Expression of yeast but not human apurinic/apyrimidinic endonuclease renders Chinese hamster cells more resistant to DNA damaging agents

TSH controls Ref-1 nuclear translocation in thyroid cells

“…In this light, the decrease of nuclear Ref-1 observed in differentiated carcinomas could reduce the DNA repair activity of the cell, facilitating the action of genotoxic agents, and thus progression toward a more aggressive phenotype. This hypothesis is supported by several observations indicating a direct relationship between the amount of nuclear Ref-1 and cell resistance to genotoxic agents (Walker et al 1994, Tomicic et al 1997, Grösh et al 1998, Ludwig et al 1998 (Tell et al 1998b). Together, this evidence suggests that Ref-1 localization may have a critical role in the control of thyroid cell functions.…”

Ganciclovir-induced apoptosis in HSV-1 thymidine kinase expressing cells: critical role of DNA breaks, Bcl-2 decline and caspase-9 activation

“…The mitochondrial and cytosolic extracts were isolated by di erential centrifugation as described (Wang and Studzinski, 1997). Protein extracts were quanti®ed (Bradford, 1976) and fractions of 10 ± 40 mg protein were separated by 10 ± 12% SDS ± PAGE, electroblotted onto nitrocellulose membrane (Schleicher and Schuel, Germany), that were incubated with antibodies as described (Tomicic et al, 1997). The used antibodies were mostly diluted (1 : 500) in 5% non-fat dry milk, 0.2% T-PBS.…”

Overexpression of Ref-1 Inhibits Lead-induced Endothelial Cell Death via the Upregulation of Catalase

“…The enzyme is particularly important under limited glutathione content conditions, such as obtain in lead (Pb)-exposed animals (Hsu, 1981;Hunaiti et al, 1995), and plays a significant role in the development of tolerance to oxidative stress in the adaptive responses of cells (Wassmann et al, 2004 (Grosch et al, 1998;Silber et al, 2002). Conversely, overexpression of Ref-1 repair functions stimulates an increase in resistance to certain alkylating agents and oxidative stresses (Tomicic et al, 1997;Grosch et al, 1998;Kim et al, 2006;Lee et al, 2009). Ref-1 and p53 proteins are required for selenium protection from DNA damage in the human and mouse fibroblasts (Fischer et al, 2006).…”