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  • Articles  (153)
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  • Articles  (153)
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  • American Association for the Advancement of Science (AAAS)  (153)
  • American Geophysical Union
  • American Meteorological Society
  • American Physical Society (APS)
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  • 1
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    Science education. Court to weigh university's decision not to hire astronomer (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-01-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Couzin-Frankel, Jennifer -- New York, N.Y. -- Science. 2010 Dec 24;330(6012):1731. doi: 10.1126/science.330.6012.1731.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21205643" target="_blank"〉PubMed〈/a〉
    Keywords: Astronomy/*education ; *Biological Evolution ; Employment/*legislation & jurisprudence ; Kentucky ; *Religion and Science ; United States ; Universities/*legislation & jurisprudence
    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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    Has the microbiota played a critical role in the evolution of the adaptive immune system? (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-01-06
    Description: Although microbes have been classically viewed as pathogens, it is now well established that the majority of host-bacterial interactions are symbiotic. During development and into adulthood, gut bacteria shape the tissues, cells, and molecular profile of our gastrointestinal immune system. This partnership, forged over many millennia of coevolution, is based on a molecular exchange involving bacterial signals that are recognized by host receptors to mediate beneficial outcomes for both microbes and humans. We explore how specific aspects of the adaptive immune system are influenced by intestinal commensal bacteria. Understanding the molecular mechanisms that mediate symbiosis between commensal bacteria and humans may redefine how we view the evolution of adaptive immunity and consequently how we approach the treatment of numerous immunologic disorders.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3159383/" 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/PMC3159383/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Yun Kyung -- Mazmanian, Sarkis K -- AI088626/AI/NIAID NIH HHS/ -- DK078938/DK/NIDDK NIH HHS/ -- DK083633/DK/NIDDK NIH HHS/ -- R01 DK078938/DK/NIDDK NIH HHS/ -- R01 DK078938-01A2/DK/NIDDK NIH HHS/ -- R01 DK078938-02/DK/NIDDK NIH HHS/ -- R01 DK078938-03/DK/NIDDK NIH HHS/ -- R01 DK078938-04/DK/NIDDK NIH HHS/ -- R21 AI088626/AI/NIAID NIH HHS/ -- R21 AI088626-01/AI/NIAID NIH HHS/ -- R21 AI088626-02/AI/NIAID NIH HHS/ -- R21 DK083633/DK/NIDDK NIH HHS/ -- R21 DK083633-01A1/DK/NIDDK NIH HHS/ -- R21 DK083633-02/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2010 Dec 24;330(6012):1768-73. doi: 10.1126/science.1195568.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology, California Institute of Technology, Pasadena, CA 91125, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21205662" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptive Immunity ; Animals ; Autoimmune Diseases/immunology ; Bacteria/immunology ; *Bacterial Physiological Phenomena ; *Biological Evolution ; Cell Differentiation ; Humans ; Immune Tolerance ; Immunity, Innate ; Immunity, Mucosal ; Intestinal Mucosa/immunology/microbiology ; Intestines/immunology/*microbiology ; Metagenome/immunology/*physiology ; Symbiosis ; T-Lymphocytes, Helper-Inducer/cytology/immunology ; T-Lymphocytes, Regulatory/cytology/immunology
    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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    Genomics. A genome for the environment (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-02-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ebert, Dieter -- New York, N.Y. -- Science. 2011 Feb 4;331(6017):539-40. doi: 10.1126/science.1202092.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Universitat Basel, Zoological Institute, Vesalgasse 1, 4059 Basel, Switzerland. dieter.ebert@unibas.ch〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21292957" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological ; Animals ; *Biological Evolution ; Daphnia/*genetics/physiology ; *Ecosystem ; *Environment ; Evolution, Molecular ; *Gene Duplication ; *Genome ; Phenotype
    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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  • 4
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    Association of TALS developmental disorder with defect in minor splicing component U4atac snRNA (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-04-09
    Description: The spliceosome, a ribonucleoprotein complex that includes proteins and small nuclear RNAs (snRNAs), catalyzes RNA splicing through intron excision and exon ligation to produce mature messenger RNAs, which, in turn serve as templates for protein translation. We identified four point mutations in the U4atac snRNA component of the minor spliceosome in patients with brain and bone malformations and unexplained postnatal death [microcephalic osteodysplastic primordial dwarfism type 1 (MOPD 1) or Taybi-Linder syndrome (TALS); Mendelian Inheritance in Man ID no. 210710]. Expression of a subgroup of genes, possibly linked to the disease phenotype, and minor intron splicing were affected in cell lines derived from TALS patients. Our findings demonstrate a crucial role of the minor spliceosome component U4atac snRNA in early human development and postnatal survival.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Edery, Patrick -- Marcaillou, Charles -- Sahbatou, Mourad -- Labalme, Audrey -- Chastang, Joelle -- Touraine, Renaud -- Tubacher, Emmanuel -- Senni, Faiza -- Bober, Michael B -- Nampoothiri, Sheela -- Jouk, Pierre-Simon -- Steichen, Elisabeth -- Berland, Siren -- Toutain, Annick -- Wise, Carol A -- Sanlaville, Damien -- Rousseau, Francis -- Clerget-Darpoux, Francoise -- Leutenegger, Anne-Louise -- New York, N.Y. -- Science. 2011 Apr 8;332(6026):240-3. doi: 10.1126/science.1202205.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Hospices Civils de Lyon, Service de Cytogenetique Constitutionnelle, Bron, F-69677, France. patrick.edery@chu-lyon.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21474761" target="_blank"〉PubMed〈/a〉
    Keywords: Base Pairing ; Cell Line ; Child, Preschool ; Chromosomes, Human, Pair 2/genetics ; Dwarfism/genetics/metabolism ; Female ; Fetal Growth Retardation/genetics/metabolism ; Humans ; Infant ; Introns ; Inverted Repeat Sequences ; Male ; Microcephaly/genetics/metabolism ; Microtubule-Associated Proteins/genetics ; Nucleic Acid Conformation ; Osteochondrodysplasias/genetics/metabolism ; Pedigree ; *Point Mutation ; RNA Splice Sites ; *RNA Splicing ; RNA, Small Nuclear/chemistry/*genetics/metabolism ; Spliceosomes/*genetics/metabolism
    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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  • 5
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    Spatial coupling of mTOR and autophagy augments secretory phenotypes (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-04-23
    Description: Protein synthesis and autophagic degradation are regulated in an opposite manner by mammalian target of rapamycin (mTOR), whereas under certain conditions it would be beneficial if they occurred in unison to handle rapid protein turnover. We observed a distinct cellular compartment at the trans side of the Golgi apparatus, the TOR-autophagy spatial coupling compartment (TASCC), where (auto)lysosomes and mTOR accumulated during Ras-induced senescence. mTOR recruitment to the TASCC was amino acid- and Rag guanosine triphosphatase-dependent, and disruption of mTOR localization to the TASCC suppressed interleukin-6/8 synthesis. TASCC formation was observed during macrophage differentiation and in glomerular podocytes; both displayed increased protein secretion. The spatial coupling of cells' catabolic and anabolic machinery could augment their respective functions and facilitate the mass synthesis of secretory proteins.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3426290/" 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/PMC3426290/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Narita, Masako -- Young, Andrew R J -- Arakawa, Satoko -- Samarajiwa, Shamith A -- Nakashima, Takayuki -- Yoshida, Sei -- Hong, Sungki -- Berry, Lorraine S -- Reichelt, Stefanie -- Ferreira, Manuela -- Tavare, Simon -- Inoki, Ken -- Shimizu, Shigeomi -- Narita, Masashi -- DK083491/DK/NIDDK NIH HHS/ -- R01 DK083491/DK/NIDDK NIH HHS/ -- R01 DK083491-03/DK/NIDDK NIH HHS/ -- Cancer Research UK/United Kingdom -- New York, N.Y. -- Science. 2011 May 20;332(6032):966-70. doi: 10.1126/science.1205407. Epub 2011 Apr 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Research UK Cambridge Research Institute (CRI), Li Ka Shing Centre, Robinson Way, Cambridge CB2 0RE, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21512002" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acids/metabolism ; Animals ; *Autophagy ; *Cell Aging ; Cell Line ; Cytoplasm/metabolism ; Cytoplasmic Vesicles/*metabolism/ultrastructure ; Endoplasmic Reticulum, Rough/ultrastructure ; Genes, ras ; Golgi Apparatus/ultrastructure ; HL-60 Cells ; Humans ; Interleukin-6/metabolism ; Interleukin-8/metabolism ; Lysosomes/metabolism/ultrastructure ; Mice ; Monomeric GTP-Binding Proteins/genetics/metabolism ; Nocodazole/pharmacology ; Phagosomes/metabolism/ultrastructure ; Phenotype ; Podocytes/metabolism/ultrastructure ; Protein Biosynthesis ; Proteins/*secretion ; TOR Serine-Threonine Kinases/*metabolism ; Vacuoles/ultrastructure ; trans-Golgi Network/metabolism/ultrastructure
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 6
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    Tet proteins can convert 5-methylcytosine to 5-formylcytosine and 5-carboxylcytosine (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-07-23
    Description: 5-methylcytosine (5mC) in DNA plays an important role in gene expression, genomic imprinting, and suppression of transposable elements. 5mC can be converted to 5-hydroxymethylcytosine (5hmC) by the Tet (ten eleven translocation) proteins. Here, we show that, in addition to 5hmC, the Tet proteins can generate 5-formylcytosine (5fC) and 5-carboxylcytosine (5caC) from 5mC in an enzymatic activity-dependent manner. Furthermore, we reveal the presence of 5fC and 5caC in genomic DNA of mouse embryonic stem cells and mouse organs. The genomic content of 5hmC, 5fC, and 5caC can be increased or reduced through overexpression or depletion of Tet proteins. Thus, we identify two previously unknown cytosine derivatives in genomic DNA as the products of Tet proteins. Our study raises the possibility that DNA demethylation may occur through Tet-catalyzed oxidation followed by decarboxylation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3495246/" 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/PMC3495246/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ito, Shinsuke -- Shen, Li -- Dai, Qing -- Wu, Susan C -- Collins, Leonard B -- Swenberg, James A -- He, Chuan -- Zhang, Yi -- GM071440/GM/NIGMS NIH HHS/ -- GM68804/GM/NIGMS NIH HHS/ -- P30 ES010126/ES/NIEHS NIH HHS/ -- P30 ES010126-11/ES/NIEHS NIH HHS/ -- P30ES10126/ES/NIEHS NIH HHS/ -- P42 ES005948/ES/NIEHS NIH HHS/ -- P42 ES005948-17/ES/NIEHS NIH HHS/ -- P42ES5948/ES/NIEHS NIH HHS/ -- R01 GM068804/GM/NIGMS NIH HHS/ -- U01 DK089565/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Sep 2;333(6047):1300-3. doi: 10.1126/science.1210597. Epub 2011 Jul 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Biochemistry and Biophysics, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7295, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21778364" target="_blank"〉PubMed〈/a〉
    Keywords: 5-Methylcytosine/*metabolism ; Animals ; Cell Line ; Cytosine/*analogs & derivatives/metabolism ; DNA/*metabolism ; DNA Methylation ; DNA-Binding Proteins/genetics/*metabolism ; Embryonic Stem Cells/metabolism ; Humans ; Mice ; Oxidation-Reduction ; Proto-Oncogene Proteins/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism
    Print ISSN: 0036-8075
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  • 7
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    Cleavage of NIK by the API2-MALT1 fusion oncoprotein leads to noncanonical NF-kappaB activation (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-01-29
    Description: Proper regulation of nuclear factor kappaB (NF-kappaB) transcriptional activity is required for normal lymphocyte function, and deregulated NF-kappaB signaling can facilitate lymphomagenesis. We demonstrate that the API2-MALT1 fusion oncoprotein created by the recurrent t(11;18)(q21;q21) in mucosa-associated lymphoid tissue (MALT) lymphoma induces proteolytic cleavage of NF-kappaB-inducing kinase (NIK) at arginine 325. NIK cleavage requires the concerted actions of both fusion partners and generates a C-terminal NIK fragment that retains kinase activity and is resistant to proteasomal degradation. The resulting deregulated NIK activity is associated with constitutive noncanonical NF-kappaB signaling, enhanced B cell adhesion, and apoptosis resistance. Our study reveals the gain-of-function proteolytic activity of a fusion oncoprotein and highlights the importance of the noncanonical NF-kappaB pathway in B lymphoproliferative disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3124150/" 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/PMC3124150/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rosebeck, Shaun -- Madden, Lisa -- Jin, Xiaohong -- Gu, Shufang -- Apel, Ingrid J -- Appert, Alex -- Hamoudi, Rifat A -- Noels, Heidi -- Sagaert, Xavier -- Van Loo, Peter -- Baens, Mathijs -- Du, Ming-Qing -- Lucas, Peter C -- McAllister-Lucas, Linda M -- R01 CA124540/CA/NCI NIH HHS/ -- R01 CA124540-04/CA/NCI NIH HHS/ -- R01 HL082914/HL/NHLBI NIH HHS/ -- R01CA124540/CA/NCI NIH HHS/ -- T32-HD07513/HD/NICHD NIH HHS/ -- T32-HL007622-21A2/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2011 Jan 28;331(6016):468-72. doi: 10.1126/science.1198946.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics and Communicable Diseases, University of Michigan, 1150 West Medical Center Drive, Ann Arbor, MI 48109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21273489" target="_blank"〉PubMed〈/a〉
    Keywords: Apoptosis ; B-Lymphocytes/*metabolism ; Cell Adhesion ; Cell Line ; Cell Line, Tumor ; Gene Expression Regulation, Neoplastic ; Humans ; I-kappa B Kinase/metabolism ; Lymphoma, B-Cell, Marginal Zone/genetics/*metabolism ; NF-kappa B/*metabolism ; NF-kappa B p52 Subunit/metabolism ; Oncogene Proteins, Fusion/chemistry/genetics/*metabolism ; Phosphorylation ; Protein Structure, Tertiary ; Protein-Serine-Threonine Kinases/genetics/*metabolism ; Proto-Oncogene Proteins/genetics/metabolism ; Signal Transduction ; Substrate Specificity
    Print ISSN: 0036-8075
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  • 8
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    Comment on "Positive selection of tyrosine loss in metazoan evolution" (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-05-21
    Description: Tan et al. (Reports, 25 September 2009, p. 1686) argued that loss of tyrosine residues from proteins in metazoans was driven by positive selection to remove potentially deleterious phosphorylation sites. We challenge this hypothesis, providing evidence that the high guanine-cytosine (GC) content of metazoan genomes was the primary driver in the loss of tyrosine residues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Su, Zhixi -- Huang, Wei -- Gu, Xun -- New York, N.Y. -- Science. 2011 May 20;332(6032):917; author reply 917. doi: 10.1126/science.1187374.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉MOE Key Laboratory of Contemporary Anthropology and Center for Evolutionary Biology, School of Life Sciences, Institutes of Biomedical Sciences, Fudan University, Shanghai 200433, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21596977" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Base Composition ; *Biological Evolution ; Choanoflagellata/chemistry/genetics ; Evolution, Molecular ; Fungal Proteins/chemistry ; *Genome ; Phosphorylation ; Protein-Tyrosine Kinases/metabolism ; Proteins/*chemistry ; Protozoan Proteins/chemistry ; Saccharomycetales/chemistry/genetics ; *Selection, Genetic ; Tyrosine/*chemistry
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  • 9
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    Evolution. How great wings can look alike (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-08-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carroll, Sean B -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Aug 26;333(6046):1100-1. doi: 10.1126/science.1211025.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Laboratory of Molecular Biology, University of Wisconsin-Madison, 201 Bock Laboratories, Madison, WI 53706, USA. sbcarrol@facstaff.wisc.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21868661" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Biological ; Animals ; *Biological Evolution ; Butterflies/anatomy & histology/*genetics ; *Genes, Insect ; Genetic Variation ; Mutation ; Phenotype ; Pigmentation/*genetics ; Regulatory Sequences, Nucleic Acid ; Selection, Genetic ; Wings, Animal/*anatomy & histology
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  • 10
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    Evolution. Living fossil younger than thought (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-11-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Renner, Susanne S -- New York, N.Y. -- Science. 2011 Nov 11;334(6057):766-7. doi: 10.1126/science.1214649.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biology Department, University of Munich, 80638 Munich, Germany. renner@lrz.uni-muenchen.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22076366" target="_blank"〉PubMed〈/a〉
    Keywords: *Biological Evolution ; *Cycadophyta ; *Fossils ; *Genetic Speciation
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