Gene interactions and pathways from curated databases and text-mining

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CASP6 — CAT

Text-mined interactions from Literome

Kashiwagi et al., Free Radic Biol Med 1999 : Kinetic analysis revealed that catalase activity decreased and caspase-3-like activity increased during normal tadpole tail atrophy ( apoptosis )
Jiang et al., J Neurochem 2001 : Genetic up-regulation of catalase not only significantly reduced cell death but also suppressed caspase 3 activity and DNA fragmentation ... However, unlike inducibly increased catalase expression and general caspase inhibition both of which protect cells from cytotoxicity, caspase 3 inhibition alone did not improve cell survival suggesting that prevention of DNA fragmentation is insufficient to prevent H ( 2 ) O ( 2 ) -mediated cell death
Lavastre et al., Clin Immunol 2002 : In addition, toxaphene was found to induce the degradation of the cytoskeletal proteins gelsolin, paxillin, and vimentin during apoptosis, and this was reversed by the addition of z-VAD-FMK ( caspase inhibitor ) or catalase , demonstrating the importance of caspases and ROS in this process
Wang et al., Zhonghua Yan Ke Za Zhi 2003 : [ Effect of N-acetyl-L-cysteine and catalase on apoptosis of lens epithelial cell and the activity of caspase-3 ]
Poh et al., Cancer Res 2005 (Prostatic Neoplasms) : Indeed, overexpression of catalase significantly blocked the amplifying effect of LY pretreatment on caspase-2 and caspase-3 activation and cell death triggered by vincristine
Yasui et al., Free radical research 2005 (Down Syndrome...) : Catalase inhibited the neutrophil apoptosis and caspase-3 activation
Kim et al., FEBS Lett 2006 (Melanoma) : On further investigating the IAA/HRP mediated apoptotic pathway, we found that the IAA/HRP reaction leads to caspase-3 activation and poly ( ADP-ribose ) polymerase ( PARP ) cleavage, which was also blocked by catalase
Yu et al., Cancer Lett 2008 (Leukemia) : The apoptosis induction ability of ETME was associated with the production of hydrogen peroxide ( H ( 2 ) O ( 2 ) ), the decrease of mitochondrial membrane potential, and the activation of caspase-3 that was blocked by catalase
Pramanik et al., PloS one 2011 (Pancreatic Neoplasms) : Our results reveal that the release of cytochrome c and cleavage of both caspase-9 and caspase-3 due to disruption of mitochondrial membrane potential were significantly blocked by catalase and EUK-134 in BxPC-3 cells