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CASP3 — MPZ

Text-mined interactions from Literome

King et al., Brain Res 2001 : To test if the activation state of the cell survival promoting phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway affects MPP induced caspase-3 activation, PI3K was inhibited with LY294002, or activated with insulin-like growth factor-1 ... MPP induced caspase-3 activation was increased by inhibition of PI3K, and decreased by stimulation of PI3K, indicative of anti-apoptotic signaling by the PI3K/Akt pathway ... MPP induced caspase-3 activity was increased by overexpression of GSK3beta ... Conversely, the GSK3beta inhibitor lithium attenuated MPP induced caspase-3 activation
D'Agostino et al., Int Immunopharmacol 2003 : CMT-1 and CMT-8 activate mainly caspase-8 as attested by the inhibitory effects of Z-VAD-fmk and Z-IEDT-fmk on CMT induced apoptosis
Shang et al., J Neurochem 2003 : MPP+ induced caspase-3-like activation and cell death are prevented by pretreatment with 5 micro mbeta-estradiol
Han et al., J Neurosci 2003 : Immunoblot and biochemical analysis also confirmed that activation of both caspase-9 and caspase-3 was induced by 6-OHDA, but not by MPP+
Kaul et al., Eur J Neurosci 2003 (Nerve Degeneration) : The superoxide dismutase mimetic, MnTBAP also effectively attenuated MPP+ induced caspase-3 activation , PKC delta cleavage, and DNA fragmentation ... Furthermore, rottlerin attenuated MPP+ induced caspase-3 activity without affecting basal activity, suggesting positive feedback activation of caspase-3 by PKC delta ... Finally, over-expression of a kinase inactive PKC delta K376R mutant prevented MPP+ induced caspase activation and DNA fragmentation, confirming the pro-apoptotic function of PKC delta in dopaminergic cell death
Yang et al., Mol Cell Neurosci 2004 (Nerve Degeneration) : The caspase-3 inhibitor Z-DEVD-FMK and the caspase-9 inhibitor Z-LEHD-FMK effectively blocked MPP ( + ) -induced PKCdelta proteolytic activation
Tian et al., J Ethnopharmacol 2005 : The activation of caspase-3 and caspase-8 was induced by MPP ( + ) in apoptosis
Kaul et al., Brain Res Mol Brain Res 2005 : Over-expression of wild-type human alpha-synuclein in mesencephalic dopaminergic neuronal cells ( N27 cells ) attenuated MPP+ induced ( 300 microM ) cytotoxicity, release of mitochondrial cytochrome c, and subsequent caspase-3 activation, without affecting reactive oxygen species ( ROS ) generation
Bo et al., Neurosci Res 2005 : In addition, puerarin also reduced MPP+ induced caspase-3-like activation
Ramachandiran et al., Toxicological sciences : an official journal of the Society of Toxicology 2007 (Parkinsonian Disorders) : Divergent mechanisms of paraquat, MPP+ , and rotenone toxicity : oxidation of thioredoxin and caspase-3 activation
Wu et al., Neuroscience bulletin 2007 : It was also shown that MPP ( + ) significantly induced the upregulation of Bax/Bcl-2 ratio and the activation of caspase-3
Anantharam et al., Neurotoxicology 2007 (MPTP Poisoning) : Similarly, co-treatment with these inhibitors also significantly attenuated MPP+ induced increases in caspase-3 enzymatic activity
Pain et al., Toxicology 2008 : A cell-permeable peptide inhibitor TAT-JBD reduces the MPP+ induced caspase-9 activation but does not prevent the dopaminergic degeneration in substantia nigra of rats ... Our results showed that MPP ( + ) induced not only an activation of c-Jun but also an early and robust stimulation of caspase-9 in midbrain of rats ... Furthermore, a preliminary intravenous injection of TAT-JBD reduced the caspase-9 activation specifically induced by MPP ( + ) suggesting a control of the JNKs pathway on the intrinsic way of apoptosis in MPP ( + ) -toxicity
Xu et al., Toxicology 2008 (Parkinson Disease) : A threefold increase in caspase-3 activity ( P < 0.001 ) and a twofold increase in DNA fragmentation ( P < 0.05 ) with MPP ( + ) treatment was decreased by 55 % ( P < 0.01 ) and 52 % ( P < 0.05 ), respectively with IP6
Ghosh et al., Free Radic Biol Med 2010 (Disease Models, Animal...) : MPP ( + ) treatment caused a dose dependent loss of tyrosine hydroxylase and membrane potential and an increase in caspase-3 activation in dopaminergic cells, which were reversed by Mito-Q ( 10 )
Sun et al., Eur J Pharmacol 2011 (Neuroblastoma) : In addition, TSG suppressed both the upregulation of the ratio of Bax to Bcl-2 and the activation of caspase-3 induced by MPP+ , and TSG inhibited apoptosis as detected by flow cytometric analysis using Annexin-V and propidium ( PI ) label
Pöltl et al., Neurotoxicology 2012 : MPP ( + ) then triggered oxidative stress and caspase activation, as well as ATP-depletion followed by cell death
Zhang et al., Mol Cell Biochem 2012 (Neuroblastoma...) : We found that pretreatment with AS-IV significantly reversed the loss of cell viability, nuclear condensation, the generation of intracellular reactive oxygen species ( ROS ), and the increase in Bax/Bcl-2 ratio and the activity of caspase-3 induced by MPP ( + )
Kitamura et al., Mol Pharmacol 1998 : It also inhibited MPP+ induced ROS production, p53 expression, and cleavages of caspase-3 and PARP