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  • Humans  (179)
  • Phylogeny  (17)
  • American Association for the Advancement of Science (AAAS)  (190)
  • American Chemical Society (ACS)
  • Copernicus
  • 2010-2014  (190)
  • 1980-1984
  • 2013  (190)
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  • 2010-2014  (190)
  • 1980-1984
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  • 11
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    Phosphoinositide 3-kinase delta gene mutation predisposes to respiratory infection and airway damage (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-10-19
    Description: Genetic mutations cause primary immunodeficiencies (PIDs) that predispose to infections. Here, we describe activated PI3K-delta syndrome (APDS), a PID associated with a dominant gain-of-function mutation in which lysine replaced glutamic acid at residue 1021 (E1021K) in the p110delta protein, the catalytic subunit of phosphoinositide 3-kinase delta (PI3Kdelta), encoded by the PIK3CD gene. We found E1021K in 17 patients from seven unrelated families, but not among 3346 healthy subjects. APDS was characterized by recurrent respiratory infections, progressive airway damage, lymphopenia, increased circulating transitional B cells, increased immunoglobulin M, and reduced immunoglobulin G2 levels in serum and impaired vaccine responses. The E1021K mutation enhanced membrane association and kinase activity of p110delta. Patient-derived lymphocytes had increased levels of phosphatidylinositol 3,4,5-trisphosphate and phosphorylated AKT protein and were prone to activation-induced cell death. Selective p110delta inhibitors IC87114 and GS-1101 reduced the activity of the mutant enzyme in vitro, which suggested a therapeutic approach for patients with APDS.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3930011/" 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/PMC3930011/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Angulo, Ivan -- Vadas, Oscar -- Garcon, Fabien -- Banham-Hall, Edward -- Plagnol, Vincent -- Leahy, Timothy R -- Baxendale, Helen -- Coulter, Tanya -- Curtis, James -- Wu, Changxin -- Blake-Palmer, Katherine -- Perisic, Olga -- Smyth, Deborah -- Maes, Mailis -- Fiddler, Christine -- Juss, Jatinder -- Cilliers, Deirdre -- Markelj, Gasper -- Chandra, Anita -- Farmer, George -- Kielkowska, Anna -- Clark, Jonathan -- Kracker, Sven -- Debre, Marianne -- Picard, Capucine -- Pellier, Isabelle -- Jabado, Nada -- Morris, James A -- Barcenas-Morales, Gabriela -- Fischer, Alain -- Stephens, Len -- Hawkins, Phillip -- Barrett, Jeffrey C -- Abinun, Mario -- Clatworthy, Menna -- Durandy, Anne -- Doffinger, Rainer -- Chilvers, Edwin R -- Cant, Andrew J -- Kumararatne, Dinakantha -- Okkenhaug, Klaus -- Williams, Roger L -- Condliffe, Alison -- Nejentsev, Sergey -- 095198/Wellcome Trust/United Kingdom -- 095198/Z/10/Z/Wellcome Trust/United Kingdom -- 095691/Wellcome Trust/United Kingdom -- BB/J004456/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- MC_U105184308/Medical Research Council/United Kingdom -- U105184308/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2013 Nov 15;342(6160):866-71. doi: 10.1126/science.1243292. Epub 2013 Oct 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Cambridge, Cambridge, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24136356" target="_blank"〉PubMed〈/a〉
    Keywords: Class I Phosphatidylinositol 3-Kinases ; *Genetic Predisposition to Disease ; Humans ; Immunologic Deficiency Syndromes/*genetics/immunology/*pathology ; Lymphocytes/immunology ; Mutation ; Pedigree ; Phosphatidylinositol 3-Kinases/*genetics ; Phosphatidylinositol Phosphates/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Respiratory Tract Infections/*genetics/immunology/*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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  • 12
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    Infectivity, transmission, and pathology of human-isolated H7N9 influenza virus in ferrets and pigs (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-05-25
    Description: The emergence of the H7N9 influenza virus in humans in Eastern China has raised concerns that a new influenza pandemic could occur. Here, we used a ferret model to evaluate the infectivity and transmissibility of A/Shanghai/2/2013 (SH2), a human H7N9 virus isolate. This virus replicated in the upper and lower respiratory tracts of the ferrets and was shed at high titers for 6 to 7 days, with ferrets showing relatively mild clinical signs. SH2 was efficiently transmitted between ferrets via direct contact, but less efficiently by airborne exposure. Pigs were productively infected by SH2 and shed virus for 6 days but were unable to transmit the virus to naive pigs or ferrets. Under appropriate conditions, human-to-human transmission of the H7N9 virus may be possible.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhu, H -- Wang, D -- Kelvin, D J -- Li, L -- Zheng, Z -- Yoon, S-W -- Wong, S-S -- Farooqui, A -- Wang, J -- Banner, D -- Chen, R -- Zheng, R -- Zhou, J -- Zhang, Y -- Hong, W -- Dong, W -- Cai, Q -- Roehrl, M H A -- Huang, S S H -- Kelvin, A A -- Yao, T -- Zhou, B -- Chen, X -- Leung, G M -- Poon, L L M -- Webster, R G -- Webby, R J -- Peiris, J S M -- Guan, Y -- Shu, Y -- HSN266200700005C/PHS HHS/ -- New York, N.Y. -- Science. 2013 Jul 12;341(6142):183-6. doi: 10.1126/science.1239844. Epub 2013 May 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Joint Influenza Research Centre [Shantou University Medical College/University of Hong Kong], Shantou University, Shantou, PR China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23704376" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Communicable Diseases, Emerging/*transmission/*virology ; Disease Models, Animal ; Ferrets ; Humans ; Influenza, Human/pathology/*transmission/*virology ; Orthomyxoviridae/classification/genetics/*pathogenicity ; Respiratory System/pathology/virology ; Sus scrofa
    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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  • 13
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    Substitutions near the receptor binding site determine major antigenic change during influenza virus evolution (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-11-23
    Description: The molecular basis of antigenic drift was determined for the hemagglutinin (HA) of human influenza A/H3N2 virus. From 1968 to 2003, antigenic change was caused mainly by single amino acid substitutions, which occurred at only seven positions in HA immediately adjacent to the receptor binding site. Most of these substitutions were involved in antigenic change more than once. Equivalent positions were responsible for the recent antigenic changes of influenza B and A/H1N1 viruses. Substitution of a single amino acid at one of these positions substantially changed the virus-specific antibody response in infected ferrets. These findings have potentially far-reaching consequences for understanding the evolutionary mechanisms that govern influenza viruses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koel, Bjorn F -- Burke, David F -- Bestebroer, Theo M -- van der Vliet, Stefan -- Zondag, Gerben C M -- Vervaet, Gaby -- Skepner, Eugene -- Lewis, Nicola S -- Spronken, Monique I J -- Russell, Colin A -- Eropkin, Mikhail Y -- Hurt, Aeron C -- Barr, Ian G -- de Jong, Jan C -- Rimmelzwaan, Guus F -- Osterhaus, Albert D M E -- Fouchier, Ron A M -- Smith, Derek J -- DP1-OD000490-01/OD/NIH HHS/ -- HHSN266200700010C/PHS HHS/ -- New York, N.Y. -- Science. 2013 Nov 22;342(6161):976-9. doi: 10.1126/science.1244730.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Viroscience, Erasmus MC, 3015GE Rotterdam, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24264991" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Substitution/genetics/immunology ; Antigens, Viral/genetics/*immunology ; Binding Sites/genetics ; *Evolution, Molecular ; Hemagglutinin Glycoproteins, Influenza Virus/genetics/*immunology ; Humans ; Influenza A Virus, H3N2 Subtype/genetics/*immunology ; Mutation
    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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  • 14
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    Don't cull wild birds yet (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-05-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yong, Ding Li -- Ng, Daniel -- Xiong, Gordon -- Fam, Shun Deng -- New York, N.Y. -- Science. 2013 May 10;340(6133):681-2. doi: 10.1126/science.340.6133.681-a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23661740" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Communicable Diseases, Emerging/*transmission/*virology ; Humans ; Influenza A virus/*physiology ; Influenza in Birds/*transmission ; Influenza, Human/*virology
    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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  • 15
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    Circulating breast tumor cells exhibit dynamic changes in epithelial and mesenchymal composition (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-02-02
    Description: Epithelial-mesenchymal transition (EMT) of adherent epithelial cells to a migratory mesenchymal state has been implicated in tumor metastasis in preclinical models. To investigate its role in human cancer, we characterized EMT in circulating tumor cells (CTCs) from breast cancer patients. Rare primary tumor cells simultaneously expressed mesenchymal and epithelial markers, but mesenchymal cells were highly enriched in CTCs. Serial CTC monitoring in 11 patients suggested an association of mesenchymal CTCs with disease progression. In an index patient, reversible shifts between these cell fates accompanied each cycle of response to therapy and disease progression. Mesenchymal CTCs occurred as both single cells and multicellular clusters, expressing known EMT regulators, including transforming growth factor (TGF)-beta pathway components and the FOXC1 transcription factor. These data support a role for EMT in the blood-borne dissemination of human breast cancer.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3760262/" 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/PMC3760262/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yu, Min -- Bardia, Aditya -- Wittner, Ben S -- Stott, Shannon L -- Smas, Malgorzata E -- Ting, David T -- Isakoff, Steven J -- Ciciliano, Jordan C -- Wells, Marissa N -- Shah, Ajay M -- Concannon, Kyle F -- Donaldson, Maria C -- Sequist, Lecia V -- Brachtel, Elena -- Sgroi, Dennis -- Baselga, Jose -- Ramaswamy, Sridhar -- Toner, Mehmet -- Haber, Daniel A -- Maheswaran, Shyamala -- EB008047/EB/NIBIB NIH HHS/ -- K12 CA087723/CA/NCI NIH HHS/ -- NCI CA129933/CA/NCI NIH HHS/ -- R01 CA129933/CA/NCI NIH HHS/ -- U01 EB012493/EB/NIBIB NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Feb 1;339(6119):580-4. doi: 10.1126/science.1228522.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Massachusetts General Hospital Cancer Center, Harvard Medical School, Charlestown, MA 02129, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23372014" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomarkers, Tumor/genetics/metabolism ; Breast Neoplasms/blood/genetics/*pathology ; Cell Count ; Cell Movement ; Epithelial Cells/pathology ; *Epithelial-Mesenchymal Transition ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Mesoderm/pathology ; Mice ; Neoplasm Transplantation ; Neoplastic Cells, Circulating/metabolism/*pathology ; RNA, Neoplasm/chemistry/genetics ; Transcription, Genetic ; Transforming Growth Factor beta/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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  • 16
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    Product-to-parent reversion of trenbolone: unrecognized risks for endocrine disruption (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-09-28
    Description: Trenbolone acetate (TBA) is a high-value steroidal growth promoter often administered to beef cattle, whose metabolites are potent endocrine-disrupting compounds. We performed laboratory and field phototransformation experiments to assess the fate of TBA metabolites and their photoproducts. Unexpectedly, we observed that the rapid photohydration of TBA metabolites is reversible under conditions representative of those in surface waters (pH 7, 25 degrees C). This product-to-parent reversion mechanism results in diurnal cycling and substantial regeneration of TBA metabolites at rates that are strongly temperature- and pH-dependent. Photoproducts can also react to produce structural analogs of TBA metabolites. These reactions also occur in structurally similar steroids, including human pharmaceuticals, which suggests that predictive fate models and regulatory risk assessment paradigms must account for transformation products of high-risk environmental contaminants such as endocrine-disrupting steroids.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4096139/" 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/PMC4096139/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Qu, Shen -- Kolodziej, Edward P -- Long, Sarah A -- Gloer, James B -- Patterson, Eric V -- Baltrusaitis, Jonas -- Jones, Gerrad D -- Benchetler, Peter V -- Cole, Emily A -- Kimbrough, Kaitlin C -- Tarnoff, Matthew D -- Cwiertny, David M -- 8 P20 GM103440-11/GM/NIGMS NIH HHS/ -- P20 GM103440/GM/NIGMS NIH HHS/ -- P30 ES005605/ES/NIEHS NIH HHS/ -- S10 RR025500/RR/NCRR NIH HHS/ -- S10-RR025500/RR/NCRR NIH HHS/ -- UL1 RR024979/RR/NCRR NIH HHS/ -- UL1RR024979/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2013 Oct 18;342(6156):347-51. doi: 10.1126/science.1243192. Epub 2013 Sep 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Civil and Environmental Engineering, University of Iowa, 4105 Seamans Center for the Engineering Arts and Sciences, Iowa City, IA 52242-1527, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24072818" target="_blank"〉PubMed〈/a〉
    Keywords: Anabolic Agents/adverse effects/*chemistry/metabolism ; Animals ; Cattle ; Darkness ; Desiccation ; Endocrine Disruptors/adverse effects/*chemistry/*metabolism ; Environmental Health ; Humans ; Hydrogen-Ion Concentration ; *Photolysis ; Risk Assessment ; Temperature ; Trenbolone Acetate/adverse effects/*chemistry/metabolism ; Water/*chemistry ; Water Pollutants/adverse effects/*chemistry/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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  • 17
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    Minimal "Self" peptides that inhibit phagocytic clearance and enhance delivery of nanoparticles (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-02-23
    Description: Foreign particles and cells are cleared from the body by phagocytes that must also recognize and avoid clearance of "self" cells. The membrane protein CD47 is reportedly a "marker of self" in mice that impedes phagocytosis of self by signaling through the phagocyte receptor CD172a. Minimal "Self" peptides were computationally designed from human CD47 and then synthesized and attached to virus-size particles for intravenous injection into mice that express a CD172a variant compatible with hCD47. Self peptides delay macrophage-mediated clearance of nanoparticles, which promotes persistent circulation that enhances dye and drug delivery to tumors. Self-peptide affinity for CD172a is near the optimum measured for human CD172a variants, and Self peptide also potently inhibits nanoparticle uptake mediated by the contractile cytoskeleton. The reductionist approach reveals the importance of human Self peptides and their utility in enhancing drug delivery and imaging.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3966479/" 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/PMC3966479/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rodriguez, Pia L -- Harada, Takamasa -- Christian, David A -- Pantano, Diego A -- Tsai, Richard K -- Discher, Dennis E -- 8UL1TR000003/TR/NCATS NIH HHS/ -- P01-DK032094/DK/NIDDK NIH HHS/ -- P30-DK090969/DK/NIDDK NIH HHS/ -- R01 EB007049/EB/NIBIB NIH HHS/ -- R01 HL062352/HL/NHLBI NIH HHS/ -- R01-EB007049/EB/NIBIB NIH HHS/ -- R01-HL062352/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2013 Feb 22;339(6122):971-5. doi: 10.1126/science.1229568.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular and Cell Biophysics and NanoBioPolymers Laboratory, University of Pennsylvania, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23430657" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antigens, CD47/chemistry/immunology/metabolism ; Antigens, Differentiation/*metabolism ; Antineoplastic Agents/administration & dosage ; Autoantigens ; Blood Circulation ; Diagnostic Imaging/methods ; Drug Delivery Systems/*methods ; Humans ; Mice ; Mice, Inbred NOD ; Mice, SCID ; *Nanoparticles/administration & dosage/analysis ; Neoplasms/chemistry/diagnosis/drug therapy ; Paclitaxel/administration & dosage ; Particle Size ; Peptide Fragments/chemical synthesis/chemistry/immunology/*metabolism ; Phagocytes/immunology/metabolism ; *Phagocytosis ; Receptors, Immunologic/immunology/*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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  • 18
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    A strategy for modulation of enzymes in the ubiquitin system (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-01-05
    Description: The ubiquitin system regulates virtually all aspects of cellular function. We report a method to target the myriad enzymes that govern ubiquitination of protein substrates. We used massively diverse combinatorial libraries of ubiquitin variants to develop inhibitors of four deubiquitinases (DUBs) and analyzed the DUB-inhibitor complexes with crystallography. We extended the selection strategy to the ubiquitin conjugating (E2) and ubiquitin ligase (E3) enzymes and found that ubiquitin variants can also enhance enzyme activity. Last, we showed that ubiquitin variants can bind selectively to ubiquitin-binding domains. Ubiquitin variants exhibit selective function in cells and thus enable orthogonal modulation of specific enzymatic steps in the ubiquitin system.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3815447/" 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/PMC3815447/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ernst, Andreas -- Avvakumov, George -- Tong, Jiefei -- Fan, Yihui -- Zhao, Yanling -- Alberts, Philipp -- Persaud, Avinash -- Walker, John R -- Neculai, Ana-Mirela -- Neculai, Dante -- Vorobyov, Andrew -- Garg, Pankaj -- Beatty, Linda -- Chan, Pak-Kei -- Juang, Yu-Chi -- Landry, Marie-Claude -- Yeh, Christina -- Zeqiraj, Elton -- Karamboulas, Konstantina -- Allali-Hassani, Abdellah -- Vedadi, Masoud -- Tyers, Mike -- Moffat, Jason -- Sicheri, Frank -- Pelletier, Laurence -- Durocher, Daniel -- Raught, Brian -- Rotin, Daniela -- Yang, Jianhua -- Moran, Michael F -- Dhe-Paganon, Sirano -- Sidhu, Sachdev S -- 092076/Wellcome Trust/United Kingdom -- 092381/Wellcome Trust/United Kingdom -- 1R01NS072420-01/Canadian Institutes of Health Research/Canada -- MOP-102536/Canadian Institutes of Health Research/Canada -- MOP-111149/Canadian Institutes of Health Research/Canada -- MOP-13494/Canadian Institutes of Health Research/Canada -- MOP-57795/Canadian Institutes of Health Research/Canada -- R01 NS072420/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2013 Feb 1;339(6119):590-5. doi: 10.1126/science.1230161. Epub 2013 Jan 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Terrence Donnelly Center for Cellular and Biomolecular Research, University of Toronto, 160 College Street, Toronto, Ontario, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23287719" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; *Combinatorial Chemistry Techniques ; Conserved Sequence ; Drug Design ; Endopeptidases/chemistry/*metabolism ; HEK293 Cells ; Humans ; Molecular Sequence Data ; Protease Inhibitors/chemistry/*isolation & purification/pharmacology ; Protein Conformation ; Protein Structure, Secondary ; Small Molecule Libraries ; Ubiquitin/chemistry/genetics/*metabolism ; Ubiquitin Thiolesterase/chemistry/*metabolism ; Ubiquitin-Conjugating Enzymes/chemistry/metabolism ; Ubiquitin-Protein Ligases/chemistry/metabolism ; Ubiquitination/*drug effects
    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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  • 19
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    Dental morphology and the phylogenetic "place" of Australopithecus sediba (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-04-13
    Description: To characterize further the Australopithecus sediba hypodigm, we describe 22 dental traits in specimens MH1 and MH2. Like other skeletal elements, the teeth present a mosaic of primitive and derived features. The new nonmetric data are then qualitatively and phenetically compared with those in eight other African hominin samples, before cladistic analyses using a gorilla outgroup. There is some distinction, largely driven by contrasting molar traits, from East African australopiths. However, Au. sediba links with Au. africanus to form a South African australopith clade. These species present five apomorphies, including shared expressions of Carabelli's upper first molar (UM1) and protostylid lower first molar (LM1). Five synapomorphies are also evident between them and monophyletic Homo habilis/rudolfensis + H. erectus. Finally, a South African australopith + Homo clade is supported by four shared derived states, including identical LM1 cusp 7 expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Irish, Joel D -- Guatelli-Steinberg, Debbie -- Legge, Scott S -- de Ruiter, Darryl J -- Berger, Lee R -- New York, N.Y. -- Science. 2013 Apr 12;340(6129):1233062. doi: 10.1126/science.1233062.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Research Centre in Evolutionary Anthropology and Palaeoecology, School of Natural Sciences and Psychology, Liverpool John Moores University, Liverpool, UK. j.d.irish@ljmu.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23580535" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Evolution ; Dentition ; Female ; *Fossils ; Gorilla gorilla/anatomy & histology ; Hominidae/*anatomy & histology/*classification ; Male ; Molar/*anatomy & histology ; Paleodontology ; Phylogeny ; South Africa ; Tooth/*anatomy & histology
    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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  • 20
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    EMRE is an essential component of the mitochondrial calcium uniporter complex (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-11-16
    Description: The mitochondrial uniporter is a highly selective calcium channel in the organelle's inner membrane. Its molecular components include the EF-hand-containing calcium-binding proteins mitochondrial calcium uptake 1 (MICU1) and MICU2 and the pore-forming subunit mitochondrial calcium uniporter (MCU). We sought to achieve a full molecular characterization of the uniporter holocomplex (uniplex). Quantitative mass spectrometry of affinity-purified uniplex recovered MICU1 and MICU2, MCU and its paralog MCUb, and essential MCU regulator (EMRE), a previously uncharacterized protein. EMRE is a 10-kilodalton, metazoan-specific protein with a single transmembrane domain. In its absence, uniporter channel activity was lost despite intact MCU expression and oligomerization. EMRE was required for the interaction of MCU with MICU1 and MICU2. Hence, EMRE is essential for in vivo uniporter current and additionally bridges the calcium-sensing role of MICU1 and MICU2 with the calcium-conducting role of MCU.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4091629/" 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/PMC4091629/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sancak, Yasemin -- Markhard, Andrew L -- Kitami, Toshimori -- Kovacs-Bogdan, Erika -- Kamer, Kimberli J -- Udeshi, Namrata D -- Carr, Steven A -- Chaudhuri, Dipayan -- Clapham, David E -- Li, Andrew A -- Calvo, Sarah E -- Goldberger, Olga -- Mootha, Vamsi K -- DK080261/DK/NIDDK NIH HHS/ -- F32 HL107021/HL/NHLBI NIH HHS/ -- F32HL107021/HL/NHLBI NIH HHS/ -- P30 HD018655/HD/NICHD NIH HHS/ -- R24 DK080261/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Dec 13;342(6164):1379-82. doi: 10.1126/science.1242993. Epub 2013 Nov 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Massachusetts General Hospital, Department of Systems Biology, Harvard Medical School, Boston, MA, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24231807" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Calcium Channels/chemistry/genetics/*metabolism ; Calcium-Binding Proteins/genetics/*metabolism ; Cation Transport Proteins/genetics/*metabolism ; Cell Membrane/*metabolism ; EF Hand Motifs ; Gene Knockdown Techniques ; HEK293 Cells ; Humans ; Mitochondria/*metabolism ; Mitochondrial Membrane Transport Proteins/genetics/*metabolism ; Molecular Sequence Data ; Phylogeny ; Protein Structure, Tertiary ; Proteomics
    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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