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Heidi B. Kaplan

Researcher at University of Texas Health Science Center at Houston

Publications -  52
Citations -  6507

Heidi B. Kaplan is an academic researcher from University of Texas Health Science Center at Houston. The author has contributed to research in topics: Myxococcus xanthus & Gene. The author has an hindex of 27, co-authored 50 publications receiving 5848 citations. Previous affiliations of Heidi B. Kaplan include Dartmouth College & Stanford University.

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Myxococcus xanthus dif Genes Are Required for Biogenesis of Cell Surface Fibrils Essential for Social Gliding Motility

TL;DR: It is demonstrated here that M. xanthus dif genes are required for the biogenesis of fibrils but not for that of type IV pili, and the developmental defects of dif mutants can be partially rescued by the addition of isolated fibril materials.
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Phage-Antibiotic Synergy Is Driven by a Unique Combination of Antibacterial Mechanism of Action and Stoichiometry

TL;DR: In this paper, a comprehensive analysis of phage-antibiotic interaction was performed against a pandemic drug-resistant clonal group of extraintestinal pathogenic Escherichia coli (ExPEC) with antibiotic levels blanketing the MIC across seven orders of viral titers.
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The Myxococcus xanthus lipopolysaccharide O‐antigen is required for social motility and multicellular development

TL;DR: It is reported here that the developmental and motility phenotypes of four mutants each containing different Tn5 insertions in LPS O‐antigen biosynthesis genes are similar to those of the original sasA locus mutants.
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Exopolysaccharide biosynthesis genes required for social motility in Myxococcus xanthus.

TL;DR: Genetic mutagenesis analysis indicates that the whole eps region is involved in the biosynthesis of fibrils and fibril EPS, confirming the involvement of these genes in M. xanthus EPS biogenesis.
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Toxin Synthesis by Clostridium difficile Is Regulated through Quorum Signaling

TL;DR: It is shown that C. difficile toxin synthesis is regulated by an accessory gene regulator quorum-signaling system, which is mediated through a small (<1,000-Da) thiolactone that can be detected directly in stools of CDI patients.