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Amanda L. Jones
Researcher at University of Washington
Publications - 15
Citations - 2584
Amanda L. Jones is an academic researcher from University of Washington. The author has contributed to research in topics: Streptococcus agalactiae & Virulence. The author has an hindex of 12, co-authored 14 publications receiving 2257 citations. Previous affiliations of Amanda L. Jones include Boston Children's Hospital.
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Journal ArticleDOI
Genome analysis of multiple pathogenic isolates of Streptococcus agalactiae: Implications for the microbial “pan-genome”
Hervé Tettelin,Vega Masignani,Michael J. Cieslewicz,Claudio Donati,Duccio Medini,Naomi L. Ward,Samuel V. Angiuoli,Jonathan Crabtree,Amanda L. Jones,A. Scott Durkin,Robert T. DeBoy,Tanja M. Davidsen,Marirosa Mora,Maria Scarselli,Immaculada Margarit Y Ros,Jeremy Peterson,Christopher R. Hauser,Jaideep P. Sundaram,William C. Nelson,Ramana Madupu,Lauren M. Brinkac,Robert J. Dodson,M. J. Rosovitz,Steven A. Sullivan,Sean C. Daugherty,Daniel H. Haft,Jeremy D. Selengut,Michelle L. Gwinn,Liwei Zhou,Nikhat Zafar,Hoda Khouri,Diana Radune,George Dimitrov,Kisha Watkins,Kevin J. B. O'Connor,Shannon Smith,Teresa Utterback,Owen White,Craig E. Rubens,Guido Grandi,Lawrence C. Madoff,Dennis L. Kasper,John L. Telford,Michael R. Wessels,Rino Rappuoli,Claire M. Fraser +45 more
TL;DR: The genomic sequence of six strains representing the five major disease-causing serotypes of Streptococcus agalactiae, the main cause of neonatal infection in humans, was generated and Mathematical extrapolation of the data suggests that the gene reservoir available for inclusion in the S. agalactic pan-genome is vast and that unique genes will continue to be identified even after sequencing hundreds of genomes.
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Identification of Streptococcus agalactiae virulence genes in the neonatal rat sepsis model using signature-tagged mutagenesis.
TL;DR: Signature‐tagged transposon mutagenesis was used to identify genes required for growth and survival of GBS in a neonatal rat sepsis infection model and revealed GBS genomic loci that encode a wide variety of functional gene classes, underscoring the diversity of bacterial processes required for the infection process.
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Staphylococcus aureus exploits cathelicidin antimicrobial peptides produced during early pneumonia to promote staphylokinase-dependent fibrinolysis.
TL;DR: Staphylokinase production may be a novel virulence mechanism by which S. aureus exploits cathelicidin to promote fibrinolysis, leading to enhanced bacterial dissemination and invasive infection.
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Penicillin-binding protein 1a promotes resistance of group B streptococcus to antimicrobial peptides.
TL;DR: This study is the first to identify a role for a PBP in resistance to host AMPs, encoded by ponA, and this novel function for PBP1a in promoting resistance of GBS to AMP did not involve an alteration in bacterial surface charge or peptidoglycan cross-linking.
Journal ArticleDOI
Penicillin-binding proteins in Streptococcus agalactiae: a novel mechanism for evasion of immune clearance
TL;DR: In this paper, the authors identified a mutant with a transposon insertion in the ponA gene that encoded an extra-cytoplasmic penicillin-binding protein PBP1a, a newly identified virulence trait for GBS that promotes resistance to phagocytic killing independent of capsular polysaccharide.