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CASP1 — CASP2

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

• IRef Hprd Interaction: Complex of CASP1-CASP3-CASP2-CASP3-CASP1-CASP2-CASP1-CASP2-CASP3 (in vivo) Walker et al., Cell 1994*
• IRef Ophid Interaction: CASP2 — CASP1 (aggregation, confirmational text mining) Walker et al., Cell 1994*
• IRef Ophid Interaction: CASP2 — CASP1 (aggregation, interologs mapping) Brown et al., Bioinformatics 2005

Text-mined interactions from Literome

de Bilbao et al., Neuroscience 2000 (Facial Nerve Injuries) : Similar results were obtained in interleukin-1 beta converting enzyme-deficient and wild-type mice, indicating that the interleukin-1 beta converting enzyme may not be required for caspase 3 activation
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
Yang et al., Nephron. Experimental nephrology 2004 (Necrosis) : Here we evaluate three caspase inhibitors : B-D-FMK ( pan caspase inhibitor ), Z-DEVDFMK ( predominantly Caspase-3 inhibitor ) and Z-VAD-FMK ( predominantly Caspase-1 and -3 inhibitor ) to ameliorate apoptosis induced by cisplatin in rat proximal tubular ( RPT ) cells
Messerli et al., Neoplasia (New York, N.Y.) 2004 (Glioma) : The specificity of this probe for caspase-1 is supported by various lines of evidence : 1 ) activation by purified caspase-1, but not another caspase in vitro ; 2 ) activation of the probe by infection of cells with a herpes simplex virus amplicon vector ( HGC-ICE-lacZ ) expressing a catalytically active caspase-1-lacZ fusion protein; 3 ) inhibition of HGC-ICE-lacZ vector induced activation of the probe by coincubation with the caspase-1 inhibitor YVAD-cmk, but not with a caspase-3 inhibitor ; and 4 ) activation of the probe following standard methods of inducing apoptosis with staurosporine, ganciclovir, or ionizing radiation in culture
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 )
Guo et al., Cell Death Differ 2006 : Caspase-1 activation of caspase-6 in human apoptotic neurons
Fang et al., J Immunol 2011 (Disease Resistance...) : Caspase-1 activation was partially impaired in NLRP3 ( -/- ) macrophages, whereas knockdown and knockout of AIM2 resulted in a clear decrease in caspase-1 activation in response to S. pneumoniae
LaRock et al., Cell Host Microbe 2012 : Caspase-1 activation antagonizes Yersinia survival in vivo, and consequently YopM inhibition of caspase-1 is required for Yersinia pathogenesis
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
Wang et al., Cell 1998 (Shock, Septic) : Murine caspase-11 , an ICE interacting protease, is essential for the activation of ICE ... Furthermore, we found that pro-caspase-11 physically interacts with pro-ICE in cells, and the expression of casp-11 is essential for activation of ICE ... Our data suggest that caspase-11 is a component of ICE complex and is required for the activation of ICE