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  • 1
    In: mBio, American Society for Microbiology, Vol. 7, No. 6 ( 2016-12-30)
    Abstract: This longitudinal study provides an opportunity to describe shifts in the microbiomes of individual patients who suffer from ulcerative colitis (UC) prior to and following inflammation. Pouchitis serves as a model for UC with a predictable incidence of disease onset and enables prospective longitudinal investigations of UC etiology prior to inflammation. Because of insufficient criteria for predicting which patients will develop UC or pouchitis, the interpretation of cross-sectional study designs suffers from lack of information about the microbiome structure and host gene expression patterns that directly correlate with the onset of disease. Our unique longitudinal study design allows each patient to serve as their own control, providing information about the state of the microbiome and host prior to and during the course of disease. Of significance to the broader community, this study identifies microbial strains that may have genetic elements that trigger the onset of disease in susceptible hosts.
    Type of Medium: Online Resource
    ISSN: 2161-2129 , 2150-7511
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2016
    detail.hit.zdb_id: 2557172-2
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  • 2
    In: Journal of Bacteriology, American Society for Microbiology, Vol. 195, No. 11 ( 2013-06), p. 2509-2517
    Abstract: Sigma B (σ B ) is an alternative sigma factor that regulates the general stress response in Bacillus subtilis and in many other Gram-positive organisms. σ B activity in B. subtilis is tightly regulated via at least three distinct pathways within a complex signal transduction cascade in response to a variety of stresses, including environmental stress, energy stress, and growth at high or low temperatures. We probed the ability of fluoro-phenyl-styrene-sulfonamide (FPSS), a small-molecule inhibitor of σ B activity in Listeria monocytogenes , to inhibit σ B activity in B. subtilis through perturbation of signal transduction cascades under various stress conditions. FPSS inhibited the activation of σ B in response to multiple categories of stress known to induce σ B activity in B. subtilis . Specifically, FPSS prevented the induction of σ B activity in response to energy stress, including entry into stationary phase, phosphate limitation, and azide stress. FPSS also inhibited chill induction of σ B activity in a Δ rsbV strain, suggesting that FPSS does not exclusively target the RsbU and RsbP phosphatases or the anti–anti-sigma factor RsbV, all of which contribute to posttranslational regulation of σ B activity. Genetic and biochemical experiments, including artificial induction of σ B , analysis of the phosphorylation state of the anti–anti-sigma factor RsbV, and in vitro transcription assays, indicate that while FPSS does not bind directly to σ B to inhibit activity, it appears to prevent the release of B. subtilis σ B from its anti-sigma factor RsbW.
    Type of Medium: Online Resource
    ISSN: 0021-9193 , 1098-5530
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2013
    detail.hit.zdb_id: 1481988-0
    SSG: 12
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