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Moira K. B. Whyte

Researcher at University of Edinburgh

Publications -  89
Citations -  3674

Moira K. B. Whyte is an academic researcher from University of Edinburgh. The author has contributed to research in topics: Inflammation & Idiopathic pulmonary fibrosis. The author has an hindex of 32, co-authored 85 publications receiving 2839 citations. Previous affiliations of Moira K. B. Whyte include Medical Research Council & University of Sheffield.

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Activation of hypoxia-inducible factor-1α (Hif-1α) delays inflammation resolution by reducing neutrophil apoptosis and reverse migration in a zebrafish inflammation model

TL;DR: It is demonstrated that Hif-1α regulates neutrophil function in complex ways during inflammation resolution in vivo, and site-directed mutagenesis of Hif in vivo reveals that hydroxylation of HIF-1 α by prolyl hydoxylases critically regulates the Hif pathway in zebrafish neutrophils.
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Genetic variants associated with susceptibility to idiopathic pulmonary fibrosis in people of European ancestry: a genome-wide association study

TL;DR: The identification of AKAP13 as a susceptibility gene for IPF increases the prospect of successfully targeting RhoA pathway inhibitors in patients with IPF.
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Simultaneous intravital imaging of macrophage and neutrophil behaviour during inflammation using a novel transgenic zebrafish

TL;DR: It is shown that macrophages were effectively ablated by addition of the prodrug metronidazole, with no effect on neutrophil number, and Tg(fms:GAL4.VP16)i186 provides a powerful tool for intravital imaging and functional manipulation of macrophage behaviour during inflammation.
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Genome-Wide Association Study of Susceptibility to Idiopathic Pulmonary Fibrosis.

Richard J. Allen, +77 more
TL;DR: The observation that decreased DEPTOR expression associates with increased susceptibility to IPF supports recent studies demonstrating the importance of mTOR signaling in lung fibrosis, and new signals of association implicating KIF15 and MAD1L1 suggest a possible role of mitotic spindle-assembly genes in IPF susceptibility.