S
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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Antitumor Effects of EGFR Antisense Guanidine-Based Peptide Nucleic Acids in Cancer Models
Sufi M. Thomas,Bichismita Sahu,Srinivas Rapireddy,Raman Bahal,Sarah E Wheeler,Eva M. Procopio,Joseph Kim,Sonali Joyce,Sarah Contrucci,Yun Wang,Simion I. Chiosea,Kira L. Lathrop,Simon C. Watkins,Jennifer R. Grandis,Bruce A. Armitage,Danith H. Ly +15 more
TL;DR: Development of cell-permeable, guanidine-based peptide nucleic acids targeting the epidermal growth factor receptor (EGFR) in preclinical models as therapeutic modality for head and neck squamous cell carcinoma and nonsmall cell lung cancer is reported.
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Automated imaging system for fast quantitation of neurons, cell morphology and neurite morphometry in vivo and in vitro
TL;DR: In this paper, the authors describe automated techniques to quantify the number and morphology of neurons (or any cell type, e.g., astrocytes) and their processes with high speed and accuracy.
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Role of glutathione conjugate efflux in cellular protection against benzo[a]pyrene-7,8-diol-9,10-epoxide–induced DNA damage
TL;DR: The results of the present study indicate that in addition to GSH conjugation, the efflux of BPD‐SG may be essential for cellular protection against (+)‐anti‐BPDE–induced DNA damage.
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The Role of Dendritic Brain-Derived Neurotrophic Factor Transcripts on Altered Inhibitory Circuitry in Depression.
Hyunjung Oh,Sean C. Piantadosi,Brad R. Rocco,David A. Lewis,Simon C. Watkins,Etienne Sibille +5 more
TL;DR: These findings provide evidence for a novel MDD-related pathological mechanism linking local neurotrophic support, pyramidal cell structure, dendritic inhibition, and mood regulation.
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Endocytosis separates EGF receptors from endogenous fluorescently labeled HRas and diminishes receptor signaling to MAP kinases in endosomes
TL;DR: It is proposed that, under physiological conditions of cell stimulation, EGFR endocytosis serves to spatially separate EGFR–Grb2 complexes and Ras, thus terminating Ras-mediated signaling.