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Gregory Dolganov

Researcher at University of California, San Francisco

Publications -  41
Citations -  7156

Gregory Dolganov is an academic researcher from University of California, San Francisco. The author has contributed to research in topics: Gene expression & Mycobacterium tuberculosis. The author has an hindex of 28, co-authored 39 publications receiving 6782 citations. Previous affiliations of Gregory Dolganov include Cardiovascular Institute Hospital & Cardiovascular Institute of the South.

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Transcriptional Adaptation of Mycobacterium tuberculosis within Macrophages Insights into the Phagosomal Environment

TL;DR: The microbial transcriptome served as a bioprobe of the MTB phagosomal environment, showing it to be nitrosative, oxidative, functionally hypoxic, carbohydrate poor, and capable of perturbing the pathogen's cell envelope.
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Inhibition of Respiration by Nitric Oxide Induces a Mycobacterium tuberculosis Dormancy Program

TL;DR: It is shown that O2 and low, nontoxic concentrations of NO competitively modulate the expression of a 48-gene regulon, which is expressed in vivo and prepares bacilli for survival during long periods of in vitro dormancy, and leads to a model postulating that, within granulomas, inhibition of respiration by NO production and O2 limitation constrains M. tuberculosis replication rates in persons with latent tuberculosis.
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Direct effects of interleukin-13 on epithelial cells cause airway hyperreactivity and mucus overproduction in asthma

TL;DR: The results demonstrate the importance of direct effects of IL-13 on epithelial cells in causing two central features of asthma, including airway hyperreactivity and mucus overproduction.
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Mild and moderate asthma is associated with airway goblet cell hyperplasia and abnormalities in mucin gene expression.

TL;DR: It is concluded that even mild asthma is associated with goblet cell hyperplasia and increased stored mucin in the airway epithelium, whereas moderate asthma isassociated with increased stored bronchial mucin and secreted mucin.
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Loss of integrin alpha(v)beta6-mediated TGF-beta activation causes Mmp12-dependent emphysema.

TL;DR: A pathway in which the loss of integrin-mediated activation of latent TGF-β causes age-dependent pulmonary emphysema through alterations of macrophage Mmp12 expression is uncovered and it is shown that a functional alteration in the T GF-β activation pathway affects susceptibility to this disease.