/cytology/physiology ; Blastula/cytology/physiology ; Cell Count ; Cell Differentiation ; Cell Proliferation ; Embryo, Nonmammalian/cytology/physiology ; Gastrula/physiology ; Heart/*embryology ; Mesoderm/cytology ; Myocytes, Cardiac/cytology/*physiology ; Receptors, Retinoic Acid/antagonists & inhibitors ; Retinal Dehydrogenase ; Retinoids/pharmacology ; *Signal Transduction ; Stem Cells/cytology/*physiology ; Tretinoin/*metabolism ; Zebrafish
    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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    Prostaglandin E2 promotes colon cancer cell growth through a Gs-axin-beta-catenin signaling axis (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-11-19
    Description: How cyclooxygenase-2 (COX-2) and its proinflammatory metabolite prostaglandin E2 (PGE2) enhance colon cancer progression remains poorly understood. We show that PGE2 stimulates colon cancer cell growth through its heterotrimeric guanine nucleotide-binding protein (G protein)-coupled receptor, EP2, by a signaling route that involves the activation of phosphoinositide 3-kinase and the protein kinase Akt by free G protein betagamma subunits and the direct association of the G protein alphas subunit with the regulator of G protein signaling (RGS) domain of axin. This leads to the inactivation and release of glycogen synthase kinase 3beta from its complex with axin, thereby relieving the inhibitory phosphorylation of beta-catenin and activating its signaling pathway. These findings may provide a molecular framework for the future evaluation of chemopreventive strategies for colorectal cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Castellone, Maria Domenica -- Teramoto, Hidemi -- Williams, Bart O -- Druey, Kirk M -- Gutkind, J Silvio -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2005 Dec 2;310(5753):1504-10. Epub 2005 Nov 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Oral and Pharyngeal Cancer Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892-4340, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16293724" target="_blank"〉PubMed〈/a〉
    Keywords: Axin Protein ; Cell Line ; Cell Proliferation ; Colonic Neoplasms/*pathology ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Dinoprostone/*physiology ; GTP-Binding Protein alpha Subunits, Gs/*metabolism ; Genes, Reporter ; Humans ; RGS Proteins/metabolism ; Receptors, Prostaglandin E/metabolism ; Receptors, Prostaglandin E, EP2 Subtype ; Repressor Proteins/*metabolism ; *Signal Transduction ; beta Catenin/*metabolism
    Print ISSN: 0036-8075
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  • 9
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    A transmembrane intracellular estrogen receptor mediates rapid cell signaling (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-02-12
    Description: The steroid hormone estrogen regulates many functionally unrelated processes in numerous tissues. Although it is traditionally thought to control transcriptional activation through the classical nuclear estrogen receptors, it also initiates many rapid nongenomic signaling events. We found that of all G protein-coupled receptors characterized to date, GPR30 is uniquely localized to the endoplasmic reticulum, where it specifically binds estrogen and fluorescent estrogen derivatives. Activating GPR30 by estrogen resulted in intracellular calcium mobilization and synthesis of phosphatidylinositol 3,4,5-trisphosphate in the nucleus. Thus, GPR30 represents an intracellular transmembrane estrogen receptor that may contribute to normal estrogen physiology as well as pathophysiology.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Revankar, Chetana M -- Cimino, Daniel F -- Sklar, Larry A -- Arterburn, Jeffrey B -- Prossnitz, Eric R -- 1 S10 RR14668/RR/NCRR NIH HHS/ -- AI36357/AI/NIAID NIH HHS/ -- EB00264/EB/NIBIB NIH HHS/ -- P20 RR11830/RR/NCRR NIH HHS/ -- R24 CA88339/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2005 Mar 11;307(5715):1625-30. Epub 2005 Feb 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology and Physiology, University of New Mexico Health Sciences Center, Albuquerque, NM 87131, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15705806" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antisense Elements (Genetics) ; Calcium/metabolism ; Cell Line ; Cell Line, Tumor ; Cell Membrane/metabolism ; Cell Nucleus/metabolism ; Endoplasmic Reticulum/*metabolism ; Estradiol/metabolism ; Estrogen Receptor alpha/metabolism ; Estrogens/*metabolism ; Humans ; Nuclear Envelope/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphatidylinositol Phosphates/metabolism ; Protein Transport ; Receptor, Epidermal Growth Factor/metabolism ; Receptors, Estrogen/*metabolism ; Receptors, G-Protein-Coupled/*metabolism ; Recombinant Fusion Proteins/metabolism ; *Signal Transduction ; Transfection
    Print ISSN: 0036-8075
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  • 10
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    Stat3 dimerization regulated by reversible acetylation of a single lysine residue (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-01-18
    Description: Upon cytokine treatment, members of the signal transducers and activators of transcription (STAT) family of proteins are phosphorylated on tyrosine and serine sites within the carboxyl-terminal region in cells. We show that in response to cytokine treatment, Stat3 is also acetylated on a single lysine residue, Lys685. Histone acetyltransferase p300-mediated Stat3 acetylation on Lys685 was reversible by type I histone deacetylase (HDAC). Use of a prostate cancer cell line (PC3) that lacks Stat3 and PC3 cells expressing wild-type Stat3 or a Stat3 mutant containing a Lys685-to-Arg substitution revealed that Lys685 acetylation was critical for Stat3 to form stable dimers required for cytokine-stimulated DNA binding and transcriptional regulation, to enhance transcription of cell growth-related genes, and to promote cell cycle progression in response to treatment with oncostatin M.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yuan, Zheng-Long -- Guan, Ying-Jie -- Chatterjee, Devasis -- Chin, Y Eugene -- New York, N.Y. -- Science. 2005 Jan 14;307(5707):269-73.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Surgery, Brown University Medical School-Rhode Island Hospital, Providence, RI 02903, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15653507" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Acetyltransferases/metabolism ; Arginine/chemistry/metabolism ; Cell Cycle ; Cell Line, Tumor ; Cell Nucleus/metabolism ; Cyclin D1/metabolism ; Cytokines/pharmacology/*physiology ; Cytoplasm/metabolism ; DNA/metabolism ; DNA-Binding Proteins/chemistry/genetics/*metabolism ; Dimerization ; HeLa Cells ; Histone Acetyltransferases ; Histone Deacetylases/metabolism ; Humans ; Interferon-alpha/pharmacology ; Lysine/*metabolism ; Mutation ; Nuclear Proteins/metabolism ; Oncostatin M ; Peptides/pharmacology ; Phosphorylation ; Protein Structure, Secondary ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Proto-Oncogene Proteins c-myc/metabolism ; Recombinant Fusion Proteins/chemistry/metabolism ; STAT3 Transcription Factor ; *Signal Transduction ; Trans-Activators/chemistry/genetics/*metabolism ; Transcriptional Activation ; bcl-X Protein ; src Homology Domains
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