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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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Ethanol inhibits the autophosphorylation of the insulin-like growth factor 1 (IGF-1) receptor and IGF-1-mediated proliferation of 3T3 cells.

TL;DR: It is demonstrated that ethanol at low concentrations markedly inhibits IGF-1 receptor autophosphorylation and IGF-2-mediated cell growth and transcription of c-myc, c-fos, and c-jun in response to IGF- 1 was inhibited by ethanol.
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Long-Term IGF-I Exposure Decreases Autophagy and Cell Viability

TL;DR: The results indicate that chronic IGF-I stimulation leads to mitochondrial dysfunction and reduced cell viability, which is a negative impact at the cellular level using quiescent human fibroblasts.
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The insulin-like growth factor 1 receptor is required for the proliferation of hemopoietic cells.

TL;DR: It is shown that expression of the IGF1 receptor is required for the entry into S phase of both stimulated lymphocytes and HL-60 cells, and a tentative temporal relationship between these three genes (c-myb, IGF1 receptors, PCNA) is proposed.
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Topical rapamycin reduces markers of senescence and aging in human skin: an exploratory, prospective, randomized trial

TL;DR: Topical rapamycin treatment is a potential anti-aging therapy with efficacy in humans, accompanied by relative improvement in clinical appearance of the skin and histological markers of aging and by an increase in collagen VII, which is critical to the integrity of the basement membrane.
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A Phosphatidylinositol 3-Kinase Inhibitor Induces a Senescent-like Growth Arrest in Human Diploid Fibroblasts

TL;DR: Growth arrest with a PI-3 kinase inhibitor induces a senescent-like phenotype that is not seen when cells are growth arrested by either serum starvation or a MEK-1 inhibitor.