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John W. Beaber

Researcher at University of California, Berkeley

Publications -  6
Citations -  400

John W. Beaber is an academic researcher from University of California, Berkeley. The author has contributed to research in topics: Bacillus anthracis & Phage display. The author has an hindex of 5, co-authored 6 publications receiving 366 citations. Previous affiliations of John W. Beaber include Howard Hughes Medical Institute.

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Genomic and Functional Analyses of SXT, an Integrating Antibiotic Resistance Gene Transfer Element Derived from Vibrio cholerae

TL;DR: Two SXT loci, designated setC and setD, whose predicted amino acid sequences were similar to those of the flagellar regulators FlhC and FlhD, were found to encode regulators that activate the transcription of genes required for SXT excision and transfer.
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Discovery of diverse and functional antibodies from large human repertoire antibody libraries

TL;DR: Both the Fab and scFv libraries show robust sequence diversity in target-specific binders and differential V-gene usage for each target tested, supporting the use of libraries that utilize multiple display formats and V- gene utilization to maximize antibody-binding diversity.
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Killed but Metabolically Active Bacillus anthracis Vaccines Induce Broad and Protective Immunity against Anthrax

TL;DR: Data demonstrate that KBMA anthrax vaccines are well tolerated and elicit potent protective immune responses, and the use of KBMA vaccines may be broadly applicable to bacterial pathogens, especially those for which the correlates of protective immunity are unknown.
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Identification of the bacterial protein FtsX as a unique target of chemokine-mediated antimicrobial activity against Bacillus anthracis.

TL;DR: It is reported that disruption of the gene ftsX, which encodes the transmembrane domain of a putative ATP-binding cassette transporter, affords resistance to CXCL10-mediated antimicrobial effects against vegetative B. anthracis bacilli, and is the first description of a bacterial component critically involved in the ability of host chemokines to target and kill a bacterial pathogen.