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William M. Shafer

Researcher at Emory University

Publications -  175
Citations -  10117

William M. Shafer is an academic researcher from Emory University. The author has contributed to research in topics: Neisseria gonorrhoeae & Efflux. The author has an hindex of 53, co-authored 166 publications receiving 8978 citations. Previous affiliations of William M. Shafer include Imperial College London & United States Department of Veterans Affairs.

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Journal ArticleDOI

Antimicrobial Resistance in Neisseria gonorrhoeae in the 21st Century: Past, Evolution, and Future

TL;DR: By understanding the evolution, emergence, and spread of AMR in N. gonorrhoeae, including its molecular and phenotypic mechanisms, resistance to antimicrobials used clinically can be anticipated, and future methods for genetic testing for AMR might permit region-specific and tailor-made antimicrobial therapy, the design of novel antimicroBials to circumvent the resistance problems can be undertaken more rationally.
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Modulation of Neisseria gonorrhoeae susceptibility to vertebrate antibacterial peptides due to a member of the resistance/nodulation/division efflux pump family

TL;DR: Genetic and biochemical evidence is reported that gonococcal susceptibility to the lethal action of PG-1 and other structurally unrelated antibacterial peptides, including a peptide that is expressed constitutively by human granulocytes and testis and inducibly by keratinocytes, is modulated by an energy-dependent efflux system termed mtr.
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Resistance of Neisseria gonorrhoeae to antimicrobial hydrophobic agents is modulated by the mtrRCDE efflux system

TL;DR: It is proposed that the 13 bp inverted-repeat sequence represents a transcriptional control element that regulates expression of the mtrRCDE gene complex, thereby modulating levels of gonococcal susceptibility to HAs.
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Cationic Antimicrobial Peptide Resistance in Neisseria meningitidis

TL;DR: Data indicated that meningococci utilize multiple mechanisms including the action of the MtrC-MtrD- MtrE efflux pump and lipid A modification as well as the type IV pilin secretion system to modulate levels of CAMP resistance.