ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
  • *Gene Expression Regulation
  • American Association for the Advancement of Science (AAAS)  (15)
  • American Meteorological Society
  • 2015-2019  (12)
  • 2010-2014  (3)
  • 1955-1959
  • 2015  (12)
  • 2012  (3)
Collection
Keywords
Publisher
Years
  • 2015-2019  (12)
  • 2010-2014  (3)
  • 1955-1959
Year
  • 1
    facet.materialart.
    Unknown
    Human genomics. Effect of predicted protein-truncating genetic variants on the human transcriptome (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-05-09
    Description: Accurate prediction of the functional effect of genetic variation is critical for clinical genome interpretation. We systematically characterized the transcriptome effects of protein-truncating variants, a class of variants expected to have profound effects on gene function, using data from the Genotype-Tissue Expression (GTEx) and Geuvadis projects. We quantitated tissue-specific and positional effects on nonsense-mediated transcript decay and present an improved predictive model for this decay. We directly measured the effect of variants both proximal and distal to splice junctions. Furthermore, we found that robustness to heterozygous gene inactivation is not due to dosage compensation. Our results illustrate the value of transcriptome data in the functional interpretation of genetic variants.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4537935/" 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/PMC4537935/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rivas, Manuel A -- Pirinen, Matti -- Conrad, Donald F -- Lek, Monkol -- Tsang, Emily K -- Karczewski, Konrad J -- Maller, Julian B -- Kukurba, Kimberly R -- DeLuca, David S -- Fromer, Menachem -- Ferreira, Pedro G -- Smith, Kevin S -- Zhang, Rui -- Zhao, Fengmei -- Banks, Eric -- Poplin, Ryan -- Ruderfer, Douglas M -- Purcell, Shaun M -- Tukiainen, Taru -- Minikel, Eric V -- Stenson, Peter D -- Cooper, David N -- Huang, Katharine H -- Sullivan, Timothy J -- Nedzel, Jared -- GTEx Consortium -- Geuvadis Consortium -- Bustamante, Carlos D -- Li, Jin Billy -- Daly, Mark J -- Guigo, Roderic -- Donnelly, Peter -- Ardlie, Kristin -- Sammeth, Michael -- Dermitzakis, Emmanouil T -- McCarthy, Mark I -- Montgomery, Stephen B -- Lappalainen, Tuuli -- MacArthur, Daniel G -- 090532/Wellcome Trust/United Kingdom -- 090532/Z/09/Z/Wellcome Trust/United Kingdom -- 095552/Wellcome Trust/United Kingdom -- 095552/Z/11/Z/Wellcome Trust/United Kingdom -- 098381/Wellcome Trust/United Kingdom -- DA006227/DA/NIDA NIH HHS/ -- HHSN261200800001E/CA/NCI NIH HHS/ -- HHSN261200800001E/PHS HHS/ -- HHSN268201000029C/HL/NHLBI NIH HHS/ -- HHSN268201000029C/PHS HHS/ -- MH090936/MH/NIMH NIH HHS/ -- MH090937/MH/NIMH NIH HHS/ -- MH090941/MH/NIMH NIH HHS/ -- MH090948/MH/NIMH NIH HHS/ -- MH090951/MH/NIMH NIH HHS/ -- P30 DK020595/DK/NIDDK NIH HHS/ -- R01 GM104371/GM/NIGMS NIH HHS/ -- R01 MH090941/MH/NIMH NIH HHS/ -- R01 MH101810/MH/NIMH NIH HHS/ -- R01 MH101814/MH/NIMH NIH HHS/ -- R01 MH101820/MH/NIMH NIH HHS/ -- R01GM104371/GM/NIGMS NIH HHS/ -- R01MH090941/MH/NIMH NIH HHS/ -- R01MH101810/MH/NIMH NIH HHS/ -- R01MH101814/MH/NIMH NIH HHS/ -- U01 HG007593/HG/NHGRI NIH HHS/ -- U01HG007593/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2015 May 8;348(6235):666-9. doi: 10.1126/science.1261877.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust Centre for Human Genetics, Nuffield Department of Clinical Medicine, University of Oxford, Oxford, UK. rivas@well.ox.ac.uk tlappalainen@nygenome.org macarthur@atgu.mgh.harvard.edu. ; FInstitute for Molecular Medicine Finland (FIMM), University of Helsinki, Helsinki, Finland. ; Washington University in St. Louis, St. Louis, MO, USA. ; Broad Institute of MIT and Harvard, Cambridge, MA, USA. Analytical and Translational Genetics Unit, Massachusetts General Hospital, Boston, MA, USA. ; Department of Genetics, Stanford University, Stanford, CA, USA. Department of Pathology, Stanford University, Stanford, CA, USA. Biomedical Informatics Program, Stanford University, Stanford, CA, USA. ; Department of Genetics, Stanford University, Stanford, CA, USA. Department of Pathology, Stanford University, Stanford, CA, USA. ; Broad Institute of MIT and Harvard, Cambridge, MA, USA. ; Broad Institute of MIT and Harvard, Cambridge, MA, USA. Analytical and Translational Genetics Unit, Massachusetts General Hospital, Boston, MA, USA. Department of Psychiatry, Mt. Sinai Hospital, NY, USA. ; Department of Genetic Medicine and Development,University of Geneva, Geneva, Switzerland. Institute for Genetics and Genomics in Geneva (iGE3), University of Geneva, Geneva, Switzerland. Swiss Institute of Bioinformatics, Geneva, Switzerland. ; Department of Genetics, Stanford University, Stanford, CA, USA. ; Department of Psychiatry, Mt. Sinai Hospital, NY, USA. Division of Psychiatric Genomics, Department of Psychiatry, Icahn School of Medicine at Mount Sinai, NY, USA. ; Broad Institute of MIT and Harvard, Cambridge, MA, USA. Analytical and Translational Genetics Unit, Massachusetts General Hospital, Boston, MA, USA. Department of Psychiatry, Mt. Sinai Hospital, NY, USA. Division of Psychiatric Genomics, Department of Psychiatry, Icahn School of Medicine at Mount Sinai, NY, USA. ; Institute of Medical Genetics, School of Medicine, Cardiff University, Heath Park, Cardiff, UK. ; Center for Genomic Regulation (CRG), Universitat Pompeu Fabra (UPF), Barcelona, Catalonia, Spain. ; Wellcome Trust Centre for Human Genetics, Nuffield Department of Clinical Medicine, University of Oxford, Oxford, UK. Department of Statistics, University of Oxford, Oxford, UK. ; Center for Genomic Regulation (CRG), Universitat Pompeu Fabra (UPF), Barcelona, Catalonia, Spain. National Institute for Scientific Computing (LNCC), Petropolis, Rio de Janeiro, Brazil. ; Wellcome Trust Centre for Human Genetics, Nuffield Department of Clinical Medicine, University of Oxford, Oxford, UK. Oxford Center for Diabetes Endocrinology and Metabolism, University of Oxford, Oxford, UK. ; Department of Genetics, Stanford University, Stanford, CA, USA. Department of Genetic Medicine and Development,University of Geneva, Geneva, Switzerland. Institute for Genetics and Genomics in Geneva (iGE3), University of Geneva, Geneva, Switzerland. Swiss Institute of Bioinformatics, Geneva, Switzerland. New York Genome Center, New York, NY, USA. Department of Systems Biology, Columbia University, New York, NY, USA. rivas@well.ox.ac.uk tlappalainen@nygenome.org macarthur@atgu.mgh.harvard.edu. ; Broad Institute of MIT and Harvard, Cambridge, MA, USA. Analytical and Translational Genetics Unit, Massachusetts General Hospital, Boston, MA, USA. Department of Medicine, Harvard Medical School, Boston, MA, USA. rivas@well.ox.ac.uk tlappalainen@nygenome.org macarthur@atgu.mgh.harvard.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25954003" target="_blank"〉PubMed〈/a〉
    Keywords: Alternative Splicing ; Gene Expression Profiling ; *Gene Expression Regulation ; Gene Silencing ; *Genetic Variation ; Genome, Human/*genetics ; Heterozygote ; Humans ; Nonsense Mediated mRNA Decay ; Phenotype ; Proteins/*genetics ; *Transcriptome
    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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 2
    facet.materialart.
    Unknown
    Human genomics. The human transcriptome across tissues and individuals (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-05-09
    Description: Transcriptional regulation and posttranscriptional processing underlie many cellular and organismal phenotypes. We used RNA sequence data generated by Genotype-Tissue Expression (GTEx) project to investigate the patterns of transcriptome variation across individuals and tissues. Tissues exhibit characteristic transcriptional signatures that show stability in postmortem samples. These signatures are dominated by a relatively small number of genes-which is most clearly seen in blood-though few are exclusive to a particular tissue and vary more across tissues than individuals. Genes exhibiting high interindividual expression variation include disease candidates associated with sex, ethnicity, and age. Primary transcription is the major driver of cellular specificity, with splicing playing mostly a complementary role; except for the brain, which exhibits a more divergent splicing program. Variation in splicing, despite its stochasticity, may play in contrast a comparatively greater role in defining individual phenotypes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4547472/" 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/PMC4547472/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mele, Marta -- Ferreira, Pedro G -- Reverter, Ferran -- DeLuca, David S -- Monlong, Jean -- Sammeth, Michael -- Young, Taylor R -- Goldmann, Jakob M -- Pervouchine, Dmitri D -- Sullivan, Timothy J -- Johnson, Rory -- Segre, Ayellet V -- Djebali, Sarah -- Niarchou, Anastasia -- GTEx Consortium -- Wright, Fred A -- Lappalainen, Tuuli -- Calvo, Miquel -- Getz, Gad -- Dermitzakis, Emmanouil T -- Ardlie, Kristin G -- Guigo, Roderic -- HHSN261200800001E/PHS HHS/ -- HHSN268201000029C/HL/NHLBI NIH HHS/ -- HHSN268201000029C/PHS HHS/ -- R01 DA006227-17/DA/NIDA NIH HHS/ -- R01 MH090936/MH/NIMH NIH HHS/ -- R01 MH090941/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2015 May 8;348(6235):660-5. doi: 10.1126/science.aaa0355.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Genomic Regulation (CRG), Barcelona, Catalonia, Spain. Harvard Department of stem cell and regenerative biology, Harvard University, Cambridge, MA, USA. ; Center for Genomic Regulation (CRG), Barcelona, Catalonia, Spain. Department of Genetic Medicine and Development, University of Geneva, Geneva, Switzerland. Institute for Genetics and Genomics in Geneva (iGE3), University of Geneva, Geneva, Switzerland. Swiss Institute of Bioinformatics, Geneva, Switzerland. ; Center for Genomic Regulation (CRG), Barcelona, Catalonia, Spain. Facultat de Biologia, Universitat de Barcelona (UB), Barcelona, Catalonia, Spain. Universitat Pompeu Fabra (UPF), Barcelona, Catalonia, Spain. ; Broad Institute of MIT and Harvard, Cambridge, MA, USA. ; Center for Genomic Regulation (CRG), Barcelona, Catalonia, Spain. Universitat Pompeu Fabra (UPF), Barcelona, Catalonia, Spain. McGill University, Montreal, Canada. ; Center for Genomic Regulation (CRG), Barcelona, Catalonia, Spain. Universitat Pompeu Fabra (UPF), Barcelona, Catalonia, Spain. National Institute for Scientific Computing (LNCC), Petropolis, Rio de Janeiro, Brazil. ; Center for Genomic Regulation (CRG), Barcelona, Catalonia, Spain. Universitat Pompeu Fabra (UPF), Barcelona, Catalonia, Spain. Radboud University, Nijmegen, Netherlands. ; Center for Genomic Regulation (CRG), Barcelona, Catalonia, Spain. Universitat Pompeu Fabra (UPF), Barcelona, Catalonia, Spain. Faculty of Bioengineering and Bioinformatics, Moscow State University, Leninskie Gory 1-73, 119992 Moscow, Russia. ; Center for Genomic Regulation (CRG), Barcelona, Catalonia, Spain. Universitat Pompeu Fabra (UPF), Barcelona, Catalonia, Spain. ; Department of Genetic Medicine and Development, University of Geneva, Geneva, Switzerland. Institute for Genetics and Genomics in Geneva (iGE3), University of Geneva, Geneva, Switzerland. Swiss Institute of Bioinformatics, Geneva, Switzerland. ; Center for Genomic Regulation (CRG), Barcelona, Catalonia, Spain. Harvard Department of stem cell and regenerative biology, Harvard University, Cambridge, MA, USA. Department of Genetic Medicine and Development, University of Geneva, Geneva, Switzerland. Institute for Genetics and Genomics in Geneva (iGE3), University of Geneva, Geneva, Switzerland. Swiss Institute of Bioinformatics, Geneva, Switzerland. Facultat de Biologia, Universitat de Barcelona (UB), Barcelona, Catalonia, Spain. Universitat Pompeu Fabra (UPF), Barcelona, Catalonia, Spain. Broad Institute of MIT and Harvard, Cambridge, MA, USA. McGill University, Montreal, Canada. National Institute for Scientific Computing (LNCC), Petropolis, Rio de Janeiro, Brazil. Radboud University, Nijmegen, Netherlands. Faculty of Bioengineering and Bioinformatics, Moscow State University, Leninskie Gory 1-73, 119992 Moscow, Russia. North Carolina State University, Raleigh, NC, USA. New York Genome Center, New York, NY, USA. Department of Systems Biology, Columbia University, New York, NY, USA. Cancer Center and Department of Pathology, Massachusetts General Hospital, Boston, MA 02114, USA. Institut Hospital del Mar d'Investigacions Mediques (IMIM), Barcelona, Catalonia, Spain. Joint CRG-Barcelona Super Computing Center (BSC)-Institut de Recerca Biomedica (IRB) Program in Computational Biology, Barcelona, Catalonia, Spain. ; North Carolina State University, Raleigh, NC, USA. ; Department of Genetic Medicine and Development, University of Geneva, Geneva, Switzerland. Institute for Genetics and Genomics in Geneva (iGE3), University of Geneva, Geneva, Switzerland. Swiss Institute of Bioinformatics, Geneva, Switzerland. New York Genome Center, New York, NY, USA. Department of Systems Biology, Columbia University, New York, NY, USA. ; Facultat de Biologia, Universitat de Barcelona (UB), Barcelona, Catalonia, Spain. ; Broad Institute of MIT and Harvard, Cambridge, MA, USA. Cancer Center and Department of Pathology, Massachusetts General Hospital, Boston, MA 02114, USA. ; Broad Institute of MIT and Harvard, Cambridge, MA, USA. kardlie@broadinstitute.org roderic.guigo@crg.cat. ; Center for Genomic Regulation (CRG), Barcelona, Catalonia, Spain. Universitat Pompeu Fabra (UPF), Barcelona, Catalonia, Spain. Institut Hospital del Mar d'Investigacions Mediques (IMIM), Barcelona, Catalonia, Spain. Joint CRG-Barcelona Super Computing Center (BSC)-Institut de Recerca Biomedica (IRB) Program in Computational Biology, Barcelona, Catalonia, Spain. kardlie@broadinstitute.org roderic.guigo@crg.cat.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25954002" target="_blank"〉PubMed〈/a〉
    Keywords: Alternative Splicing ; Female ; Gene Expression Profiling ; *Gene Expression Regulation ; Genome, Human/*genetics ; Humans ; Male ; Organ Specificity/genetics ; Phenotype ; Polymorphism, Single Nucleotide ; Sequence Analysis, RNA ; Sex Factors ; *Transcriptome
    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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 3
    facet.materialart.
    Unknown
    Loss of motoneuron-specific microRNA-218 causes systemic neuromuscular failure (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-12-19
    Description: Dysfunction of microRNA (miRNA) metabolism is thought to underlie diseases affecting motoneurons. One miRNA, miR-218, is abundantly and selectively expressed by developing and mature motoneurons. Here we show that mutant mice lacking miR-218 die neonatally and exhibit neuromuscular junction defects, motoneuron hyperexcitability, and progressive motoneuron cell loss, all of which are hallmarks of motoneuron diseases such as amyotrophic lateral sclerosis and spinal muscular atrophy. Gene profiling reveals that miR-218 modestly represses a cohort of hundreds of genes that are neuronally enriched but are not specific to a single neuron subpopulation. Thus, the set of messenger RNAs targeted by miR-218, designated TARGET(218), defines a neuronal gene network that is selectively tuned down in motoneurons to prevent neuromuscular failure and neurodegeneration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Amin, Neal D -- Bai, Ge -- Klug, Jason R -- Bonanomi, Dario -- Pankratz, Matthew T -- Gifford, Wesley D -- Hinckley, Christopher A -- Sternfeld, Matthew J -- Driscoll, Shawn P -- Dominguez, Bertha -- Lee, Kuo-Fen -- Jin, Xin -- Pfaff, Samuel L -- F31-NS080340-03/NS/NINDS NIH HHS/ -- P30 CA014195/CA/NCI NIH HHS/ -- P30 NS072031/NS/NINDS NIH HHS/ -- R01AG0476669/AG/NIA NIH HHS/ -- R01GM088278/GM/NIGMS NIH HHS/ -- R01NS044420/NS/NINDS NIH HHS/ -- R01NS054154/NS/NINDS NIH HHS/ -- R01NS060833/NS/NINDS NIH HHS/ -- R21NS084254/NS/NINDS NIH HHS/ -- T32-GM007198/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2015 Dec 18;350(6267):1525-9. doi: 10.1126/science.aad2509.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Gene Expression Laboratory, Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA. Medical Scientist Training Program, University of California, San Diego (UCSD), 9500 Gilman Drive, La Jolla, CA 92037, USA. Biomedical Sciences Graduate Program, UCSD, 9500 Gilman Drive, La Jolla, CA 92037, USA. ; Howard Hughes Medical Institute and Gene Expression Laboratory, Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA. ; Molecular Neurobiology Laboratory, Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA. ; Howard Hughes Medical Institute and Gene Expression Laboratory, Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA. Medical Scientist Training Program, University of California, San Diego (UCSD), 9500 Gilman Drive, La Jolla, CA 92037, USA. Neurosciences Graduate Program, UCSD, 9500 Gilman Drive, La Jolla, CA 92037, USA. ; Howard Hughes Medical Institute and Gene Expression Laboratory, Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA. Biological Sciences Graduate Program, UCSD, 9500 Gilman Drive, La Jolla, CA 92037, USA. ; Peptide Biology Laboratory, Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA. ; Howard Hughes Medical Institute and Gene Expression Laboratory, Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA. pfaff@salk.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26680198" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Gene Expression Regulation ; Gene Regulatory Networks ; Mice ; Mice, Knockout ; MicroRNAs/genetics/*physiology ; Motor Neuron Disease/*genetics/physiopathology ; Motor Neurons/metabolism/pathology/*physiology ; Neurodegenerative Diseases/*genetics/pathology ; Spinal Cord/metabolism/physiopathology
    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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 4
    facet.materialart.
    Unknown
    GENE REGULATION. Discrete functions of nuclear receptor Rev-erbalpha couple metabolism to the clock (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-06-06
    Description: Circadian and metabolic physiology are intricately intertwined, as illustrated by Rev-erbalpha, a transcription factor (TF) that functions both as a core repressive component of the cell-autonomous clock and as a regulator of metabolic genes. Here, we show that Rev-erbalpha modulates the clock and metabolism by different genomic mechanisms. Clock control requires Rev-erbalpha to bind directly to the genome at its cognate sites, where it competes with activating ROR TFs. By contrast, Rev-erbalpha regulates metabolic genes primarily by recruiting the HDAC3 co-repressor to sites to which it is tethered by cell type-specific transcription factors. Thus, direct competition between Rev-erbalpha and ROR TFs provides a universal mechanism for self-sustained control of the molecular clock across all tissues, whereas Rev-erbalpha uses lineage-determining factors to convey a tissue-specific epigenomic rhythm that regulates metabolism tailored to the specific need of that tissue.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4613749/" 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/PMC4613749/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Yuxiang -- Fang, Bin -- Emmett, Matthew J -- Damle, Manashree -- Sun, Zheng -- Feng, Dan -- Armour, Sean M -- Remsberg, Jarrett R -- Jager, Jennifer -- Soccio, Raymond E -- Steger, David J -- Lazar, Mitchell A -- F30 DK104513/DK/NIDDK NIH HHS/ -- F32 DK102284/DK/NIDDK NIH HHS/ -- K08 DK094968/DK/NIDDK NIH HHS/ -- P30 DK019525/DK/NIDDK NIH HHS/ -- P30 DK050306/DK/NIDDK NIH HHS/ -- P30 DK19525/DK/NIDDK NIH HHS/ -- R00 DK099443/DK/NIDDK NIH HHS/ -- R01 DK045586/DK/NIDDK NIH HHS/ -- R01 DK098542/DK/NIDDK NIH HHS/ -- R01 DK45586/DK/NIDDK NIH HHS/ -- T32 GM0008275/GM/NIGMS NIH HHS/ -- T32 GM008275/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2015 Jun 26;348(6242):1488-92. doi: 10.1126/science.aab3021. Epub 2015 Jun 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, Department of Genetics, and the Institute for Diabetes, Obesity, and Metabolism, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. ; Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, Department of Genetics, and the Institute for Diabetes, Obesity, and Metabolism, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. Department of Molecular and Cellular Biology, Division of Diabetes, Endocrinology and Metabolism, Department of Medicine, Baylor College of Medicine, Houston, TX 77030, USA. ; Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, Department of Genetics, and the Institute for Diabetes, Obesity, and Metabolism, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. lazar@mail.med.upenn.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26044300" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CLOCK Proteins/*genetics ; Circadian Clocks/*genetics ; Circadian Rhythm/*genetics ; *Gene Expression Regulation ; Hepatocyte Nuclear Factor 6/metabolism ; Histone Deacetylases/*metabolism ; Lipid Metabolism/genetics ; Liver/metabolism ; Male ; Metabolism/*genetics ; Mice, Inbred C57BL ; Mice, Knockout ; Nuclear Receptor Subfamily 1, Group D, Member 1/genetics/*metabolism ; Nuclear Receptor Subfamily 1, Group F, Member 1/metabolism ; Organ Specificity ; Protein Binding ; Tissue Distribution
    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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 5
    facet.materialart.
    Unknown
    CTCF establishes discrete functional chromatin domains at the Hox clusters during differentiation (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-02-28
    Description: Polycomb and Trithorax group proteins encode the epigenetic memory of cellular positional identity by establishing inheritable domains of repressive and active chromatin within the Hox clusters. Here we demonstrate that the CCCTC-binding factor (CTCF) functions to insulate these adjacent yet antagonistic chromatin domains during embryonic stem cell differentiation into cervical motor neurons. Deletion of CTCF binding sites within the Hox clusters results in the expansion of active chromatin into the repressive domain. CTCF functions as an insulator by organizing Hox clusters into spatially disjoint domains. Ablation of CTCF binding disrupts topological boundaries such that caudal Hox genes leave the repressed domain and become subject to transcriptional activation. Hence, CTCF is required to insulate facultative heterochromatin from impinging euchromatin to produce discrete positional identities.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4428148/" 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/PMC4428148/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Narendra, Varun -- Rocha, Pedro P -- An, Disi -- Raviram, Ramya -- Skok, Jane A -- Mazzoni, Esteban O -- Reinberg, Danny -- GM-64844/GM/NIGMS NIH HHS/ -- GM086852/GM/NIGMS NIH HHS/ -- GM112192/GM/NIGMS NIH HHS/ -- P30 CA016087/CA/NCI NIH HHS/ -- R01 GM086852/GM/NIGMS NIH HHS/ -- R01 GM112192/GM/NIGMS NIH HHS/ -- R01 HD079682/HD/NICHD NIH HHS/ -- R01HD079682/HD/NICHD NIH HHS/ -- R37-37120/PHS HHS/ -- T32 GM007238/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2015 Feb 27;347(6225):1017-21. doi: 10.1126/science.1262088.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Chevy Chase, MD 20815, USA. Department of Biochemistry and Molecular Pharmacology, New York University School of Medicine, New York, NY 10016, USA. ; Department of Pathology, New York University School of Medicine, New York, NY 10016, USA. ; Department of Biology, New York University, New York, NY 10003, USA. ; Department of Biology, New York University, New York, NY 10003, USA. danny.reinberg@nyumc.org eom204@nyu.edu. ; Howard Hughes Medical Institute, Chevy Chase, MD 20815, USA. Department of Biochemistry and Molecular Pharmacology, New York University School of Medicine, New York, NY 10016, USA. danny.reinberg@nyumc.org eom204@nyu.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25722416" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation/*genetics ; Chromatin/chemistry/genetics/*metabolism ; Dogs ; Embryonic Stem Cells/*cytology ; *Gene Expression Regulation ; *Genes, Homeobox ; Humans ; Mice ; Motor Neurons/*cytology ; Multigene Family ; Neck ; Protein Structure, Tertiary ; Rats ; Repressor Proteins/chemistry/genetics/*metabolism
    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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 6
    facet.materialart.
    Unknown
    The Symbiodinium kawagutii genome illuminates dinoflagellate gene expression and coral symbiosis (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-11-07
    Description: Dinoflagellates are important components of marine ecosystems and essential coral symbionts, yet little is known about their genomes. We report here on the analysis of a high-quality assembly from the 1180-megabase genome of Symbiodinium kawagutii. We annotated protein-coding genes and identified Symbiodinium-specific gene families. No whole-genome duplication was observed, but instead we found active (retro)transposition and gene family expansion, especially in processes important for successful symbiosis with corals. We also documented genes potentially governing sexual reproduction and cyst formation, novel promoter elements, and a microRNA system potentially regulating gene expression in both symbiont and coral. We found biochemical complementarity between genomes of S. kawagutii and the anthozoan Acropora, indicative of host-symbiont coevolution, providing a resource for studying the molecular basis and evolution of coral symbiosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lin, Senjie -- Cheng, Shifeng -- Song, Bo -- Zhong, Xiao -- Lin, Xin -- Li, Wujiao -- Li, Ling -- Zhang, Yaqun -- Zhang, Huan -- Ji, Zhiliang -- Cai, Meichun -- Zhuang, Yunyun -- Shi, Xinguo -- Lin, Lingxiao -- Wang, Lu -- Wang, Zhaobao -- Liu, Xin -- Yu, Sheng -- Zeng, Peng -- Hao, Han -- Zou, Quan -- Chen, Chengxuan -- Li, Yanjun -- Wang, Ying -- Xu, Chunyan -- Meng, Shanshan -- Xu, Xun -- Wang, Jun -- Yang, Huanming -- Campbell, David A -- Sturm, Nancy R -- Dagenais-Bellefeuille, Steve -- Morse, David -- AI056034/AI/NIAID NIH HHS/ -- AI073806/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2015 Nov 6;350(6261):691-4. doi: 10.1126/science.aad0408.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉State Key Laboratory of Marine Environmental Science and Marine Biodiversity and Global Change Research Center, Xiamen University, Xiamen 361101, China. Department of Marine Sciences, University of Connecticut, Groton, CT 06340, USA. senjie.lin@uconn.edu. ; Beijing Genomics Institute (BGI)-Shenzhen, Shenzhen, 518083, China. Hong Kong University (HKU)-BGI Bioinformatics Algorithms and Core Technology Research Laboratory, The Computer Science Department, The University of Hong Kong, Hong Kong, China. School of Biological Sciences, The University of Hong Kong, Pokfulam, Hong Kong, China. ; Beijing Genomics Institute (BGI)-Shenzhen, Shenzhen, 518083, China. ; State Key Laboratory of Marine Environmental Science and Marine Biodiversity and Global Change Research Center, Xiamen University, Xiamen 361101, China. ; Department of Marine Sciences, University of Connecticut, Groton, CT 06340, USA. ; State Key Laboratory of Stress Cell Biology, School of Life Sciences, Xiamen University, Xiamen 361101, China. ; Bioinformatics Institute, Agency for Science, Technology and Research, Singapore. ; Beijing Genomics Institute (BGI)-Shenzhen, Shenzhen, 518083, China. Department of Biology, University of Copenhagen, DK-2200 Copenhagen, Denmark. Princess Al Jawhara Center of Excellence in the Research of Hereditary Disorders, King Abdulaziz University, Jeddah, Saudi Arabia. ; Beijing Genomics Institute (BGI)-Shenzhen, Shenzhen, 518083, China. Princess Al Jawhara Center of Excellence in the Research of Hereditary Disorders, King Abdulaziz University, Jeddah, Saudi Arabia. James D. Watson Institute of Genome Science, Hangzhou, China. ; Department of Microbiology, Immunology, and Molecular Genetics, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, CA 90095, USA. ; Institut de Recherche en Biologie Vegetale, Departement de Sciences Biologiques, Universite de Montreal, Montreal, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26542574" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anthozoa/*physiology ; Biological Evolution ; *Coral Reefs ; Dinoflagellida/*genetics ; *Gene Expression Regulation ; Gene Targeting ; *Genome, Protozoan ; MicroRNAs/genetics ; Symbiosis/*genetics
    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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 7
    facet.materialart.
    Unknown
    Molecular biology. Epigenetic islands in a genetic ocean (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-11-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schubeler, Dirk -- New York, N.Y. -- Science. 2012 Nov 9;338(6108):756-7. doi: 10.1126/science.1227243.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Friedrich Miescher Institute for Biomedical Research, Basel, Switzerland. dirk@fmi.ch〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23139324" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; *CpG Islands ; *DNA Methylation ; DNA-Binding Proteins/metabolism ; Enhancer Elements, Genetic ; *Epigenesis, Genetic ; *Gene Expression Regulation ; Humans ; Promoter Regions, Genetic ; Transcription Factors/metabolism
    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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 8
    facet.materialart.
    Unknown
    C/EBP transcription factors mediate epicardial activation during heart development and injury (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-11-20
    Description: The epicardium encapsulates the heart and functions as a source of multipotent progenitor cells and paracrine factors essential for cardiac development and repair. Injury of the adult heart results in reactivation of a developmental gene program in the epicardium, but the transcriptional basis of epicardial gene expression has not been delineated. We established a mouse embryonic heart organ culture and gene expression system that facilitated the identification of epicardial enhancers activated during heart development and injury. Epicardial activation of these enhancers depends on a combinatorial transcriptional code centered on CCAAT/enhancer binding protein (C/EBP) transcription factors. Disruption of C/EBP signaling in the adult epicardium reduced injury-induced neutrophil infiltration and improved cardiac function. These findings reveal a transcriptional basis for epicardial activation and heart injury, providing a platform for enhancing cardiac regeneration.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3613149/" 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/PMC3613149/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, Guo N -- Thatcher, Jeffrey E -- McAnally, John -- Kong, Yongli -- Qi, Xiaoxia -- Tan, Wei -- DiMaio, J Michael -- Amatruda, James F -- Gerard, Robert D -- Hill, Joseph A -- Bassel-Duby, Rhonda -- Olson, Eric N -- 1K99HL114738/HL/NHLBI NIH HHS/ -- HL100401-01/HL/NHLBI NIH HHS/ -- K99 HL114738/HL/NHLBI NIH HHS/ -- R01 HL077439/HL/NHLBI NIH HHS/ -- R01 HL093039/HL/NHLBI NIH HHS/ -- R01 HL111665/HL/NHLBI NIH HHS/ -- U01 HL100401/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2012 Dec 21;338(6114):1599-603. doi: 10.1126/science.1229765. Epub 2012 Nov 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23160954" target="_blank"〉PubMed〈/a〉
    Keywords: Aldehyde Oxidoreductases/genetics/metabolism ; Animals ; Binding Sites ; CCAAT-Enhancer-Binding Protein-beta/genetics/metabolism ; CCAAT-Enhancer-Binding Protein-delta/genetics/metabolism ; CCAAT-Enhancer-Binding Proteins/genetics/*metabolism ; Enhancer Elements, Genetic ; Female ; *Gene Expression Regulation ; Gene Expression Regulation, Developmental ; Heart/embryology/*physiopathology ; Male ; Mice ; Mice, Transgenic ; Models, Genetic ; Myocardial Contraction ; Myocardial Infarction/*genetics/metabolism ; Myocardial Reperfusion Injury/*genetics/metabolism ; Neutrophil Infiltration ; Oligonucleotide Array Sequence Analysis ; Organ Culture Techniques ; Pericardium/cytology/*embryology/*metabolism ; Signal Transduction ; Uroplakin III/genetics/metabolism ; Ventricular Remodeling ; WT1 Proteins/genetics/metabolism
    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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 9
    facet.materialart.
    Unknown
    Evidence of abundant purifying selection in humans for recently acquired regulatory functions (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-09-08
    Description: Although only 5% of the human genome is conserved across mammals, a substantially larger portion is biochemically active, raising the question of whether the additional elements evolve neutrally or confer a lineage-specific fitness advantage. To address this question, we integrate human variation information from the 1000 Genomes Project and activity data from the ENCODE Project. A broad range of transcribed and regulatory nonconserved elements show decreased human diversity, suggesting lineage-specific purifying selection. Conversely, conserved elements lacking activity show increased human diversity, suggesting that some recently became nonfunctional. Regulatory elements under human constraint in nonconserved regions were found near color vision and nerve-growth genes, consistent with purifying selection for recently evolved functions. Our results suggest continued turnover in regulatory regions, with at least an additional 4% of the human genome subject to lineage-specific constraint.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4104271/" 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/PMC4104271/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ward, Lucas D -- Kellis, Manolis -- R01 HG004037/HG/NHGRI NIH HHS/ -- R01HG004037/HG/NHGRI NIH HHS/ -- RC1 HG005334/HG/NHGRI NIH HHS/ -- RC1HG005334/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2012 Sep 28;337(6102):1675-8. Epub 2012 Sep 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Computer Science and Artificial Intelligence Laboratory, Massachusetts Institute of Technology (MIT), Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22956687" target="_blank"〉PubMed〈/a〉
    Keywords: Conserved Sequence ; Disease/genetics ; *Gene Expression Regulation ; *Genetic Variation ; Genome, Human/*genetics ; Humans ; Polymorphism, Single Nucleotide ; Regulatory Sequences, Nucleic Acid/*genetics ; *Selection, Genetic ; Transcription, Genetic
    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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 10
    facet.materialart.
    Unknown
    Gene expression. MicroRNA control of protein expression noise (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-04-04
    Description: MicroRNAs (miRNAs) repress the expression of many genes in metazoans by accelerating messenger RNA degradation and inhibiting translation, thereby reducing the level of protein. However, miRNAs only slightly reduce the mean expression of most targeted proteins, leading to speculation about their role in the variability, or noise, of protein expression. We used mathematical modeling and single-cell reporter assays to show that miRNAs, in conjunction with increased transcription, decrease protein expression noise for lowly expressed genes but increase noise for highly expressed genes. Genes that are regulated by multiple miRNAs show more-pronounced noise reduction. We estimate that hundreds of (lowly expressed) genes in mouse embryonic stem cells have reduced noise due to substantial miRNA regulation. Our findings suggest that miRNAs confer precision to protein expression and thus offer plausible explanations for the commonly observed combinatorial targeting of endogenous genes by multiple miRNAs, as well as the preferential targeting of lowly expressed genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schmiedel, Jorn M -- Klemm, Sandy L -- Zheng, Yannan -- Sahay, Apratim -- Bluthgen, Nils -- Marks, Debora S -- van Oudenaarden, Alexander -- New York, N.Y. -- Science. 2015 Apr 3;348(6230):128-32. doi: 10.1126/science.aaa1738.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Integrative Research Institute for the Life Sciences and Institute for Theoretical Biology, Humboldt Universitat, 10115 Berlin, Germany. Institute of Pathology, Charite-Universitatsmedizin, 10117 Berlin, Germany. Department of Physics, Massachusetts Institute of Technology (MIT), Cambridge MA 02139, USA. ; Department of Electrical Engineering and Computer Science, MIT, Cambridge, MA 02139, USA. ; Department of Physics, Massachusetts Institute of Technology (MIT), Cambridge MA 02139, USA. ; Integrative Research Institute for the Life Sciences and Institute for Theoretical Biology, Humboldt Universitat, 10115 Berlin, Germany. Institute of Pathology, Charite-Universitatsmedizin, 10117 Berlin, Germany. nils.bluethgen@charite.de debbie@hms.harvard.edu a.vanoudenaarden@hubrecht.eu. ; Department of Systems Biology, Harvard Medical School, Longwood Avenue, Boston, MA 02115, USA. nils.bluethgen@charite.de debbie@hms.harvard.edu a.vanoudenaarden@hubrecht.eu. ; Department of Physics, Massachusetts Institute of Technology (MIT), Cambridge MA 02139, USA. Department of Biology, MIT, Cambridge, MA 02139, USA. Hubrecht Institute, Royal Netherlands Academy of Arts and Sciences, and University Medical Center Utrecht, Uppsalalaan 8, 3584 CT, Utrecht, Netherlands. nils.bluethgen@charite.de debbie@hms.harvard.edu a.vanoudenaarden@hubrecht.eu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25838385" target="_blank"〉PubMed〈/a〉
    Keywords: 3' Untranslated Regions/genetics/physiology ; Animals ; Embryonic Stem Cells/metabolism ; *Gene Expression Regulation ; Mice ; MicroRNAs/genetics/*physiology ; Models, Genetic ; Protein Biosynthesis/*genetics ; RNA, Messenger/biosynthesis ; Single-Cell Analysis ; Transcription, Genetic
    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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...