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  • Mice  (51)
  • ASTROPHYSICS
  • Analytical Chemistry and Spectroscopy
  • Life and Medical Sciences
  • Polymer and Materials Science
  • 2000-2004  (51)
  • 2003  (51)
  • 1
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    Human chromosome 7: DNA sequence and biology (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-04-12
    Description: DNA sequence and annotation of the entire human chromosome 7, encompassing nearly 158 million nucleotides of DNA and 1917 gene structures, are presented. To generate a higher order description, additional structural features such as imprinted genes, fragile sites, and segmental duplications were integrated at the level of the DNA sequence with medical genetic data, including 440 chromosome rearrangement breakpoints associated with disease. This approach enabled the discovery of candidate genes for developmental diseases including autism.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2882961/" 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/PMC2882961/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scherer, Stephen W -- Cheung, Joseph -- MacDonald, Jeffrey R -- Osborne, Lucy R -- Nakabayashi, Kazuhiko -- Herbrick, Jo-Anne -- Carson, Andrew R -- Parker-Katiraee, Layla -- Skaug, Jennifer -- Khaja, Razi -- Zhang, Junjun -- Hudek, Alexander K -- Li, Martin -- Haddad, May -- Duggan, Gavin E -- Fernandez, Bridget A -- Kanematsu, Emiko -- Gentles, Simone -- Christopoulos, Constantine C -- Choufani, Sanaa -- Kwasnicka, Dorota -- Zheng, Xiangqun H -- Lai, Zhongwu -- Nusskern, Deborah -- Zhang, Qing -- Gu, Zhiping -- Lu, Fu -- Zeesman, Susan -- Nowaczyk, Malgorzata J -- Teshima, Ikuko -- Chitayat, David -- Shuman, Cheryl -- Weksberg, Rosanna -- Zackai, Elaine H -- Grebe, Theresa A -- Cox, Sarah R -- Kirkpatrick, Susan J -- Rahman, Nazneen -- Friedman, Jan M -- Heng, Henry H Q -- Pelicci, Pier Giuseppe -- Lo-Coco, Francesco -- Belloni, Elena -- Shaffer, Lisa G -- Pober, Barbara -- Morton, Cynthia C -- Gusella, James F -- Bruns, Gail A P -- Korf, Bruce R -- Quade, Bradley J -- Ligon, Azra H -- Ferguson, Heather -- Higgins, Anne W -- Leach, Natalia T -- Herrick, Steven R -- Lemyre, Emmanuelle -- Farra, Chantal G -- Kim, Hyung-Goo -- Summers, Anne M -- Gripp, Karen W -- Roberts, Wendy -- Szatmari, Peter -- Winsor, Elizabeth J T -- Grzeschik, Karl-Heinz -- Teebi, Ahmed -- Minassian, Berge A -- Kere, Juha -- Armengol, Lluis -- Pujana, Miguel Angel -- Estivill, Xavier -- Wilson, Michael D -- Koop, Ben F -- Tosi, Sabrina -- Moore, Gudrun E -- Boright, Andrew P -- Zlotorynski, Eitan -- Kerem, Batsheva -- Kroisel, Peter M -- Petek, Erwin -- Oscier, David G -- Mould, Sarah J -- Dohner, Hartmut -- Dohner, Konstanze -- Rommens, Johanna M -- Vincent, John B -- Venter, J Craig -- Li, Peter W -- Mural, Richard J -- Adams, Mark D -- Tsui, Lap-Chee -- 38103/Canadian Institutes of Health Research/Canada -- P01 GM061354/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2003 May 2;300(5620):767-72. Epub 2003 Apr 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics and Genomic Biology, The Hospital for Sick Children, Toronto, Ontario, Canada, M5G 1X8. steve@genet.sickkids.on.ca〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12690205" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autistic Disorder/genetics ; Chromosome Aberrations ; Chromosome Fragile Sites ; Chromosome Fragility ; Chromosome Mapping ; Chromosomes, Human, Pair 7/*genetics ; Computational Biology ; Congenital Abnormalities/genetics ; CpG Islands ; DNA, Complementary ; Databases, Genetic ; Euchromatin/genetics ; Expressed Sequence Tags ; Gene Duplication ; Genes, Overlapping ; Genetic Diseases, Inborn/genetics ; Genomic Imprinting ; Humans ; In Situ Hybridization, Fluorescence ; Limb Deformities, Congenital/genetics ; Mice ; Molecular Sequence Data ; Mutation ; Neoplasms/genetics ; Pseudogenes ; RNA/genetics ; Retroelements ; *Sequence Analysis, DNA ; Williams Syndrome/genetics
    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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    Allosteric activators of glucokinase: potential role in diabetes therapy (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-07-19
    Description: Glucokinase (GK) plays a key role in whole-body glucose homeostasis by catalyzing the phosphorylation of glucose in cells that express this enzyme, such as pancreatic beta cells and hepatocytes. We describe a class of antidiabetic agents that act as nonessential, mixed-type GK activators (GKAs) that increase the glucose affinity and maximum velocity (Vmax) of GK. GKAs augment both hepatic glucose metabolism and glucose-induced insulin secretion from isolated rodent pancreatic islets, consistent with the expression and function of GK in both cell types. In several rodent models of type 2 diabetes mellitus, GKAs lowered blood glucose levels, improved the results of glucose tolerance tests, and increased hepatic glucose uptake. These findings may lead to the development of new drug therapies for diabetes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grimsby, Joseph -- Sarabu, Ramakanth -- Corbett, Wendy L -- Haynes, Nancy-Ellen -- Bizzarro, Fred T -- Coffey, John W -- Guertin, Kevin R -- Hilliard, Darryl W -- Kester, Robert F -- Mahaney, Paige E -- Marcus, Linda -- Qi, Lida -- Spence, Cheryl L -- Tengi, John -- Magnuson, Mark A -- Chu, Chang An -- Dvorozniak, Mark T -- Matschinsky, Franz M -- Grippo, Joseph F -- New York, N.Y. -- Science. 2003 Jul 18;301(5631):370-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Metabolic Diseases, Hoffmann-La Roche Inc., Nutley, NJ 07110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12869762" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Allosteric Regulation ; Animals ; Blood Glucose/metabolism ; *Carrier Proteins ; Diabetes Mellitus, Type 2/*drug therapy/metabolism ; Dose-Response Relationship, Drug ; Drug Evaluation, Preclinical ; Enzyme Activation ; Enzyme Activators/chemistry/pharmacology ; Glucokinase/*metabolism ; Glucose/*metabolism ; Glucose Tolerance Test ; Homeostasis ; Humans ; Hypoglycemic Agents/chemistry/pharmacology ; Insulin/blood/*secretion ; Islets of Langerhans/*drug effects/secretion ; Keto Acids/metabolism ; Liver/*drug effects/metabolism ; Liver Glycogen/biosynthesis ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Obese ; Proteins/metabolism/pharmacology ; Rats ; Rats, Wistar ; Recombinant Proteins/metabolism ; Stereoisomerism ; Thiazoles/chemistry/*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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  • 3
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    Prevention of organ allograft rejection by a specific Janus kinase 3 inhibitor (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-11-01
    Description: Because of its requirement for signaling by multiple cytokines, Janus kinase 3 (JAK3) is an excellent target for clinical immunosuppression. We report the development of a specific, orally active inhibitor of JAK3, CP-690,550, that significantly prolonged survival in a murine model of heart transplantation and in cynomolgus monkeys receiving kidney transplants. CP-690,550 treatment was not associated with hypertension, hyperlipidemia, or lymphoproliferative disease. On the basis of these preclinical results, we believe JAK3 blockade by CP-690,550 has potential for therapeutically desirable immunosuppression in human organ transplantation and in other clinical settings.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Changelian, Paul S -- Flanagan, Mark E -- Ball, Douglas J -- Kent, Craig R -- Magnuson, Kelly S -- Martin, William H -- Rizzuti, Bonnie J -- Sawyer, Perry S -- Perry, Bret D -- Brissette, William H -- McCurdy, Sandra P -- Kudlacz, Elizabeth M -- Conklyn, Maryrose J -- Elliott, Eileen A -- Koslov, Erika R -- Fisher, Michael B -- Strelevitz, Timothy J -- Yoon, Kwansik -- Whipple, David A -- Sun, Jianmin -- Munchhof, Michael J -- Doty, John L -- Casavant, Jeffrey M -- Blumenkopf, Todd A -- Hines, Michael -- Brown, Matthew F -- Lillie, Brett M -- Subramanyam, Chakrapani -- Shang-Poa, Chang -- Milici, Anthony J -- Beckius, Gretchen E -- Moyer, James D -- Su, Chunyan -- Woodworth, Thasia G -- Gaweco, Anderson S -- Beals, Chan R -- Littman, Bruce H -- Fisher, Douglas A -- Smith, James F -- Zagouras, Panayiotis -- Magna, Holly A -- Saltarelli, Mary J -- Johnson, Kimberly S -- Nelms, Linda F -- Des Etages, Shelley G -- Hayes, Lisa S -- Kawabata, Thomas T -- Finco-Kent, Deborah -- Baker, Deanna L -- Larson, Michael -- Si, Ming-Sing -- Paniagua, Ricardo -- Higgins, John -- Holm, Bari -- Reitz, Bruce -- Zhou, Yong-Jie -- Morris, Randall E -- O'Shea, John J -- Borie, Dominic C -- New York, N.Y. -- Science. 2003 Oct 31;302(5646):875-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunology Group, Department of Antibacterials and Immunology, Pfizer Global Researchand Development, Groton, CT 06340, USA. paul_s_changelian@groton.pfizer.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14593182" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Enzyme Inhibitors/administration & dosage/pharmacology/therapeutic use/toxicity ; Gene Expression Regulation/drug effects ; Graft Rejection/*prevention & control ; Graft Survival/drug effects ; *Heart Transplantation ; Humans ; Immunosuppressive Agents/administration & dosage/*pharmacology/therapeutic ; use/toxicity ; Interleukin-2/immunology ; Janus Kinase 3 ; *Kidney Transplantation ; Lymphocyte Activation/drug effects ; Lymphocyte Count ; Lymphocyte Culture Test, Mixed ; Lymphocyte Subsets/drug effects ; Macaca fascicularis ; Mice ; Mice, Inbred C57BL ; Mice, Inbred DBA ; Myocardium/metabolism ; Piperidines ; Protein-Tyrosine Kinases/*antagonists & inhibitors/metabolism ; Pyrimidines/administration & dosage/*pharmacology/therapeutic use/toxicity ; Pyrroles/administration & dosage/*pharmacology/therapeutic use/toxicity ; Transplantation, Heterotopic ; Transplantation, Homologous ; Tumor Cells, Cultured
    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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    Abnormal coronary function in mice deficient in alpha1H T-type Ca2+ channels (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-11-25
    Description: Calcium ion (Ca2+) influx through voltage-gated Ca2+ channels is important for the regulation of vascular tone. Activation of L-type Ca2+ channels initiates muscle contraction; however, the role of T-type Ca2+ channels (T-channels) is not clear. We show that mice deficient in the alpha1H T-type Ca2+ channel (alpha(1)3.2-null) have constitutively constricted coronary arterioles and focal myocardial fibrosis. Coronary arteries isolated from alpha(1)3.2-null arteries showed normal contractile responses, but reduced relaxation in response to acetylcholine and nitroprusside. Furthermore, acute blockade of T-channels with Ni2+ prevented relaxation of wild-type coronary arteries. Thus, Ca2+ influx through alpha1H T-type Ca2+ channels is essential for normal relaxation of coronary arteries.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Chien-Chang -- Lamping, Kathryn G -- Nuno, Daniel W -- Barresi, Rita -- Prouty, Sally J -- Lavoie, Julie L -- Cribbs, Leanne L -- England, Sarah K -- Sigmund, Curt D -- Weiss, Robert M -- Williamson, Roger A -- Hill, Joseph A -- Campbell, Kevin P -- New York, N.Y. -- Science. 2003 Nov 21;302(5649):1416-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of Iowa, Iowa City, IA 52242, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14631046" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholine/pharmacology ; Animals ; Arteries/drug effects/*physiology ; Calcium/*metabolism ; Calcium Channels, T-Type/genetics/*physiology ; Coronary Vessels/drug effects/pathology/*physiology ; Echocardiography ; Electrocardiography ; Endothelium, Vascular/drug effects/physiology ; Female ; Fibrosis ; Ganglia, Spinal/cytology ; Gene Targeting ; Heart/physiology ; Heart Rate ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Muscle, Smooth, Vascular/physiology ; Myocardium/pathology ; Neurons/metabolism ; Nickel/pharmacology ; Nitric Oxide/physiology ; Nitric Oxide Donors/pharmacology ; Nitroprusside/pharmacology ; Patch-Clamp Techniques ; Vasoconstriction/drug effects ; *Vasodilation/drug effects
    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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    Critical roles for Rac1 and Rac2 GTPases in B cell development and signaling (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-10-18
    Description: The Rac1 guanosine triphosphatase (GTPase) has been implicated in multiple cellular functions, including actin dynamics, proliferation, apoptosis, adhesion, and migration resulting from signaling by multiple receptors, including the B cell antigen receptor (BCR). We used conditional gene targeting to generate mice with specific Rac1 deficiency in the B cell lineage. In the absence of both Rac1 and the highly related Rac2, B cell development was almost completely blocked. Both GTPases were required to transduce BCR signals leading to proliferation, survival and up-regulation of BAFF-R, a receptor for BAFF, a key survival molecule required for B cell development and maintenance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Walmsley, Marita J -- Ooi, Steen K T -- Reynolds, Lucinda F -- Smith, Susan Harless -- Ruf, Sandra -- Mathiot, Anne -- Vanes, Lesley -- Williams, David A -- Cancro, Michael P -- Tybulewicz, Victor L J -- R01 AI042990/AI/NIAID NIH HHS/ -- R01 AI054488/AI/NIAID NIH HHS/ -- R01 DK62757/DK/NIDDK NIH HHS/ -- T32 CA009140/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2003 Oct 17;302(5644):459-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Immune Cell Biology, National Institute for Medical Research, The Ridgeway, Mill Hill, London, NW7 1AA, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14564011" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Cell Activating Factor ; B-Cell Activation Factor Receptor ; B-Lymphocyte Subsets/physiology ; B-Lymphocytes/*physiology ; Cell Differentiation ; Cell Division ; Cell Lineage ; Cell Survival ; Female ; Gene Targeting ; Lymphocyte Activation ; Male ; Membrane Proteins/metabolism ; Mice ; Mice, Inbred C57BL ; Receptors, Antigen, B-Cell/*metabolism ; Receptors, Tumor Necrosis Factor/genetics/metabolism ; Recombination, Genetic ; *Signal Transduction ; Spleen/cytology ; Tumor Necrosis Factor-alpha/metabolism ; Up-Regulation ; rac GTP-Binding Proteins/*physiology ; rac1 GTP-Binding Protein/*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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  • 6
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    Design and chemical synthesis of a homogeneous polymer-modified erythropoiesis protein (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-02-08
    Description: We report the design and total chemical synthesis of "synthetic erythropoiesis protein" (SEP), a 51-kilodalton protein-polymer construct consisting of a 166-amino-acid polypeptide chain and two covalently attached, branched, and monodisperse polymer moieties that are negatively charged. The ability to control the chemistry allowed us to synthesize a macromolecule of precisely defined covalent structure. SEP was homogeneous as shown by high-resolution analytical techniques, with a mass of 50,825 +/-10 daltons by electrospray mass spectrometry, and with a pI of 5.0. In cell and animal assays for erythropoiesis, SEP displayed potent biological activity and had significantly prolonged duration of action in vivo. These chemical methods are a powerful tool in the rational design of protein constructs with potential therapeutic applications.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kochendoerfer, Gerd G -- Chen, Shiah-Yun -- Mao, Feng -- Cressman, Sonya -- Traviglia, Stacey -- Shao, Haiyan -- Hunter, Christie L -- Low, Donald W -- Cagle, E Neil -- Carnevali, Maia -- Gueriguian, Vincent -- Keogh, Peter J -- Porter, Heather -- Stratton, Stephen M -- Wiedeke, M Con -- Wilken, Jill -- Tang, Jie -- Levy, Jay J -- Miranda, Les P -- Crnogorac, Milan M -- Kalbag, Suresh -- Botti, Paolo -- Schindler-Horvat, Janice -- Savatski, Laura -- Adamson, John W -- Kung, Ada -- Kent, Stephen B H -- Bradburne, James A -- New York, N.Y. -- Science. 2003 Feb 7;299(5608):884-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gryphon Therapeutics, 250 East Grand Avenue, Suite 90, South San Francisco, CA 94080, USA. Gkochendoerfer@gryphonRX.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12574628" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Line ; Circular Dichroism ; *Drug Design ; Drug Stability ; Electrophoresis, Polyacrylamide Gel ; *Erythropoiesis ; Erythropoietin/chemistry/pharmacology ; Hematocrit ; Humans ; Isoelectric Point ; Mice ; Molecular Sequence Data ; Molecular Structure ; Molecular Weight ; *Polymers/*chemical synthesis/*chemistry/pharmacokinetics/pharmacology ; Protein Folding ; Proteins/*chemical synthesis/*chemistry/pharmacokinetics/pharmacology ; Rats ; Receptors, Erythropoietin/drug effects/metabolism ; Recombinant Proteins ; Spectrometry, Mass, Electrospray Ionization
    Print ISSN: 0036-8075
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  • 7
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    Epidermal viral immunity induced by CD8alpha+ dendritic cells but not by Langerhans cells (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-09-27
    Description: The classical paradigm for dendritic cell function derives from the study of Langerhans cells, which predominate within skin epidermis. After an encounter with foreign agents, Langerhans cells are thought to migrate to draining lymph nodes, where they initiate T cell priming. Contrary to this, we show here that infection of murine epidermis by herpes simplex virus did not result in the priming of virus-specific cytotoxic T lymphocytes by Langerhans cells. Rather, the priming response required a distinct CD8alpha+ dendritic cell subset. Thus, the traditional view of Langerhans cells in epidermal immunity needs to be revisited to accommodate a requirement for other dendritic cells in this response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Allan, Rhys S -- Smith, Chris M -- Belz, Gabrielle T -- van Lint, Allison L -- Wakim, Linda M -- Heath, William R -- Carbone, Francis R -- New York, N.Y. -- Science. 2003 Sep 26;301(5641):1925-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, The University of Melbourne, Melbourne, Victoria 3010, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14512632" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen Presentation ; Antigens, CD/analysis ; Antigens, CD8/*analysis ; Antigens, Viral/immunology ; Cell Separation ; Chimera ; Cytotoxicity, Immunologic ; Dendritic Cells/*immunology ; Epidermis/*immunology ; H-2 Antigens/analysis/immunology ; Herpes Simplex/*immunology ; Herpesvirus 1, Human/*immunology ; Histocompatibility Antigens Class II/analysis ; Langerhans Cells/*immunology ; Lectins, C-Type/analysis ; Lymph Nodes/immunology ; Lymphocyte Activation ; Mice ; Mice, Inbred C57BL ; Mice, Inbred Strains ; Mice, Transgenic ; Receptors, Cell Surface/analysis ; T-Lymphocytes, Cytotoxic/*immunology ; Viral Envelope Proteins/immunology
    Print ISSN: 0036-8075
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  • 8
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    Dishevelled 2 recruits beta-arrestin 2 to mediate Wnt5A-stimulated endocytosis of Frizzled 4 (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-09-06
    Description: Wnt proteins, regulators of development in many organisms, bind to seven transmembrane-spanning (7TMS) receptors called frizzleds, thereby recruiting the cytoplasmic molecule dishevelled (Dvl) to the plasma membrane.Frizzled-mediated endocytosis of Wg (a Drosophila Wnt protein) and lysosomal degradation may regulate the formation of morphogen gradients. Endocytosis of Frizzled 4 (Fz4) in human embryonic kidney 293 cells was dependent on added Wnt5A protein and was accomplished by the multifunctional adaptor protein beta-arrestin 2 (betaarr2), which was recruited to Fz4 by binding to phosphorylated Dvl2. These findings provide a previously unrecognized mechanism for receptor recruitment of beta-arrestin and demonstrate that Dvl plays an important role in the endocytosis of frizzled, as well as in promoting signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Wei -- ten Berge, Derk -- Brown, Jeff -- Ahn, Seungkirl -- Hu, Liaoyuan A -- Miller, William E -- Caron, Marc G -- Barak, Larry S -- Nusse, Roel -- Lefkowitz, Robert J -- HL 16037/HL/NHLBI NIH HHS/ -- HL 61365/HL/NHLBI NIH HHS/ -- NS 19576/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2003 Sep 5;301(5638):1391-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Departments of Medicine and Biochemistry, Duke University Medical Center, Durham, NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12958364" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Animals ; Arrestins/genetics/*metabolism ; Cell Line ; Cell Membrane/metabolism ; Clathrin/metabolism ; Cytoplasm/metabolism ; *Endocytosis ; Frizzled Receptors ; Humans ; Mice ; Phosphoproteins/metabolism ; Phosphorylation ; Protein Kinase C/antagonists & inhibitors/metabolism ; Proteins/genetics/*metabolism ; Proto-Oncogene Proteins/*metabolism/pharmacology ; RNA, Small Interfering ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Wnt Proteins
    Print ISSN: 0036-8075
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  • 9
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    Nuclear membrane proteins with potential disease links found by subtractive proteomics (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-09-06
    Description: To comprehensively identify integral membrane proteins of the nuclear envelope (NE), we prepared separately NEs and organelles known to cofractionate with them from liver. Proteins detected by multidimensional protein identification technology in the cofractionating organelles were subtracted from the NE data set. In addition to all 13 known NE integral proteins, 67 uncharacterized open reading frames with predicted membrane-spanning regions were identified. All of the eight proteins tested targeted to the NE, indicating that there are substantially more integral proteins of the NE than previously thought. Furthermore, 23 of these mapped within chromosome regions linked to a variety of dystrophies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schirmer, Eric C -- Florens, Laurence -- Guan, Tinglu -- Yates, John R 3rd -- Gerace, Larry -- F32 GM19085/GM/NIGMS NIH HHS/ -- GM28521/GM/NIGMS NIH HHS/ -- RR11823/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2003 Sep 5;301(5638):1380-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Scripps Research Institute, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12958361" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Animals ; Cell Fractionation ; Chromosome Mapping ; DNA, Complementary ; Genetic Diseases, Inborn/*genetics ; Genetic Linkage ; Humans ; Liver/chemistry/ultrastructure ; Membrane Proteins/*analysis/genetics/isolation & purification ; Mice ; Mice, Inbred Strains ; Nuclear Envelope/*chemistry ; Nuclear Proteins/*analysis/genetics/isolation & purification ; Open Reading Frames ; Protein Structure, Tertiary ; *Proteomics ; Rats ; Rats, Sprague-Dawley
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  • 10
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    Control of effector CD8+ T cell function by the transcription factor Eomesodermin (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-11-08
    Description: Activated CD8+ T cells play a critical role in host defense against viruses, intracellular microbes, and tumors. It is not clear if a key regulatory transcription factor unites the effector functions of CD8+ T cells. We now show that Eomesodermin (Eomes), a paralogue of T-bet, is induced in effector CD8+ T cells in vitro and in vivo. Ectopic expression of Eomes was sufficient to invoke attributes of effector CD8+ T cells, including interferon-gamma (IFN-gamma), perforin, and granzyme B. Loss-of-function analysis suggests Eomes may also be necessary for full effector differentiation of CD8+ T cells. We suggest that Eomesodermin is likely to complement the actions of T-bet and act as a key regulatory gene in the development of cell-mediated immunity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pearce, Erika L -- Mullen, Alan C -- Martins, Gislaine A -- Krawczyk, Connie M -- Hutchins, Anne S -- Zediak, Valerie P -- Banica, Monica -- DiCioccio, Catherine B -- Gross, Darrick A -- Mao, Chai-An -- Shen, Hao -- Cereb, Nezih -- Yang, Soo Y -- Lindsten, Tullia -- Rossant, Janet -- Hunter, Christopher A -- Reiner, Steven L -- AI-042370/AI/NIAID NIH HHS/ -- GM-07229/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2003 Nov 7;302(5647):1041-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Abramson Family Cancer Research Institute, and Department of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14605368" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Arenaviridae Infections/immunology ; Base Sequence ; CD8-Positive T-Lymphocytes/*immunology/physiology ; Cell Differentiation ; Cytotoxicity, Immunologic ; Gene Expression Regulation ; Granzymes ; Interferon-gamma/biosynthesis ; Lymphocyte Activation ; Lymphocytic choriomeningitis virus/immunology ; Membrane Glycoproteins/biosynthesis/genetics ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Molecular Sequence Data ; Perforin ; Pore Forming Cytotoxic Proteins ; RNA, Messenger/genetics/metabolism ; Serine Endopeptidases/biosynthesis/genetics ; T-Box Domain Proteins/chemistry/genetics/*physiology ; Th2 Cells/immunology/physiology ; Transcription Factors/chemistry/genetics/physiology
    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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