Gene interactions and pathways from curated databases and text-mining

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CASP7 — PRKDC

Pathways - manually collected, often from reviews:

Text-mined interactions from Literome

Wu et al., Blood Cells Mol Dis 1999 : The ability of lactacystin to promote DNA fragmentation was abrogated by TPCK, but not by caspase inhibitors, whereas the ability of lactacystin to promote degradation of DNA-PKcs was blocked by caspase inhibitors, but not by TPCK
Mandal et al., Biochem Biophys Res Commun 1999 (Colorectal Neoplasms) : Here we report that in cells treated with butyric acid, the cleavage of DNA-PKcs was paralleled or preceded by the induction of activation of caspase-3 , and these events were inhibited by Bcl-2 overexpression
Boldogh et al., Toxicology 2003 (Ovarian Neoplasms) : The decreased kinase activity of DNA-PKcs was not due to a change in its amount or the levels of Ku70 and Ku86, their subcellular distribution, cell cycle progression or caspase mediated degradation of DNA-PK
Pajonk et al., BMC cancer 2005 : We conclude that caspase dependent cleavage of DNA-PKcs during apoptosis does not contribute to the radiosensitizing effects of MG-132
Shi et al., Cell 2009 : DNA-PKcs-PIDDosome : a nuclear caspase-2 activating complex with role in G2/M checkpoint maintenance
Seo et al., Molecular cancer 2010 : Moreover, TRAIL inhibited P-gp efflux function via caspase-3 dependent degradation of P-gp as well as DNA-PKcs and subsequently sensitized MDR cells to MDR related drugs such as vinblastine and doxorubicin
Kim et al., Molecular cancer 2011 (Colonic Neoplasms...) : Moreover, the suppression of DNA-PKcs level with siRNA in the cells induced the up-regulation of DR5 and active caspase-8 , -9, and -3