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  • Mice  (7)
  • American Association for the Advancement of Science (AAAS)  (7)
  • Elsevier
  • 2005-2009  (7)
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Year
  • 1
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    Structural insight into pre-B cell receptor function (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-04-14
    Description: The pre-B cell receptor (pre-BCR) serves as a checkpoint in B cell development. In the 2.7 angstrom structure of a human pre-BCR Fab-like fragment, consisting of an antibody heavy chain (HC) paired with the surrogate light chain, the "unique regions" of VpreB and lambda5 replace the complementarity-determining region 3 (CDR3) loop of an antibody light chain and appear to "probe" the HC CDR3, potentially influencing the selection of the antibody repertoire. Biochemical analysis indicates that the pre-BCR is impaired in its ability to recognize antigen, which, together with electron microscopic visualization of a pre-BCR dimer, suggests ligand-independent oligomerization as the likely signaling mechanism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bankovich, Alexander J -- Raunser, Stefan -- Juo, Z Sean -- Walz, Thomas -- Davis, Mark M -- Garcia, K Christopher -- T32 AI007290/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2007 Apr 13;316(5822):291-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17431183" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Complementarity Determining Regions/chemistry/physiology ; Crystallography, X-Ray ; Humans ; Immunoglobulin Heavy Chains/chemistry/physiology ; Immunoglobulin Light Chains/chemistry/physiology ; Immunoglobulin Light Chains, Surrogate ; Membrane Glycoproteins/*chemistry/physiology/ultrastructure ; Mice ; Models, Molecular ; Pre-B Cell Receptors ; Protein Conformation ; Receptors, Antigen, B-Cell/*chemistry/physiology/ultrastructure ; Recombinant Proteins ; Structure-Activity Relationship
    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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  • 2
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    A stress signaling pathway in adipose tissue regulates hepatic insulin resistance (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-12-06
    Description: A high-fat diet causes activation of the regulatory protein c-Jun NH2-terminal kinase 1 (JNK1) and triggers development of insulin resistance. JNK1 is therefore a potential target for therapeutic treatment of metabolic syndrome. We explored the mechanism of JNK1 signaling by engineering mice in which the Jnk1 gene was ablated selectively in adipose tissue. JNK1 deficiency in adipose tissue suppressed high-fat diet-induced insulin resistance in the liver. JNK1-dependent secretion of the inflammatory cytokine interleukin-6 by adipose tissue caused increased expression of liver SOCS3, a protein that induces hepatic insulin resistance. Thus, JNK1 activation in adipose tissue can cause insulin resistance in the liver.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2643026/" 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/PMC2643026/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sabio, Guadalupe -- Das, Madhumita -- Mora, Alfonso -- Zhang, Zhiyou -- Jun, John Y -- Ko, Hwi Jin -- Barrett, Tamera -- Kim, Jason K -- Davis, Roger J -- DK52530/DK/NIDDK NIH HHS/ -- R01 CA065861/CA/NCI NIH HHS/ -- R01 CA065861-14/CA/NCI NIH HHS/ -- R01 DK080756/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Dec 5;322(5907):1539-43. doi: 10.1126/science.1160794.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, 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/19056984" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes/enzymology/*metabolism ; Adipose Tissue/enzymology/metabolism ; Animals ; Dietary Fats/administration & dosage ; Enzyme Activation ; Glucose/metabolism ; Insulin/metabolism ; Insulin Receptor Substrate Proteins/metabolism ; *Insulin Resistance ; Interleukin-6/administration & dosage/metabolism ; Liver/*metabolism ; MAP Kinase Signaling System ; Mice ; Mitogen-Activated Protein Kinase 8/deficiency/genetics/*metabolism ; Phosphorylation ; Proto-Oncogene Proteins c-akt/metabolism ; *Signal Transduction ; *Stress, Physiological ; Suppressor of Cytokine Signaling Proteins/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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    Mutations in the FUS/TLS gene on chromosome 16 cause familial amyotrophic lateral sclerosis (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-03-03
    Description: Amyotrophic lateral sclerosis (ALS) is a fatal degenerative motor neuron disorder. Ten percent of cases are inherited; most involve unidentified genes. We report here 13 mutations in the fused in sarcoma/translated in liposarcoma (FUS/TLS) gene on chromosome 16 that were specific for familial ALS. The FUS/TLS protein binds to RNA, functions in diverse processes, and is normally located predominantly in the nucleus. In contrast, the mutant forms of FUS/TLS accumulated in the cytoplasm of neurons, a pathology that is similar to that of the gene TAR DNA-binding protein 43 (TDP43), whose mutations also cause ALS. Neuronal cytoplasmic protein aggregation and defective RNA metabolism thus appear to be common pathogenic mechanisms involved in ALS and possibly in other neurodegenerative disorders.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kwiatkowski, T J Jr -- Bosco, D A -- Leclerc, A L -- Tamrazian, E -- Vanderburg, C R -- Russ, C -- Davis, A -- Gilchrist, J -- Kasarskis, E J -- Munsat, T -- Valdmanis, P -- Rouleau, G A -- Hosler, B A -- Cortelli, P -- de Jong, P J -- Yoshinaga, Y -- Haines, J L -- Pericak-Vance, M A -- Yan, J -- Ticozzi, N -- Siddique, T -- McKenna-Yasek, D -- Sapp, P C -- Horvitz, H R -- Landers, J E -- Brown, R H Jr -- New York, N.Y. -- Science. 2009 Feb 27;323(5918):1205-8. doi: 10.1126/science.1166066.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Massachusetts General Hospital, 114 16th Street, Charlestown, MA 02129, USA. tkwiatkowski@partners.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19251627" target="_blank"〉PubMed〈/a〉
    Keywords: Age of Onset ; Amino Acid Substitution ; Amyotrophic Lateral Sclerosis/*genetics/metabolism/pathology ; Animals ; Brain/pathology ; Cell Line, Tumor ; Cell Nucleus/metabolism ; Chromosomes, Human, Pair 16/*genetics ; Cytoplasm/metabolism ; DNA-Binding Proteins/genetics/metabolism ; Exons ; Female ; Humans ; Male ; Mice ; Motor Neurons/chemistry/metabolism/ultrastructure ; Mutant Proteins/chemistry/genetics/metabolism ; *Mutation, Missense ; Neurons/metabolism/ultrastructure ; RNA/metabolism ; RNA-Binding Protein FUS/chemistry/*genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Sequence Analysis, DNA ; Spinal Cord/pathology
    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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    Sequence variants in SLITRK1 are associated with Tourette's syndrome (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-10-15
    Description: Tourette's syndrome (TS) is a genetically influenced developmental neuropsychiatric disorder characterized by chronic vocal and motor tics. We studied Slit and Trk-like 1 (SLITRK1) as a candidate gene on chromosome 13q31.1 because of its proximity to a de novo chromosomal inversion in a child with TS. Among 174 unrelated probands, we identified a frameshift mutation and two independent occurrences of the identical variant in the binding site for microRNA hsa-miR-189. These variants were absent from 3600 control chromosomes. SLITRK1 mRNA and hsa-miR-189 showed an overlapping expression pattern in brain regions previously implicated in TS. Wild-type SLITRK1, but not the frameshift mutant, enhanced dendritic growth in primary neuronal cultures. Collectively, these findings support the association of rare SLITRK1 sequence variants with TS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Abelson, Jesse F -- Kwan, Kenneth Y -- O'Roak, Brian J -- Baek, Danielle Y -- Stillman, Althea A -- Morgan, Thomas M -- Mathews, Carol A -- Pauls, David L -- Rasin, Mladen-Roko -- Gunel, Murat -- Davis, Nicole R -- Ercan-Sencicek, A Gulhan -- Guez, Danielle H -- Spertus, John A -- Leckman, James F -- Dure, Leon S 4th -- Kurlan, Roger -- Singer, Harvey S -- Gilbert, Donald L -- Farhi, Anita -- Louvi, Angeliki -- Lifton, Richard P -- Sestan, Nenad -- State, Matthew W -- K23 RR16118/RR/NCRR NIH HHS/ -- R01 NS054273/NS/NINDS NIH HHS/ -- R01 NS43520/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2005 Oct 14;310(5746):317-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Child Study Center, 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/16224024" target="_blank"〉PubMed〈/a〉
    Keywords: 3' Untranslated Regions ; Adolescent ; Animals ; Attention Deficit Disorder with Hyperactivity/complications/genetics ; Brain/metabolism ; Child ; Child, Preschool ; Chromosome Inversion ; Chromosome Mapping ; *Chromosomes, Human, Pair 13 ; Dna ; DNA Mutational Analysis ; Female ; Frameshift Mutation ; Humans ; In Situ Hybridization, Fluorescence ; Male ; Membrane Proteins/*genetics ; Mice ; *Mutation ; Nerve Tissue Proteins/*genetics ; Pedigree ; Sequence Analysis, DNA ; Tourette Syndrome/complications/*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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  • 5
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    Human IRGM induces autophagy to eliminate intracellular mycobacteria (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-08-05
    Description: Immunity-related p47 guanosine triphosphatases (IRG) play a role in defense against intracellular pathogens. We found that the murine Irgm1 (LRG-47) guanosine triphosphatase induced autophagy and generated large autolysosomal organelles as a mechanism for the elimination of intracellular Mycobacterium tuberculosis. We also identified a function for a human IRG protein in the control of intracellular pathogens and report that the human Irgm1 ortholog, IRGM, plays a role in autophagy and in the reduction of intracellular bacillary load.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Singh, Sudha B -- Davis, Alexander S -- Taylor, Gregory A -- Deretic, Vojo -- AI42999/AI/NIAID NIH HHS/ -- AI45148/AI/NIAID NIH HHS/ -- AI57831/AI/NIAID NIH HHS/ -- R01 AI057831/AI/NIAID NIH HHS/ -- T32 AI007538/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2006 Sep 8;313(5792):1438-41. Epub 2006 Aug 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics and Microbiology, University of New Mexico School of Medicine, Albuquerque, NM 87131, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16888103" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Autophagy ; Cell Line ; Cytosol/metabolism ; GTP-Binding Proteins/genetics/*physiology ; HeLa Cells ; Humans ; Interferon-gamma/immunology ; Lysosomes/metabolism/microbiology/ultrastructure ; Macrophages/*immunology/*microbiology ; Mice ; Microbial Viability ; Microtubule-Associated Proteins/metabolism ; Mycobacterium bovis/*immunology/physiology ; Phagosomes/metabolism/microbiology/*ultrastructure ; RNA, Small Interfering ; Transfection ; Vacuoles/metabolism/ultrastructure
    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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    Phosphorylation by p38 MAPK as an alternative pathway for GSK3beta inactivation (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-05-03
    Description: Glycogen synthase kinase 3beta (GSK3beta) is involved in metabolism, neurodegeneration, and cancer. Inhibition of GSK3beta activity is the primary mechanism that regulates this widely expressed active kinase. Although the protein kinase Akt inhibits GSK3beta by phosphorylation at the N terminus, preventing Akt-mediated phosphorylation does not affect the cell-survival pathway activated through the GSK3beta substrate beta-catenin. Here, we show that p38 mitogen-activated protein kinase (MAPK) also inactivates GSK3beta by direct phosphorylation at its C terminus, and this inactivation can lead to an accumulation of beta-catenin. p38 MAPK-mediated phosphorylation of GSK3beta occurs primarily in the brain and thymocytes. Activation of beta-catenin-mediated signaling through GSK3beta inhibition provides a potential mechanism for p38 MAPK-mediated survival in specific tissues.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2597039/" 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/PMC2597039/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thornton, Tina M -- Pedraza-Alva, Gustavo -- Deng, Bin -- Wood, C David -- Aronshtam, Alexander -- Clements, James L -- Sabio, Guadalupe -- Davis, Roger J -- Matthews, Dwight E -- Doble, Bradley -- Rincon, Mercedes -- P20 RR021905/RR/NCRR NIH HHS/ -- P20 RR15557/RR/NCRR NIH HHS/ -- P20 RR16462/RR/NCRR NIH HHS/ -- R01 AI051454/AI/NIAID NIH HHS/ -- R01 AI051454-01A1/AI/NIAID NIH HHS/ -- R01 AI051454-02/AI/NIAID NIH HHS/ -- R01 AI051454-03/AI/NIAID NIH HHS/ -- R01 AI051454-04/AI/NIAID NIH HHS/ -- R01 AI051454-05/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2008 May 2;320(5876):667-70. doi: 10.1126/science.1156037.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine/Immunobiology Program, University of Vermont, Burlington, VT 05405-0068, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18451303" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/enzymology ; Glycogen Synthase Kinase 3/*antagonists & inhibitors/immunology/metabolism ; Humans ; Mice ; Phosphorylation ; Protein Kinase Inhibitors/*metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Serine/metabolism ; Thymus Gland/cytology/enzymology ; beta Catenin/metabolism ; p38 Mitogen-Activated Protein Kinases/*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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  • 7
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    Apicomplexan parasites co-opt host calpains to facilitate their escape from infected cells (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-04-04
    Description: Apicomplexan parasites, including Plasmodium falciparum and Toxoplasma gondii (the causative agents of malaria and toxoplasmosis, respectively), are responsible for considerable morbidity and mortality worldwide. These pathogenic protozoa replicate within an intracellular vacuole inside of infected host cells, from which they must escape to initiate a new lytic cycle. By integrating cell biological, pharmacological, and genetic approaches, we provide evidence that both Plasmodium and Toxoplasma hijack host cell calpain proteases to facilitate parasite egress. Immunodepletion or inhibition of calpain-1 in hypotonically lysed and resealed erythrocytes prevented the escape of P. falciparum parasites, which was restored by adding purified calpain-1. Similarly, efficient egress of T. gondii from mammalian fibroblasts was blocked by either small interfering RNA-mediated suppression or genetic deletion of calpain activity and could be restored by genetic complementation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3391539/" 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/PMC3391539/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chandramohanadas, Rajesh -- Davis, Paul H -- Beiting, Daniel P -- Harbut, Michael B -- Darling, Claire -- Velmourougane, Geetha -- Lee, Ming Yeh -- Greer, Peter A -- Roos, David S -- Greenbaum, Doron C -- F32 AI075846/AI/NIAID NIH HHS/ -- F32 AI075846-02/AI/NIAID NIH HHS/ -- F32 AI077268/AI/NIAID NIH HHS/ -- F32 AI077268-02/AI/NIAID NIH HHS/ -- R37 AI028724/AI/NIAID NIH HHS/ -- R37 AI028724-17/AI/NIAID NIH HHS/ -- T32 GM008076/GM/NIGMS NIH HHS/ -- T32 GM008076-24/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2009 May 8;324(5928):794-7. doi: 10.1126/science.1171085. Epub 2009 Apr 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of Pennsylvania, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19342550" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calpain/blood/genetics/*metabolism ; Cell Line ; Cell Line, Tumor ; Erythrocytes/*parasitology ; Fibroblasts/parasitology ; Humans ; Leucine/analogs & derivatives/pharmacology ; Life Cycle Stages ; Merozoites/physiology ; Mice ; Mice, Knockout ; Plasmodium falciparum/growth & development/metabolism/*pathogenicity/physiology ; RNA, Small Interfering ; Schizonts/physiology ; Toxoplasma/growth & development/metabolism/*pathogenicity/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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