M
Michael F. McDermott
Researcher at University of Leeds
Publications - 153
Citations - 16117
Michael F. McDermott is an academic researcher from University of Leeds. The author has contributed to research in topics: Familial Mediterranean fever & Tumor necrosis factor alpha. The author has an hindex of 55, co-authored 148 publications receiving 14562 citations. Previous affiliations of Michael F. McDermott include Royal London Hospital & National Institute for Health Research.
Papers
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Journal ArticleDOI
Modelling the Major Histocompatibility Complex Susceptibility to RA Using the MASC Method
Emmanuelle Génin,Marie-Claude Babron,Michael F. McDermott,B. Mulcahy,F. Waldron-Lynch,Claire Adams,Daniel O. Clegg,Ryk Ward,Fergus Shanahan,M. G. Molloy,Fergal O'Gara,Françoise Clerget-Darpoux +11 more
TL;DR: The TNF data provided additional information for a better understanding of genetic susceptibility to RA than was previously possible using only HLA‐DR data and the advisability of using different linked markers in a candidate region for modelling the contribution of this region in disease susceptibility is addressed.
Journal Article
BMS-561392. Bristol-Myers Squibb.
TL;DR: Bristol-Myers Squibb Pharma Co is developing the tumor necrosis factor-alpha converting enzyme inhibitor BMS-561392 (DPC-333) for the potential treatment of diseases characterized by overproduction of TNF alpha, such as rheumatoid arthritis.
Journal ArticleDOI
Pancreatitis in fibrocalculous pancreatic diabetes mellitus is not associated with common mutations in the trypsinogen gene
Zahid Hassan,Viswanathan Mohan,Michael F. McDermott,Liaquat Ali,W Ogunkolade,Ebun Aganna,Paul G. Cassell,Raj Deepa,A.K.Azad Khan,Graham A. Hitman +9 more
TL;DR: The hypothesis that mutations in exons 2 and 3 of the trypsinogen gene might also predispose to FCPD is investigated.
SUMMARY Primer: inflammasomes and interleukin 1β in inflammatory disorders
TL;DR: In this paper, the NALP-like inflammasome pathways cooperate with Toll-like receptor pathways to mediate a rapid and appropriate response to pathogens and genotoxic stress, and aberrant IL-1β processing has been reported in several autoinflammatory conditions.
Journal ArticleDOI
Differential cytokine secretion results from p65 and c-Rel NF-κB subunit signaling in peripheral blood mononuclear cells of TNF receptor-associated periodic syndrome patients
Belinda Nedjai,Graham A. Hitman,Leigh D Church,Kirsten Minden,Margo Whiteford,Shane McKee,Susanna Stjernberg,Tom Pettersson,Annamari Ranki,Philip N. Hawkins,Peter D. Arkwright,Michael F. McDermott,Mark D. Turner +12 more
TL;DR: While all six TNFRSF1A mutations showed enhanced NF-κB activity, different mutations stimulated distinct NF-σκB family subunit activities, and this in turn resulted in the generation of unique cytokine secretory profiles.