R
Randall J. Ruch
Researcher at University of Toledo Medical Center
Publications - 67
Citations - 5615
Randall J. Ruch is an academic researcher from University of Toledo Medical Center. The author has contributed to research in topics: Connexin & Cell culture. The author has an hindex of 37, co-authored 67 publications receiving 5368 citations.
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Journal ArticleDOI
Prevention of cytotoxicity and inhibition of intercellular communication by antioxidant catechins isolated from Chinese green tea
TL;DR: An antioxidant fraction of Chinese green tea, containing several catechins, has been previously shown to inhibit 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced tumor promotion in mouse skin and was shown to have antioxidative activity toward hydrogen peroxide and the superoxide radical.
Journal ArticleDOI
Cell-cell communication in carcinogenesis.
James E. Trosko,Randall J. Ruch +1 more
TL;DR: The review examines how GJIC can be either transiently or stably modulated by endogenous or exogenesis chemicals or by oncogenes and tumor suppressor genes at the transcriptional, translational, or posttranslational levels.
Journal ArticleDOI
Gap‐junction disassembly and connexin 43 dephosphorylation induced by 18β‐glycyrrhetinic acid
TL;DR: In this article, the authors provided morphological evidence that 18 beta-glycyrrhetinic acid (18 beta-GA), a saponin isolated from licorice root that is an inhibitor of gap junctional communication, caused the disassembly of gap-junction plaques in WB-F344 rat liver epithelial cells.
Journal ArticleDOI
Changes in gap-junction permeability, phosphorylation, and number mediated by phorbol ester and non-phorbol-ester tumor promoters in rat liver epithelial cells.
TL;DR: Results suggest that TPA‐induced hyperphosphorylation of connexin 43 occurred fast enough to account for inhibition of GJIC, and dieldrin and heptachlor epoxide modulated connexIn phosphorylation in a manner different from TPA by promoting hypophosphorylated of con Nexin 43, and redistribution of plasma membrane gap‐junctional plaques after treatment with phorbol ester and non‐phorbol‐ester tumor promoters occurred
Book ChapterDOI
Role of inhibition of intercellular communication in carcinogenesis.
James E. Klaunig,Randall J. Ruch +1 more
TL;DR: The hypothesis that tumor promoters stimulate cell proliferation of initiated cells by inhibiting gap junctional intercellular communication in the initiated cells is proposed.