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  • 1
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    B cell antigen receptor signaling: roles in cell development and disease (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-06-01
    Description: Signals propagated through the B cell antigen receptor (BCR) are vital for the development and survival of B lymphocytes in both the bone marrow and the periphery. These signals not only guide maturation and activation but also affect the removal of potentially self-reactive B lymphocytes. Interestingly, these signals are known to be either ligand-independent ("tonic" signals) or induced by ligand (antigen) binding to the BCR. We focus on the problems that occur in B cell development due to defects in signals emanating from the BCR. In addition, we present the B Cell Antigen Receptor Pathway, an STKE Connections Map that illustrates the events involved in B cell signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gauld, Stephen B -- Dal Porto, Joseph M -- Cambier, John C -- New York, N.Y. -- Science. 2002 May 31;296(5573):1641-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Integrated Department of Immunology, University of Colorado Health Sciences Center, and National Jewish Medical Research Center, 1400 Jackson Street, Denver, CO 80206, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12040177" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD19/metabolism ; Autoimmune Diseases/immunology ; B-Lymphocytes/*immunology/metabolism/physiology ; Humans ; Immunologic Deficiency Syndromes/immunology ; Lymphocyte Activation ; Phosphorylation ; Protein-Tyrosine Kinases/metabolism ; Receptors, Antigen, B-Cell/chemistry/*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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  • 2
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    Hematopoietic stem cell gene therapy with a lentiviral vector in X-linked adrenoleukodystrophy (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-11-07
    Description: X-linked adrenoleukodystrophy (ALD) is a severe brain demyelinating disease in boys that is caused by a deficiency in ALD protein, an adenosine triphosphate-binding cassette transporter encoded by the ABCD1 gene. ALD progression can be halted by allogeneic hematopoietic cell transplantation (HCT). We initiated a gene therapy trial in two ALD patients for whom there were no matched donors. Autologous CD34+ cells were removed from the patients, genetically corrected ex vivo with a lentiviral vector encoding wild-type ABCD1, and then re-infused into the patients after they had received myeloablative treatment. Over a span of 24 to 30 months of follow-up, we detected polyclonal reconstitution, with 9 to 14% of granulocytes, monocytes, and T and B lymphocytes expressing the ALD protein. These results strongly suggest that hematopoietic stem cells were transduced in the patients. Beginning 14 to 16 months after infusion of the genetically corrected cells, progressive cerebral demyelination in the two patients stopped, a clinical outcome comparable to that achieved by allogeneic HCT. Thus, lentiviral-mediated gene therapy of hematopoietic stem cells can provide clinical benefits in ALD.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cartier, Nathalie -- Hacein-Bey-Abina, Salima -- Bartholomae, Cynthia C -- Veres, Gabor -- Schmidt, Manfred -- Kutschera, Ina -- Vidaud, Michel -- Abel, Ulrich -- Dal-Cortivo, Liliane -- Caccavelli, Laure -- Mahlaoui, Nizar -- Kiermer, Veronique -- Mittelstaedt, Denice -- Bellesme, Celine -- Lahlou, Najiba -- Lefrere, Francois -- Blanche, Stephane -- Audit, Muriel -- Payen, Emmanuel -- Leboulch, Philippe -- l'Homme, Bruno -- Bougneres, Pierre -- Von Kalle, Christof -- Fischer, Alain -- Cavazzana-Calvo, Marina -- Aubourg, Patrick -- New York, N.Y. -- Science. 2009 Nov 6;326(5954):818-23. doi: 10.1126/science.1171242.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉INSERM UMR745, University Paris-Descartes, 75279 Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19892975" target="_blank"〉PubMed〈/a〉
    Keywords: ATP-Binding Cassette Transporters/*genetics ; Adrenoleukodystrophy/genetics/pathology/*therapy ; Animals ; Brain/pathology ; Cell Differentiation ; Cell Lineage ; Child ; Disease Progression ; Fatty Acids/blood ; Female ; Gene Expression ; *Genetic Therapy ; *Genetic Vectors ; HIV-1/*genetics ; Hematopoiesis ; *Hematopoietic Stem Cell Transplantation ; Hematopoietic Stem Cells/*physiology/virology ; Humans ; Leukocytes, Mononuclear/metabolism ; Male ; Mice ; Microglia/cytology/metabolism ; Myeloablative Agonists/therapeutic use ; Transduction, Genetic ; Transplantation Conditioning ; Transplantation, Autologous ; Virus Integration
    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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    Ebola virus entry requires the cholesterol transporter Niemann-Pick C1 (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-08-26
    Description: Infections by the Ebola and Marburg filoviruses cause a rapidly fatal haemorrhagic fever in humans for which no approved antivirals are available. Filovirus entry is mediated by the viral spike glycoprotein (GP), which attaches viral particles to the cell surface, delivers them to endosomes and catalyses fusion between viral and endosomal membranes. Additional host factors in the endosomal compartment are probably required for viral membrane fusion; however, despite considerable efforts, these critical host factors have defied molecular identification. Here we describe a genome-wide haploid genetic screen in human cells to identify host factors required for Ebola virus entry. Our screen uncovered 67 mutations disrupting all six members of the homotypic fusion and vacuole protein-sorting (HOPS) multisubunit tethering complex, which is involved in the fusion of endosomes to lysosomes, and 39 independent mutations that disrupt the endo/lysosomal cholesterol transporter protein Niemann-Pick C1 (NPC1). Cells defective for the HOPS complex or NPC1 function, including primary fibroblasts derived from human Niemann-Pick type C1 disease patients, are resistant to infection by Ebola virus and Marburg virus, but remain fully susceptible to a suite of unrelated viruses. We show that membrane fusion mediated by filovirus glycoproteins and viral escape from the vesicular compartment require the NPC1 protein, independent of its known function in cholesterol transport. Our findings uncover unique features of the entry pathway used by filoviruses and indicate potential antiviral strategies to combat these deadly agents.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3175325/" 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/PMC3175325/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carette, Jan E -- Raaben, Matthijs -- Wong, Anthony C -- Herbert, Andrew S -- Obernosterer, Gregor -- Mulherkar, Nirupama -- Kuehne, Ana I -- Kranzusch, Philip J -- Griffin, April M -- Ruthel, Gordon -- Dal Cin, Paola -- Dye, John M -- Whelan, Sean P -- Chandran, Kartik -- Brummelkamp, Thijn R -- AI081842/AI/NIAID NIH HHS/ -- R01 AI081842/AI/NIAID NIH HHS/ -- R01 AI081842-03/AI/NIAID NIH HHS/ -- R01 AI088027/AI/NIAID NIH HHS/ -- R01 AI088027-03/AI/NIAID NIH HHS/ -- R21 HG004938/HG/NHGRI NIH HHS/ -- R21 HG004938-01/HG/NHGRI NIH HHS/ -- T32 AI070117/AI/NIAID NIH HHS/ -- T32 GM007288/GM/NIGMS NIH HHS/ -- U54 AI057159/AI/NIAID NIH HHS/ -- U54 AI057159-09/AI/NIAID NIH HHS/ -- England -- Nature. 2011 Aug 24;477(7364):340-3. doi: 10.1038/nature10348.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Nine Cambridge Center, Cambridge, Massachusetts 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21866103" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Transport ; Carrier Proteins/genetics/*metabolism ; Cell Line ; Cholesterol/*metabolism ; Ebolavirus/*physiology ; Endosomes/metabolism ; Fibroblasts/metabolism/pathology/virology ; Genome, Human/genetics ; Glycoproteins/metabolism ; Haploidy ; Hemorrhagic Fever, Ebola/drug therapy/metabolism ; Host-Pathogen Interactions/genetics ; Humans ; Lysosomes/metabolism ; Marburg Virus Disease/drug therapy/metabolism ; Marburgvirus/physiology ; Membrane Fusion/genetics/physiology ; Membrane Glycoproteins/deficiency/genetics/*metabolism ; Multiprotein Complexes/chemistry/deficiency/genetics/metabolism ; Mutation/genetics ; Niemann-Pick Diseases/pathology/virology ; Receptors, Virus/metabolism ; Viral Fusion Proteins/metabolism ; *Virus Internalization
    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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  • 4
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    Functional screening identifies miRNAs inducing cardiac regeneration (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-12-12
    Description: In mammals, enlargement of the heart during embryonic development is primarily dependent on the increase in cardiomyocyte numbers. Shortly after birth, however, cardiomyocytes stop proliferating and further growth of the myocardium occurs through hypertrophic enlargement of the existing myocytes. As a consequence of the minimal renewal of cardiomyocytes during adult life, repair of cardiac damage through myocardial regeneration is very limited. Here we show that the exogenous administration of selected microRNAs (miRNAs) markedly stimulates cardiomyocyte proliferation and promotes cardiac repair. We performed a high-content microscopy, high-throughput functional screening for human miRNAs that promoted neonatal cardiomyocyte proliferation using a whole-genome miRNA library. Forty miRNAs strongly increased both DNA synthesis and cytokinesis in neonatal mouse and rat cardiomyocytes. Two of these miRNAs (hsa-miR-590 and hsa-miR-199a) were further selected for testing and were shown to promote cell cycle re-entry of adult cardiomyocytes ex vivo and to promote cardiomyocyte proliferation in both neonatal and adult animals. After myocardial infarction in mice, these miRNAs stimulated marked cardiac regeneration and almost complete recovery of cardiac functional parameters. The miRNAs identified hold great promise for the treatment of cardiac pathologies consequent to cardiomyocyte loss.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Eulalio, Ana -- Mano, Miguel -- Dal Ferro, Matteo -- Zentilin, Lorena -- Sinagra, Gianfranco -- Zacchigna, Serena -- Giacca, Mauro -- England -- Nature. 2012 Dec 20;492(7429):376-81. doi: 10.1038/nature11739. Epub 2012 Dec 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Medicine Laboratory, International Centre for Genetic Engineering and Biotechnology, 34149 Trieste, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23222520" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Proliferation ; Cytokinesis ; DNA/biosynthesis ; Down-Regulation ; Gene Library ; Genetic Therapy ; Heart/growth & development ; Humans ; Mice ; MicroRNAs/*analysis/*genetics/therapeutic use ; Myocardial Infarction/genetics/pathology/prevention & control/therapy ; Myocardium/*cytology/metabolism ; Myocytes, Cardiac/cytology/metabolism ; Rats ; Rats, Wistar ; Regeneration/*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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  • 5
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    Motor neuron degeneration in mice that express a human Cu,Zn superoxide dismutase mutation (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-06-17
    Description: Mutations of human Cu,Zn superoxide dismutase (SOD) are found in about 20 percent of patients with familial amyotrophic lateral sclerosis (ALS). Expression of high levels of human SOD containing a substitution of glycine to alanine at position 93--a change that has little effect on enzyme activity--caused motor neuron disease in transgenic mice. The mice became paralyzed in one or more limbs as a result of motor neuron loss from the spinal cord and died by 5 to 6 months of age. The results show that dominant, gain-of-function mutations in SOD contribute to the pathogenesis of familial ALS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gurney, M E -- Pu, H -- Chiu, A Y -- Dal Canto, M C -- Polchow, C Y -- Alexander, D D -- Caliendo, J -- Hentati, A -- Kwon, Y W -- Deng, H X -- New York, N.Y. -- Science. 1994 Jun 17;264(5166):1772-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell and Molecular Biology, Northwestern University Medical School, Chicago, IL 60611.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8209258" target="_blank"〉PubMed〈/a〉
    Keywords: Amyotrophic Lateral Sclerosis/enzymology/*genetics/pathology ; Animals ; Brain/enzymology ; Disease Models, Animal ; Female ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Motor Endplate/pathology ; Motor Neuron Disease/enzymology/*genetics/pathology ; Motor Neurons/enzymology/pathology ; Muscles/innervation/pathology ; Mutation ; Pedigree ; Spinal Cord/pathology ; Superoxide Dismutase/*genetics/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Semiaquatic adaptations in a giant predatory dinosaur (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-09-13
    Description: We describe adaptations for a semiaquatic lifestyle in the dinosaur Spinosaurus aegyptiacus. These adaptations include retraction of the fleshy nostrils to a position near the mid-region of the skull and an elongate neck and trunk that shift the center of body mass anterior to the knee joint. Unlike terrestrial theropods, the pelvic girdle is downsized, the hindlimbs are short, and all of the limb bones are solid without an open medullary cavity, for buoyancy control in water. The short, robust femur with hypertrophied flexor attachment and the low, flat-bottomed pedal claws are consistent with aquatic foot-propelled locomotion. Surface striations and bone microstructure suggest that the dorsal "sail" may have been enveloped in skin that functioned primarily for display on land and in water.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ibrahim, Nizar -- Sereno, Paul C -- Dal Sasso, Cristiano -- Maganuco, Simone -- Fabbri, Matteo -- Martill, David M -- Zouhri, Samir -- Myhrvold, Nathan -- Iurino, Dawid A -- New York, N.Y. -- Science. 2014 Sep 26;345(6204):1613-6. doi: 10.1126/science.1258750. Epub 2014 Sep 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Organismal Biology and Anatomy, University of Chicago, Chicago, IL 60637, USA. nibrahim@uchicago.edu. ; Department of Organismal Biology and Anatomy, University of Chicago, Chicago, IL 60637, USA. ; Museo di Storia Naturale di Milano, Corso Venezia 55, 20121 Milan, Italy. ; School of Earth Sciences, University of Bristol, Queen's Road, Bristol, BS8 1RJ, UK. ; School of Earth and Environmental Sciences, University of Portsmouth, Burnaby Road, Portsmouth, PO1 3QL, UK. ; Laboratoire de Geosciences, Faculte des Sciences Ain Chock, Universite Hassan II, Casablanca, Morocco. ; Intellectual Ventures, 3150 139th Avenue Southeast, Bellevue, WA 98005, USA. ; Dipartimento di Scienze della Terra, Sapienza Universita di Roma, Piazzale Aldo Moro 5, 00185 Rome, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25213375" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptation, Physiological ; Animals ; Bone and Bones/anatomy & histology/physiology/ultrastructure ; Dinosaurs/*anatomy & histology/*physiology ; Femur/anatomy & histology/physiology ; Food Chain ; Hindlimb/anatomy & histology/physiology ; *Swimming ; Tail/anatomy & histology/physiology ; Water
    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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