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Stephen J. Weiss
Researcher at University of Michigan
Publications - 162
Citations - 30233
Stephen J. Weiss is an academic researcher from University of Michigan. The author has contributed to research in topics: Extracellular matrix & Matrix metalloproteinase. The author has an hindex of 80, co-authored 153 publications receiving 28547 citations. Previous affiliations of Stephen J. Weiss include Life Sciences Institute.
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Journal ArticleDOI
Tissue Destruction by Neutrophils
TL;DR: With increasing frequency, the human neutrophil is being implicated as a mediator of tissue-destructive events in inflammatory diseases ranging from rheumatoid arthritis and myocardial reperfusion injury to respiratory distress syndromes, blistering skin disorders, and ulcerative colitis.
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EZH2 is a marker of aggressive breast cancer and promotes neoplastic transformation of breast epithelial cells
Celina G. Kleer,Qi Cao,Sooryanarayana Varambally,Ronglai Shen,Ichiro Ota,Scott A. Tomlins,Debashis Ghosh,Richard George Antonius Bernardus Sewalt,Arie P. Otte,Daniel F. Hayes,Michael S. Sabel,Donna L. Livant,Stephen J. Weiss,Mark A. Rubin,Arul M. Chinnaiyan +14 more
TL;DR: Tissue microarray analysis demonstrated that EZH2 protein levels were strongly associated with breast cancer aggressiveness and provided compelling evidence for a functional link between dysregulated cellular memory, transcriptional repression, and neoplastic transformation.
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Physical limits of cell migration: Control by ECM space and nuclear deformation and tuning by proteolysis and traction force
Katarina Wolf,Mariska te Lindert,Marina Krause,Stephanie Alexander,Joost te Riet,Amanda L. Willis,Robert M. Hoffman,Carl G. Figdor,Stephen J. Weiss,Peter Friedl +9 more
TL;DR: The physical limits of cell migration in dense porous environments are dependent upon the available space and the deformability of the nucleus and are modulated by matrix metalloproteinases, integrins and actomyosin function.
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Regulation of transendothelial neutrophil migration by endogenous interleukin-8
TL;DR: Endothelial cell production of a 77-amino acid variant of interleukin-8 (IL-8) was found to be a requirement for the invasion of neutrophils through a vessel wall model and regulates transvenular traffic during acute inflammatory responses.
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Chlorination of taurine by human neutrophils. Evidence for hypochlorous acid generation.
TL;DR: It appears that stimulated human neutrophils can utilize the hydrogen peroxide-myeloperoxidase-chloride system to generate taurine chloramine, and the biologic reactivity and cytotoxic potential of hypochlorous acid and its chloramine derivatives suggest that these oxidants play an important role in the inflammatory response and host defense.