His primary areas of investigation include Microbiology, Streptococcus pneumoniae, Virulence, Pneumolysin and Pneumococcal infections. His Microbiology research integrates issues from Gene, Escherichia coli, Virology and Immunology. His work is dedicated to discovering how Streptococcus pneumoniae, Serotype are connected with Genotype and other disciplines.
His research integrates issues of Mutation, Autolysin, Mutant, Mutagenesis and Molecular biology in his study of Virulence. His Pneumolysin research is multidisciplinary, incorporating perspectives in Virulence factor, Complement system, Antigen, TLR4 and Cytolysin. While the research belongs to areas of Pneumococcal infections, James C. Paton spends his time largely on the problem of Toxoid, intersecting his research to questions surrounding Adjuvant.
His primary areas of study are Microbiology, Streptococcus pneumoniae, Virulence, Pneumolysin and Escherichia coli. His Microbiology research is mostly focused on the topic Toxin. His Streptococcus pneumoniae research incorporates themes from Serotype, Immunology and Antigen.
His biological study spans a wide range of topics, including Pathogen, Pathogenesis, Mutation, Mutagenesis and Autolysin. James C. Paton has included themes like Virulence factor, Streptococcaceae and Toxoid in his Pneumolysin study. In his research on the topic of Escherichia coli, Nucleic acid sequence and Unfolded protein response is strongly related with Molecular biology.
James C. Paton mostly deals with Microbiology, Streptococcus pneumoniae, Cell biology, Endoplasmic reticulum and Unfolded protein response. His Microbiology research includes themes of Shiga toxin, Escherichia coli and Mutant. His Streptococcus pneumoniae research is multidisciplinary, incorporating elements of Serotype, Virology and Gene, Virulence.
His Virulence study is concerned with Biochemistry in general. As a member of one scientific family, James C. Paton mostly works in the field of Cell biology, focusing on Cellular differentiation and, on occasion, Stem cell. His studies deal with areas such as Protein folding, Chaperone, Intracellular and Signal peptide as well as Endoplasmic reticulum.
His main research concerns Microbiology, Streptococcus pneumoniae, Cell biology, Biochemistry and Endoplasmic reticulum. His study in Pneumolysin and Antibiotic resistance is carried out as part of his Microbiology studies. His research in Streptococcus pneumoniae intersects with topics in Pathogen, Immune system and Virulence.
His Virulence research is multidisciplinary, relying on both Molecular genetics and Mutant. James C. Paton combines subjects such as XBP1, Receptor, Messenger RNA and Protein kinase domain with his study of Cell biology. The various areas that James C. Paton examines in his Endoplasmic reticulum study include Heat shock protein, Chaperone, Pancreas, Proinsulin and Cellular compartment.
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Pathogenesis and Diagnosis of Shiga Toxin-Producing Escherichia coli Infections
James C. Paton;Adrienne W. Paton.
Clinical Microbiology Reviews (1998)
Detection and characterization of Shiga toxigenic Escherichia coli by using multiplex PCR assays for stx1, stx2, eaeA, enterohemorrhagic E. coli hlyA, rfbO111, and rfbO157
Adrienne W. Paton;James C. Paton.
Journal of Clinical Microbiology (1998)
The role of Streptococcus pneumoniae virulence factors in host respiratory colonization and disease.
Aras Kadioglu;Jeffrey N. Weiser;James C. Paton;Peter W. Andrew.
Nature Reviews Microbiology (2008)
Recognition of pneumolysin by Toll-like receptor 4 confers resistance to pneumococcal infection.
Richard Malley;Philipp Henneke;Sarah C. Morse;Michael J. Cieslewicz.
Proceedings of the National Academy of Sciences of the United States of America (2003)
Antibody Response to Pneumococcal Vaccination in Children Younger than Five Years of Age
R. M. Douglas;J. C. Paton;S. J. Duncan;D. J. Hansman.
The Journal of Infectious Diseases (1983)
The classical pathway is the dominant complement pathway required for innate immunity to Streptococcus pneumoniae infection in mice
Jeremy S. Brown;Tracy Hussell;Sarah M. Gilliland;David W. Holden.
Proceedings of the National Academy of Sciences of the United States of America (2002)
Opposing unfolded-protein-response signals converge on death receptor 5 to control apoptosis.
Min Lu;David A. Lawrence;Scot Marsters;Diego Acosta-Alvear.
Reduced virulence of a defined pneumolysin-negative mutant of Streptococcus pneumoniae.
A M Berry;J Yother;D E Briles;D Hansman.
Infection and Immunity (1989)
Characterization of Saa, a Novel Autoagglutinating Adhesin Produced by Locus of Enterocyte Effacement-Negative Shiga-Toxigenic Escherichia coli Strains That Are Virulent for Humans
Adrienne W. Paton;Potjanee Srimanote;Matthew C. Woodrow;James C. Paton.
Infection and Immunity (2001)
Molecular microbiological investigation of an outbreak of hemolytic-uremic syndrome caused by dry fermented sausage contaminated with Shiga-like toxin-producing Escherichia coli.
A W Paton;R M Ratcliff;R M Doyle;J Seymour-Murray.
Journal of Clinical Microbiology (1996)
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