◀ Back to CASP1
CASP1 — CASP3
Pathways - manually collected, often from reviews:
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Sun et al., Oncogene 1999
(Adenocarcinoma...) :
The
caspase inhibitors ( Z-DEVD-FMK and Z-VAD-FMK )
suppressed CD437 induced
CPP32-like caspase activation and apoptosis in both cell lines
Selznick et al., J Neuropathol Exp Neurol 2000
:
Caspase-3 deficiency, or pharmacological
inhibition of
caspase activity, prevented caspase-3 activation and blocked the appearance of apoptotic nuclear features but not Abeta induced neuronal death
Nakatsuka et al., Neurosci Lett 2000
(Ischemic Attack, Transient) :
Although
pro-caspase-3 was strongly detected,
active caspase-3 was not
detected before and until 84 h after 5-min ischemia
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
De Saint Jean et al., Invest Ophthalmol Vis Sci 2000
:
Apoptosis was confirmed by a cleavage of PARP and
CPP32 , by
caspase-8 activation , and by an index Hoechst/neutral red greater than one
Zhang et al., J Neurosci 2000
(Alzheimer Disease) :
Caspase-3 induces neuronal apoptosis in 20 % of the cells, whereas
caspase-7 or -8 do not induce apoptosis
Tomicic et al., Biochem Biophys Res Commun 2001
:
Caspase-3- and caspase-9 mediated cleavage of Bcl-2 was efficiently
blocked by
caspase-3 ( zDEVD ) and caspase-9 ( zLEHD ) inhibitor, respectively
Kagawa et al., Clin Cancer Res 2001
:
Caspase-3 deficiency, however, did not
affect Bax induced levels of poly ( ADP-ribose ) polymerase cleavage,
caspase-6 activation, and lamin B cleavage
Kumi-Diaka et al., Biol Cell 2000
(Carcinoma...) :
The major findings of these studies are : i ) genistein inhibits growth and proliferation of both LNCaP and DU145 cells via apoptosis mainly, and necrosis at higher concentrations ; ii ) genistein induces activation and expression of caspase-3 ( CPP32 ) in both target cells ; iii ) genistein induced apoptosis and
CPP32 activation could be significantly
inhibited by the
caspase-3 inhibitor, z-VAD-fmk ( N-benzyloxycarbonyl-Val-Asp-fluoromethyl-ketone ), thus confirming a mediator role of CPP32 in the genistein induced apoptotic pathway in the target cells
Stadelman et al., Brain Pathol 2001
(Fetal Death...) :
Expression of apoptosis associated proteins p53, bcl-2, bax, and
caspase-3/CPP32 ,
activation of
caspase-3 , and modification of proteins via poly ( ADP-ribosyl ) ation was studied in pontosubicular neuron necrosis ( PSN ), a form of perinatal brain damage revealing the morphological hallmarks of neuronal apoptosis
Kwon et al., Exp Mol Med 2002
:
Caspase-3 selective inhibitor, Ac-DEVD-CHO,
prevented both the activation of
caspase-3 and cleavage of poly ( ADP-ribose ) polymerase ( PARP )
Chandra et al., J Biol Chem 2003
:
Here we present evidence that the mitochondrially localized
active caspase-9 and -3 result mostly from translocation from the cytosol ( into the intermembrane space ) and partly from
caspase mediated activation in the organelle rather than from the Apaf-1 mediated activation
Xu et al., Anticancer Res 2003
(Pancreatic Neoplasms) :
Caspase-8 and -3 activities were increased by TRAIL treatment and apoptosis was largely
blocked by
caspase-8 and -3 inhibitors
Schoemaker et al., J Hepatol 2003
(Cholestasis...) :
Apoptosis was determined by TUNEL staining,
active caspase-3 staining,
activation of
caspase-8 , -9 and -3
Du et al., World J Gastroenterol 2003
(Carcinoma, Hepatocellular...) :
The levels of
CPP32-like protease activity in HepG2 and SMMC-7721 increased by 2.8- and 3.0-fold ( P < 0.05 ) at 48 h, and the levels of
ICE-like protease activity also
increased by 2.6- and 3.2-fold ( P < 0.05 ) respectively
Aouad et al., J Immunol 2004
:
Caspase-3 is a component of Fas death inducing signaling complex in lipid rafts and its activity is
required for complete
caspase-8 activation during Fas mediated cell death
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 ... 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
Kusunoki et al., BMC pharmacology 2004
(Arthritis, Rheumatoid) :
Caspase-3 activity was increased by treatment with triptolide and was
suppressed by
caspase inhibitors
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
Guo et al., Cell Death Differ 2006
:
Caspase-1 activation of
caspase-6 in human apoptotic neurons
Liszewska et al., Prostaglandins Other Lipid Mediat 2005
:
Treatment of luteal cells with P4 and PGE2 for 24 h decreased ( P < 0.05 ) level of
active caspase-3 while aminoglutethimide ( P < 0.05 ), spermine NONOate ( P < 0.05 ), and staurosporine ( P < 0.001 )
increased caspase-3 activity in the cells
Shankar et al., J Neurosci 2006
:
Rhgas6 and
caspase inhibitors also
reduced active caspase-3 immunoreactivity relative to TNFalpha-only treated cultures
Nakadai et al., Toxicology 2006
:
Chlorpyrifos also induced an increase of intracellular
active caspase-3 in U937 cells in a dose dependent manner, and a
caspase-3 inhibitor, Z-DEVD-FMK, significantly
inhibited the chlorpyrifos induced apoptosis
Yang et al., Apoptosis 2006
:
Caspase-3 mediated-feedback and
activation of
caspase-8 and -9 in MCF-7/C3 cells is further supported by an increase in the cleavage of caspase-8 and 9 substrates and cytochrome c release
Koo et al., Am J Chin Med 2007
:
Caspase-3 activation and subsequent apoptotic cell death in MGG treated cells were partially blocked by the
caspase-3 inhibitor, Z-DEVD-FMK
Ikeda et al., Exp Cell Res 2007
:
Caspase-3 activation is also induced, but the
caspase inhibitor, Z-VAD-FMK, does not block RASSF6 mediated apoptosis
Wong et al., Biochim Biophys Acta 2007
:
Caspase-3 is
activated by cleavage of
caspase-8 and caspase-9
Denault et al., Biochem J 2007
:
Caspase 3 attenuates XIAP ( X-linked inhibitor of apoptosis protein ) -mediated inhibition of
caspase 9
Feng et al., J Huazhong Univ Sci Technolog Med Sci 2007
:
Caspase-3 inhibitors can
suppress caspase-3 activity and reduce the apoptosis rate significantly
Li et al., Toxicology 2007
:
DDVP also induced an increase of intracellular
active caspase-3 in NK-92CI in a dose- and time dependent manner, and a
caspase-3 inhibitor, Z-DEVD-FMK, significantly
inhibited DDVP induced apoptosis, suggesting that this apoptosis is partially mediated by activation of intracellular caspase-3
Wei et al., Zhonghua Xue Ye Xue Za Zhi 2007
:
The
caspase-3 activity was markedly enhanced, and the
active caspase-3 in K562/ADM cells
increased by about 40 % compared to liposome alone and non silencing controls
Audo et al., Arthritis Res Ther 2007
(Arthritis, Rheumatoid) :
Caspase 3 , a key mediator of apoptosis, was not activated in celecoxib treated RA FLSs, and the presence of specific
caspase 3 or pan-caspase inhibitors did not
affect celecoxib induced cell death
Scarlatti et al., Cell Death Differ 2008
(Breast Neoplasms) :
Here we show that resveratrol arrests cell proliferation, triggers death and decreases the number of colonies of cells that are sensitive to
caspase-3 dependent apoptosis ( MCF-7
casp-3 ) and also those that are unresponsive to it ( MCF-7vc )
Li et al., Toxicology 2009
:
Chlorpyrifos also induced an increase in intracellular
active caspase-3 in Jurkat T cells in a dose- and time dependent manner, and a
caspase-3 inhibitor, Z-DEVD-FMK, significantly
inhibited chlorpyrifos induced apoptosis
Tang et al., Oncol Rep 2009
(Adenocarcinoma...) :
Caspase-9 and -3 inhibitors almost completely
suppressed HCT induced
caspase-9 and -3 activities
Li et al., Arch Toxicol 2011
(Necrosis) :
DNA fragmentation was detected when cells were treated with 0.5, 1, or 2 µM ziram for 24 h. Ziram also induced an increase in intracellular
active caspase-3 in U937 cells in a dose dependent manner, and a
caspase-3 inhibitor, Z-DEVD-FMK, significantly
inhibited the ziram induced apoptosis
Xiao et al., Apoptosis 2011
:
Caspase-3 activity was 10-fold higher in myotubes compared to myoblasts, and Stsp
caused a significant
caspase-3 induction in both
Jeyasuria et al., Biol Reprod 2011
:
The IAP family members are the only endogenous inhibitors of
active caspase 3 , and MCL1 limits
activation of
caspase 3 by suppressing proapoptotic signaling
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
Aras et al., Brain Res 2012
(Gliosis) :
Reactive neonatal and adult astrocytes demonstrated an
increase in total
caspase activity with a corresponding increase in the expression of
active caspase-3 in the absence of cell death
Edgington et al., Chem Biol 2012
:
We also demonstrate that
caspase-6 activation does not
require active caspase-3/-7 , suggesting that it may autoactivate or be cleaved by other proteases
Nelson et al., Crit Care Med 2012
(Muscular Atrophy) :
These findings support our hypothesis that a regulatory calpain/caspase-3 cross-talk exists whereby calpain can promote
caspase-3 activation and
active caspase-3 can
enhance calpain activity in diaphragm muscle during prolonged mechanical ventilation
Chan et al., J Virol 2012
:
However, HCMV infection does
induce a temporal activation of
caspase 3, with only a low level of
active caspase 3 being observed after the 48-h viability checkpoint
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
Wu et al., Food Chem Toxicol 2013
:
Caspase-3 inhibitor also efficiently
blocked CD95 ( APO-1/CD95 ) and Bax expression,
caspase-3 activation and PARP cleavage, whereas antioxidant N-acetyl-l-cysteine, AMPK inhibitor and AMPK siRNA effectively blocked the AMPK phosphorylation
Enari et al., Nature 1996
:
The
CPP32 inhibitor
inhibited ICE- or CPP32 induced apoptosis in the cell-free system, whereas the ICE-inhibitor only inhibited ICE induced apoptosis
Armstrong et al., J Biol Chem 1996
:
Fas induced activation of the cell death related protease
CPP32 Is
inhibited by Bcl-2 and by
ICE family protease inhibitors
Armstrong et al., J Neurosci 1997
(Necrosis) :
CPP32 activation
requires macromolecular synthesis and
CED3/ICE protease activity
Wright et al., J Exp Med 1997
(Lymphoma) :
Only the
caspase inhibitors, however,
prevented activation of
CPP32-like activity as revealed by cleavage of the synthetic substrate, DEVD-pNa, by cell cytosols, and also by in vivo cleavage of poly ( ADP-ribosyl ) polymerase, a known substrate of CPP32
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
Deveraux et al., EMBO J 1998
:
In contrast, these IAP family proteins did not
prevent caspase-8 induced proteolytic activation of
pro-caspase-3 ; however, they subsequently inhibited
active caspase-3 directly, thus blocking downstream apoptotic events such as further activation of caspases