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Christian Sell

Researcher at Drexel University

Publications -  99
Citations -  15242

Christian Sell is an academic researcher from Drexel University. The author has contributed to research in topics: Senescence & Growth factor. The author has an hindex of 36, co-authored 96 publications receiving 13442 citations. Previous affiliations of Christian Sell include Lankenau Institute for Medical Research & Thomas Jefferson University.

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Role of the Raf/MEK/ERK and the PI3K/Akt(PKB) pathways in fibroblast senescence

TL;DR: Although they can be fully activated in the cytosol of both early and late passage cells, the Raf/MEK/ERK and the PI3K/Akt pathways, which are essential for cellular proliferation, are down regulated in the nuclei of senescent cells.
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Insulin-like growth factor I-mediated degradation of insulin receptor substrate-1 is inhibited by epidermal growth factor in prostate epithelial cells

TL;DR: These two growth factors, IGF-I and EGF, had antagonistic effects on IRS-1 protein levels in prostate epithelial cells, which reveals a novel level of cross-talk between the IGF-i and E GF signal pathways, which may have implications in tumors that harbor activating mutations in the EGF receptor.
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Ras mutation impairs epithelial barrier function to a wide range of nonelectrolytes.

TL;DR: An increase in extracellular signal-regulated kinase-2 phosphorylation suggests that the downstream effects on the tight junction may be due to changes in the mitogen-activated protein kinase signaling pathway, and selective changes in permeability may influence tumorigenesis by the types of solutes now able to cross the epithelial barrier.
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Mice Producing Reduced Levels of Insulin-Like Growth Factor Type 1 Display an Increase in Maximum, but not Mean, Life Span

TL;DR: The results are consistent with a significant role for IGF-1 in the modulation of life span but contrast with the published life-span data for the hypopituitary Ames and Snell dwarf mice and growth hormone receptor null mice, indicating that a reduction in IGF- 1 alone is insufficient to increase both mean and maximal life span in mice.
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Rapamycin increases oxidative metabolism and enhances metabolic flexibility in human cardiac fibroblasts

TL;DR: Senescence is accompanied by elevated glycolysis and increased oxidative phosphorylation, which are both reduced by rapamycin, and long-term treatment withRapamycin increases expression of the mitochondrial carrier protein UCP2, which facilitates the movement of metabolic intermediates across the mitochondrial membrane.