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Simon C. Watkins

Researcher at University of Pittsburgh

Publications -  999
Citations -  75771

Simon C. Watkins is an academic researcher from University of Pittsburgh. The author has contributed to research in topics: Apoptosis & Immune system. The author has an hindex of 135, co-authored 950 publications receiving 68358 citations. Previous affiliations of Simon C. Watkins include Harvard University & Children's National Medical Center.

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Myocardial extracellular matrix remodeling in transgenic mice overexpressing tumor necrosis factor alpha can be modulated by anti-tumor necrosis factor alpha therapy.

TL;DR: The results suggest a critical role of TNF-alpha and MMPs in myocardial matrix remodeling and functional regulation and support the hypothesis that both TNFs and M MPs may serve as potential therapeutic targets in the treatment of heart failure.
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Internalization of circulating apoptotic cells by splenic marginal zone dendritic cells: dependence on complement receptors and effect on cytokine production

TL;DR: Characterization of apoptotic cell/DC interaction and its outcome provides insight into the mechanisms by which apoptotic cells affect DC function without disrupting peripheral tolerance.
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The recruitment of Raf-1 to membranes is mediated by direct interaction with phosphatidic acid and is independent of association with Ras.

TL;DR: It is reported that insulin stimulation of HIRcB fibroblasts leads to accumulation of Ras, Raf-1, phosphorylated MEK,osphorylated MAPK, and PA on endosomal membranes and results indicate that agonist-dependent Raf- 1 translocation is primarily mediated by a direct interaction with PA and is independent of association with Ras.
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Disabled-2 exhibits the properties of a cargo-selective endocytic clathrin adaptor

TL;DR: It is proposed that Dab2 is a typical member of a growing family of cargo‐specific adaptor proteins, including β‐arrestin, AP180, epsin, HIP1 and numb, which regulate clathrin‐coat assembly at the plasma membrane by synchronizing cargo selection and lattice polymerization events.
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Somatic reversion/suppression of the mouse mdx phenotype in vivo.

TL;DR: The mdx mouse has a myopathy caused by dystrophin deficiency, and is therefore biochemically and genetically homologous to human Duchenne muscular dystrophy and a possible estimate of the somatic reversion rate of the mdx mutation in vivo is considered.