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CASP2 — CASP5

Text-mined interactions from Literome

Justo et al., J Am Soc Nephrol 2003 : Caspase-2 , caspase-3, and caspase-9 were activated, and specific caspase inhibitor prevented apoptosis and increased long-term survival
Fu et al., Cardiovasc Res 2004 : Caspase-2 , -3, -6 and -9 were activated during apoptosis and caspase-2 inhibitor ( Z-VDVAD-FMK ) and caspase-3 inhibitor ( Z-DEVD-FMK ) significantly attenuated the apoptosis
Perchellet et al., Anticancer Drugs 2004 : Caspase-2 and -8 may both act upstream of mitochondria to promote Cyt c release, but caspase-2 is already maximally activated 6 h after 4 microM DAU or TT13 treatments, whereas DAU- or TT-induced caspase-8 and -9 activities peak at 9 h. Pre-treatments with 15 microM of the caspase-2 inhibitor benzyloxycarbonyl ( z ) -Val-Asp-Val-Ala-Asp ( VDVAD ) -fluoromethyl ketone ( fmk ) totally block DAU- and TT13 induced caspase-2, -8 and -9 activities, whereas pre-treatments with 15 microM of the caspase-8 inhibitor z-Ile-Glu-Thr-Asp ( IETD ) -fmk prevent DAU and TT13 from inducing caspase-8 activities without affecting their caspase-2- and -9-inducing activities, suggesting that the induction of apical caspase-2 activity by these drugs may be a critical upstream event required for the activation of other downstream caspases, including caspase-9 and the mitochondrial amplification loop through caspase-8
Ho et al., FEBS J 2005 : Caspase-2 is resistant to inhibition by inhibitor of apoptosis proteins ( IAPs ) and can activate caspase-7
Lombard et al., Leuk Res 2005 (Leukemia, T-Cell) : Caspase-2 inhibitor blocked THC induced caspase-3 in wild-type Jurkat cells but not loss of Deltapsi ( m )
Stefanis et al., J Neurochem 1997 : We have shown previously that selective cysteine aspartase ( caspase ) inhibitors protect PC12 cells and sympathetic neurons from such death, and that the caspase Nedd-2 is required for this type of death to occur