R
Robert D. Fleischmann
Researcher at J. Craig Venter Institute
Publications - 68
Citations - 23631
Robert D. Fleischmann is an academic researcher from J. Craig Venter Institute. The author has contributed to research in topics: Genome & Gene. The author has an hindex of 38, co-authored 68 publications receiving 23105 citations. Previous affiliations of Robert D. Fleischmann include Human Genome Sciences & Philips.
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Journal ArticleDOI
The complete genome sequence of the gastric pathogen Helicobacter pylori
Jean-F. Tomb,Owen White,Anthony R. Kerlavage,Rebecca A. Clayton,Granger G. Sutton,Robert D. Fleischmann,Karen A. Ketchum,Hans-Peter Klenk,Steven R. Gill,Brian Dougherty,Karen E. Nelson,John Quackenbush,Lixin Zhou,Ewen F. Kirkness,Scott N. Peterson,Brendan J. Loftus,Delwood Richardson,Robert J. Dodson,Hanif Khalak,Anna Glodek,Keith McKenney,Lisa M. Fitzegerald,Norman H. Lee,Mark Raymond Adams,Erin Hickey,Douglas E. Berg,Jeanine D. Gocayne,Teresa Utterback,Jeremy Peterson,Jenny M. Kelley,Matthew D. Cotton,J. Weidman,Claire Fujii,Cheryl Bowman,Larry Watthey,Erik Wallin,William S. Hayes,Mark Borodovsky,Peter D. Karp,Hamilton O. Smith,Claire M. Fraser,J. Craig Venter +41 more
TL;DR: Sequence analysis indicates that H. pylori has well-developed systems for motility, for scavenging iron, and for DNA restriction and modification, and consistent with its restricted niche, it has a few regulatory networks, and a limited metabolic repertoire and biosynthetic capacity.
Journal ArticleDOI
The minimal gene complement of Mycoplasma genitalium
Claire M. Fraser,Jeannine D. Gocayne,Owen White,Mark Raymond Adams,Rebecca A. Clayton,Robert D. Fleischmann,Carol J. Bult,Anthony R. Kerlavage,Granger G. Sutton,Jenny M. Kelley,Janice L. Fritchman,Janice Weidman,Keith V. Small,Mina Sandusky,Joyce Fuhrmann,David Nguyen,Teresa Utterback,D. Saudek,Cheryl Phillips,Joseph M. Merrick,J F Tomb,Brian Dougherty,Kenneth F. Bott,Ping Chuan Hu,Thomas Lucier,Scott N. Peterson,Hamilton O. Smith,Clyde A. Hutchison,J. Craig Venter +28 more
TL;DR: Comparison of the Mycoplasma genitalium genome to that of Haemophilus influenzae suggests that differences in genome content are reflected as profound differences in physiology and metabolic capacity between these two organisms.
Journal ArticleDOI
Genomic sequence of a Lyme disease spirochaete, Borrelia burgdorferi
Claire M. Fraser,Sherwood R. Casjens,Wai Mun Huang,Granger G. Sutton,Rebecca A. Clayton,Raju Lathigra,Owen White,Karen A. Ketchum,Robert J. Dodson,Erin Hickey,Michelle L. Gwinn,Brian Dougherty,J F Tomb,Robert D. Fleischmann,Delwood Richardson,Jeremy Peterson,Anthony R. Kerlavage,John Quackenbush,Steven L. Salzberg,Mark S. Hanson,René Van Vugt,Nanette Palmer,Mark Raymond Adams,Jeannine D. Gocayne,Janice Weidman,Teresa Utterback,Larry Watthey,Lisa McDonald,Patricia Artiach,Cheryl Bowman,Stacey Garland,Claire Fujii,Matthew D. Cotton,Kurt Horst,Kevin Roberts,Bonnie Hatch,Hamilton O. Smith,J. Craig Venter +37 more
TL;DR: The genome of the bacterium Borrelia burgdorferi B31, the aetiologic agent of Lyme disease, contains a linear chromosome of 910,725 base pairs and at least 17 linear and circular plasmids with a combined size of more than 533,000 base pairs, which suggest their limited metabolic capacities reflect convergent evolution by gene loss from more metabolically competent progenitors.
Journal ArticleDOI
Mutation of a mutL homolog in hereditary colon cancer
Nickolas Papadopoulos,Nicholas C. Nicolaides,Ying Fei Wei,Steven M. Ruben,Kenneth C. Carter,Craig A. Rosen,William A. Haseltine,Robert D. Fleischmann,Claire M. Fraser,Mark Raymond Adams,J. Craig Venter,Stanley R. Hamilton,Gloria M. Petersen,Patrice Watson,Henry T. Lynch,Päivi Peltomäki,Jukka-Pekka Mecklin,Albert de la Chapelle,Kenneth W. Kinzler,Bert Vogelstein +19 more
TL;DR: A search of a large database of expressed sequence tags derived from random complementary DNA clones revealed three additional human mismatch repair genes, all related to the bacterial mutL gene, demonstrating that this gene is responsible for HNPCC.
Journal ArticleDOI
Mutations of two PMS homologues in hereditary nonpolyposis colon cancer.
Nicholas C. Nicolaides,Nickolas Papadopoulos,Bo Liu,Ying Fei Weit,Kenneth C. Carter,Steven M. Ruben,Craig A. Rosen,William A. Haseltine,Robert D. Fleischmann,Claire M. Fraser,Mark Raymond Adams,J. Craig Venter,Malcolm G. Dunlop,Stanley R. Hamilton,Gloria M. Petersen,Albert de la Chapelle,Bert Vogelstein,Kenneth W. Kinzler +17 more
TL;DR: Two additional homologues of the prokaryotic mutL gene were found to be mutated in the germline of HNPCC patients, which doubles the number of genes implicated in H NPCC and may help explain the relatively high incidence of this disease.