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Continuous Cell Substrate Considerations
Published in Anthony S. Lubiniecki, Large-Scale Mammalian Cell Culture Technology, 2018
Several types of activated oncogene DNAs can “transform” susceptible cells in vitro (11, 21); such transfected cell lines are frequently tumori genic upon implementation in immunosuppressed rodents (22). Fung et al. (23) showed that the v-src oncogene DNA could produce nodules in inoculated chickens which regressed after several weeks. Finally, some oncogenes are capable of causing tumors if introduced transgenically via retroviral vectors (24). This laboratory evidence supports the theoretical possibility of cellular transformation due to contaminating oncogenic DNA but is of uncertain relevance to most examples of product delivery to humans.
Targeting gap junctional intercellular communication by hepatocarcinogenic compounds
Published in Journal of Toxicology and Environmental Health, Part B, 2020
Kaat Leroy, Alanah Pieters, Andrés Tabernilla, Axelle Cooreman, Raf Van Campenhout, Bruno Cogliati, Mathieu Vinken
GJIC is mainly controlled at 2 levels, namely at the expression level and at the functionality level (Figure 2) (Nielsen et al. 2012). The latter, also called gap junction gating, encompasses many different factors, such as pH, calcium levels, transmembrane voltage, redox potential, interactions with other proteins and posttranslational modifications, including phosphorylation, glycosylation, N-acetylation, ubiquitination, methylation, S-tyrosination and SUMOylation (Garcia et al. 2018; Leithe, Mesnil, and Aasen 2018; Sorgen et al. 2018; Vinken 2016). Phosphorylation is probably the best-studied posttranslational connexin modification, being well documented for Cx43. Phosphorylation predominantly occurs at serine, threonine and tyrosine residues of the C-terminal tail, and might be generated by a multitude of kinases, such as protein kinase C (PKC), protein kinase A, tyrosine kinase 2, mitogen-activated protein kinase (MAPK), Rous sarcoma oncogene (v-Src) and casein kinase 1 (Leithe, Mesnil, and Aasen 2018). Another gating mechanism relates to changes in intracellular pH or calcium levels (Garciarena et al. 2018; Wei et al. 2019). Thus, Cx43 gap junctions open in alkaline conditions, whereas they close upon acidification (Garciarena et al. 2018). Gating in response to calcium is mediated by calmodulin, since gap junctions themselves do not possess high affinity for this ion (Peracchia 2020). Further, functional control also includes voltage gating depending upon the voltage gradient alongside the pore (Bargiello et al. 2018).