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CASP3 — PRNP
Text-mined interactions from Literome
Sáez-Valero et al., Neurosci Lett 2000
:
Thus, although beta 25-35 and
PrP 106-126 robustly
activated CPP32 , their neurotoxic effect was independent of this caspase activation
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