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Christophe Herman

Researcher at Baylor College of Medicine

Publications -  55
Citations -  3502

Christophe Herman is an academic researcher from Baylor College of Medicine. The author has contributed to research in topics: RNA polymerase & Transcription (biology). The author has an hindex of 28, co-authored 47 publications receiving 3077 citations. Previous affiliations of Christophe Herman include Baylor University & University of California, San Francisco.

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Degradation of sigma 32, the heat shock regulator in Escherichia coli, is governed by HflB.

TL;DR: The heat shock response in Escherichia coli is governed by the concentration of the highly unstable sigma factor sigma 32, and the essential protein HflB (FtsH), known to control proteolysis of the phage lambda cII protein, also governs sigma32 degradation.
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Regulon and promoter analysis of the E. coli heat-shock factor, σ32, reveals a multifaceted cellular response to heat stress

TL;DR: It is suggested that the heat-shock response protects the cell membrane and responds to its status: Fully 25% of sigma32 regulon members reside in the membrane and alter its functionality; moreover, a disproportionate fraction of overexpressed proteins that induce the response are membrane localized.
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Degradation of carboxy-terminal-tagged cytoplasmic proteins by the Escherichia coli protease HflB (FtsH)

TL;DR: It is shown that the ATP-dependent zinc protease HflB (FtsH) is involved in the degradation of four unstable derivatives of the amino-terminal domain of the lambdacI repressor: three with nonpolar pentapeptide tails and one with the SsrA tag (cI-SsrA).
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Microbial Genetic Composition Tunes Host Longevity.

TL;DR: Together, the results identified molecular targets for developing pro-longevity microbes and a bacterial metabolite acting on host mitochondria to promote longevity.
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A chaperone network controls the heat shock response in E. coli

TL;DR: It is demonstrated that increasing the level of GroEL/S leads to a decrease in sigma32 activity in vivo and this effect can be eliminated by co-overexpression of a Groel/S-specific substrate, and it is shown that depletion of Gro EL/S in vivo leads to up-regulation of s Sigma32 by increasing thelevel of sigma 32.