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Neil Q. McDonald
Researcher at Francis Crick Institute
Publications - 129
Citations - 15251
Neil Q. McDonald is an academic researcher from Francis Crick Institute. The author has contributed to research in topics: Protein kinase C & Phosphorylation. The author has an hindex of 48, co-authored 125 publications receiving 13931 citations. Previous affiliations of Neil Q. McDonald include Cancer Research UK & Birkbeck, University of London.
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Intratumor heterogeneity and branched evolution revealed by multiregion sequencing.
Marco Gerlinger,Andrew Rowan,Stuart Horswell,James Larkin,David Endesfelder,Eva Grönroos,Pierre Martinez,Nicholas Matthews,Aengus Stewart,Patrick S. Tarpey,Ignacio Varela,Benjamin Phillimore,Sharmin Begum,Neil Q. McDonald,Adam Butler,David T. Jones,Keiran Raine,Calli Latimer,Claudio R. Santos,Mahrokh Nohadani,Aron Charles Eklund,Bradley Spencer-Dene,Graham Clark,Lisa Pickering,Gordon Stamp,Martin Gore,Zoltan Szallasi,Zoltan Szallasi,Julian Downward,P. Andrew Futreal,Charles Swanton +30 more
TL;DR: Intratumor heterogeneity can lead to underestimation of the tumor genomics landscape portrayed from single tumor-biopsy samples and may present major challenges to personalized-medicine and biomarker development.
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A structural superfamily of growth factors containing a cystine knot motif.
TL;DR: The determination of the crystal structure of dimeric NGF revealed a novel three-dimensional fold that contains a cystine knot motif and the evolutionary and functional implications that arise are discussed here.
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New protein fold revealed by a 2.3-Å resolution crystal structure of nerve growth factor
TL;DR: The crystal structure of the murine NGF dimer is reported, which reveals a novel protomer structure consisting of three antiparallel pairs of β strands, together forming a flat surface that provides a model for rational design of analogues of NGF and its relatives and for testing the NGF-receptor recognition determinants critical for signal transduction.
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The mitochondrial protease HtrA2 is regulated by Parkinson's disease-associated kinase PINK1
Helene Plun-Favreau,Kristina Klupsch,Nicoleta Moisoi,Sonia Gandhi,Svend Kjaer,David Frith,Kirsten Harvey,Emma Deas,Robert J. Harvey,Neil Q. McDonald,Nicholas W. Wood,L. Miguel Martins,Julian Downward +12 more
TL;DR: It is suggested that PINK1-dependent phosphorylation of HtrA2 might modulate its proteolytic activity, thereby contributing to an increased resistance of cells to mitochondrial stress.
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Disruption of methylarginine metabolism impairs vascular homeostasis
James Leiper,Manasi Nandi,Belen Torondel,Judith Murray-Rust,Judith Murray-Rust,Mohammed Malaki,Bernard O’Hara,Sharon Rossiter,Shelagh Anthony,Melanie Madhani,David L. Selwood,Caroline L. Smith,Beata Wojciak-Stothard,Alain Rudiger,Ray Stidwill,Neil Q. McDonald,Neil Q. McDonald,Patrick Vallance,Patrick Vallance +18 more
TL;DR: It is shown that loss of DDAH-1 activity leads to accumulation of ADMA and reduction in NO signaling, which causes vascular pathophysiology, including endothelial dysfunction, increased systemic vascular resistance and elevated systemic and pulmonary blood pressure, and it is suggested that DDAh inhibition could be harnessed therapeutically to reduce the vascular collapse associated with sepsis.