Institution
University of Maryland Biotechnology Institute
About: University of Maryland Biotechnology Institute is a based out in . It is known for research contribution in the topics: Gene & Population. The organization has 1565 authors who have published 2458 publications receiving 171434 citations. The organization is also known as: UMBI.
Topics: Gene, Population, Protein structure, Vibrio cholerae, Binding site
Papers published on a yearly basis
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TL;DR: MOLREP is an automated program for molecular replacement that utilizes a number of original approaches to rotational and translational search and data preparation that includes weighting of the X-ray data and search models, multi-copy search, fitting the model into electron density, structural superposition of two models and rigid-body refinement.
Abstract: MOLREP is an automated program for molecular replacement that utilizes a number of original approaches to rotational and translational search and data preparation. Since the first publication describing the program, MOLREP has acquired a variety of features that include weighting of the X-ray data and search models, multi-copy search, fitting the model into electron density, structural superposition of two models and rigid-body refinement. The program can run in a fully automatic mode using optimized parameters calculated from the input data.
3,073 citations
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Celera Corporation1, Centre national de la recherche scientifique2, Cornell University3, National Institutes of Health4, Bar-Ilan University5, TigerLogic6, University of California, Riverside7, Virginia Tech8, University of Notre Dame9, Wellcome Trust Sanger Institute10, University of Maryland Biotechnology Institute11, University of Crete12, European Bioinformatics Institute13, Sapienza University of Rome14, Pasteur Institute15
TL;DR: Analysis of the PEST strain of A. gambiae revealed strong evidence for about 14,000 protein-encoding transcripts, and prominent expansions in specific families of proteins likely involved in cell adhesion and immunity were noted.
Abstract: Anopheles gambiae is the principal vector of malaria, a disease that afflicts more than 500 million people and causes more than 1 million deaths each year. Tenfold shotgun sequence coverage was obtained from the PEST strain of A. gambiae and assembled into scaffolds that span 278 million base pairs. A total of 91% of the genome was organized in 303 scaffolds; the largest scaffold was 23.1 million base pairs. There was substantial genetic variation within this strain, and the apparent existence of two haplotypes of approximately equal frequency ("dual haplotypes") in a substantial fraction of the genome likely reflects the outbred nature of the PEST strain. The sequence produced a conservative inference of more than 400,000 single-nucleotide polymorphisms that showed a markedly bimodal density distribution. Analysis of the genome sequence revealed strong evidence for about 14,000 protein-encoding transcripts. Prominent expansions in specific families of proteins likely involved in cell adhesion and immunity were noted. An expressed sequence tag analysis of genes regulated by blood feeding provided insights into the physiological adaptations of a hematophagous insect.
2,033 citations
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TL;DR: The V. cholerae genomic sequence provides a starting point for understanding how a free-living, environmental organism emerged to become a significant human bacterial pathogen.
Abstract: Here we determine the complete genomic sequence of the Gram negative, g-Proteobacterium Vibrio cholerae El Tor N16961 to be 4,033,460 base pairs (bp). The genome consists of two circular chromosomes of 2,961,146 bp and 1,072,314 bp that together encode 3,885 open reading frames. The vast majority of recognizable genes for essential cell functions (such as DNA replication, transcription, translation and cell-wall biosynthesis) and pathogenicity (for example, toxins, surface antigens and adhesins) are located on the large chromosome. In contrast, the small chromosome contains a larger fraction (59%) of hypothetical genes compared with the large chromosome (42%), and also contains many more genes that appear to have origins other than the g-Proteobacteria. The small chromosome also carries a gene capture system (the integron island) and host ‘addiction’ genes that are typically found on plasmids; thus, the small chromosome may have originally been a megaplasmid that was captured by an ancestral Vibrio species. The V. cholerae genomic sequence provides a starting point for understanding how a free-living, environmental organism emerged to become a significant human bacterial pathogen.
1,785 citations
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Cornell University1, University of Maryland, College Park2, North Carolina State University3, University of Maryland Biotechnology Institute4, Harvard University5, University of Southern Mississippi6, Old Dominion University7, University of South Florida St. Petersburg8, Erasmus University Rotterdam9, University of Georgia10, University of South Carolina Aiken11
TL;DR: A dramatic global increase in the severity of coral bleaching in 1997-98 is coincident with high El Niño temperatures, which climate-mediated, physiological stresses may compromise host resistance and increase frequency of opportunistic diseases.
Abstract: Mass mortalities due to disease outbreaks have recently affected major taxa in the oceans. For closely monitored groups like corals and marine mammals, reports of the frequency of epidemics and the number of new diseases have increased recently. A dramatic global increase in the severity of coral bleaching in 1997—98 is coincident with high El Nino temperatures. Such climate-mediated, physiological stresses may compromise host resistance and increase frequency of opportunistic diseases. Where documented, new diseases typically have emerged through host or range shifts of known pathogens. Both climate and human activities may have also accelerated global transport of species, bringing together pathogens and previously unexposed host populations. T he oceans harbor enormous biodiver- sity by terrestrial terms (1), much of which is still poorly described taxo- nomically. Even less well known are the dy- namics of intermittent, ephemeral, threshold phenomena such as disease outbreaks. De- spite decades of intense study of the biolog- ical agents structuring natural communities, the ecological and evolutionary impact of diseases in the ocean remains unknown, even when these diseases affect economically and ecologically important species. The paucity of baseline and epidemiological information on normal disease levels in the ocean chal- lenges our ability to assess the novelty of a recent spate of disease outbreaks and to de- termine the relative importance of increased pathogen transmission versus decreased host resistance in facilitating the outbreaks. Our objectives here are to review the prevalence of diseases of marine taxa to evaluate wheth- er it can be concluded that there has been a recent increase. We also assess the contribut- ing roles of human activity and global cli- mate, and evaluate the role of the oceans as incubators and conveyors of human disease agents. Is There an Increase in Diseases in the Ocean?
1,778 citations
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TL;DR: Transformation of the cloned wild-type NPR1 gene into npr1 mutants not only restored the responsiveness to SAR induction with respect to PR-gene expression and resistance to infections, but also rendered the transgenic plants more resistant to infection by P. syringae in the absence of SAR induction.
1,449 citations
Authors
Showing all 1565 results
Name | H-index | Papers | Citations |
---|---|---|---|
Stanley B. Prusiner | 168 | 745 | 97528 |
Robert C. Gallo | 145 | 825 | 68212 |
Thomas J. Smith | 140 | 1775 | 113919 |
J. D. Hansen | 122 | 975 | 76198 |
Stephen Mann | 120 | 669 | 55008 |
Donald M. Bers | 118 | 570 | 52757 |
Jon Clardy | 116 | 983 | 56617 |
Rita R. Colwell | 115 | 781 | 55229 |
Joseph R. Lakowicz | 104 | 850 | 76257 |
Patrick M. Schlievert | 90 | 444 | 32037 |
Mitsuhiko Ikura | 89 | 316 | 34132 |
Jeremy Thorner | 87 | 234 | 29999 |
Lawrence E. Samelson | 87 | 209 | 27398 |
Jacques Ravel | 86 | 323 | 45793 |
W. J. Lederer | 79 | 213 | 25509 |