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CASP12 — PRNP

Text-mined interactions from Literome

Stewart et al., J Neurosci Res 2001 (Prion Diseases) : These inhibitors also prevented PrP106-126 induced caspase 3 activation and annexin V binding, indicating a central role for the 5-LOX pathway in PrP106-126 mediated proapoptosis
Gavín et al., FEBS Lett 2005 : We show that PrP ( 106-126 ) induces the activation of subsets of intracellular kinases ( e.g., ERK1/2 ), early growth response 1 synthesis and induces caspase-3 activity, all of which are mediated by nicotinamide adenine dinucleotide phosphate hydrogen-oxidase activity and oxidative stress
Ferreiro et al., J Neurochem 2008 (Teratocarcinoma) : In this study, we show that PrP ( 106-126 ) induces ER stress in both cell lines, given that ER Ca2+ content is low, glucose regulated protein 78 levels are increased and caspase 4 is activated
Ferreiro et al., J Alzheimers Dis 2007 (Alzheimer Disease) : Furthermore, Bcl-2 overexpression protected from loss of cell viability and caspase-9 and -3 activation induced by Abeta ( 25-35 ) and PrP ( 106-126 ), showing that Bcl-2 is neuroprotective against apoptotic cell death caused by amyloidogenic peptides
Pan et al., J Biochem Mol Toxicol 2010 : Mechanistically, PrP106-126 decreased PC 12 intracellular glutathione ( GSH ) concentrations, decreased superoxide dismutase ( SOD ) enzyme activity, increased concentrations of the oxidation end product malondialdehyde ( MDA ), depolarized the mitochondrial membrane, and increased caspase-3 activity