M
Mark M. Davis
Researcher at Stanford University
Publications - 623
Citations - 84251
Mark M. Davis is an academic researcher from Stanford University. The author has contributed to research in topics: T cell & T-cell receptor. The author has an hindex of 144, co-authored 581 publications receiving 74358 citations. Previous affiliations of Mark M. Davis include Washington University in St. Louis & University of Chicago.
Papers
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Mycobacterium tuberculosis-specific T cell activation identifies individuals at high risk of tuberculosis disease
Cheleka A M Mpande,Munyaradzi Musvosvi,Virginie Rozot,Boitumelo Mosito,Timothy D. Reid,Constance Schreuder,Tessa Lloyd,Nicole Bilek,Huang Huang,Gerlinde Obermoser,Mark M. Davis,Morten Ruhwald,Mark Hatherill,Thomas J. Scriba,Elisa Nemes,Acs Study Team +15 more
TL;DR: The {Delta}HLA-DR MFI biomarker can identify individuals with recent TBI and those with disease progression, allowing targeted provision of TPT to those at highest risk of tuberculosis.
Journal Article
Pillars Article: A Human T Cell-Specific Molecule Is a Member of a New Gene Family. J. Immunol . 1988. 141: 1018–1025
Thomas J. Schall,Jan Jongstra,Bradley J. Dyer,Jeffrey L. Jorgensen,Carol Clayberger,Mark M. Davis,Alan M. Krensky +6 more
Journal ArticleDOI
Unclassified white matter disorders: A diagnostic journey requiring close collaboration between clinical and laboratory services.
Chloe A Stutterd,Adeline Vanderver,Paul J. Lockhart,Guy Helman,Kate Pope,Eloise Uebergang,Christina Eguizabal Love,Martin B. Delatycki,David R. Thorburn,Melissa MacKay,Heidi Peters,Andrew J. Kornberg,Chirag Patel,Victoria Rodriguez-Casero,Michaela Waak,Jonathon M. Silberstein,Adriane J Sinclair,Matthew Nolan,Michael Field,Mark M. Davis,Michael C Fahey,Ingrid E. Scheffer,Jeremy L. Freeman,Nicole I. Wolf,Ryan J. Taft,Marjo S. van der Knaap,Christine Simons,Richard J. Leventer +27 more
TL;DR: In this paper , the authors identify the genetic causes for a group of individuals with unclassified white matter disorders with suspected genetic aetiology and highlight the investigations required when the initial testing is non-diagnostic.
Journal ArticleDOI
Corrigendum: T cell killing does not require the formation of a stable mature immunological synapse
TL;DR: The authors regret having omitted reference to M. Faroudi et al. (2004), Lytic versus stimulatorysynapse in cytotoxic T lymphocyte/target cell interaction: manifestation of a dual activation threshold.
Posted ContentDOI
Biallelic loss-of-function OBSCN variants predispose individuals to severe, recurrent rhabdomyolysis
Cabrera-Serrano M,Caccavelli L,Marco Savarese,Anna Vihola,Manu Jokela,Mridul Johari,Thierry Capiod,Madrange M,Enrico Bugiardini,Brady S,Ros Quinlivan,A. Merve,Renata S Scalco,David Hilton-Jones,Henry Houlden,Aydin H,Ceylaner S,Jerry Vockley,Rhonda L. Taylor,Rhonda L. Taylor,Hayley Goullee,Hayley Goullee,Emil Ylikallio,Mari Auranen,Henna Tyynismaa,Bjarne Udd,Mark M. Davis,Alistair R. R. Forrest,Alistair R. R. Forrest,Drago Bratkovic,Nicholas Manton,Robertson T,Pamela A. McCombe,Pamela A. McCombe,Nigel G. Laing,Nigel G. Laing,Phillips L,Phillips L,Delonlay P,G. Ravenscroft,G. Ravenscroft +40 more
TL;DR: In this article, the authors identified ten bi-allelic loss-of-function variants in the gene encoding obscurin (OBSCN) co-segregating with disease.