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CASP16 — STS
Text-mined interactions from Literome
Feng et al., Am J Physiol Gastrointest Liver Physiol 2002
(Necrosis) :
These findings point to a novel pathway for
caspase-3 activation by
STS in primary hepatocytes
Shiohara et al., Biochem Biophys Res Commun 2002
(Inflammation) :
The Fas mediated induction of
ASC was
inhibited by a general
caspase inhibitor, z-VAD-fmk, and an immunocytochemical study showed that ASC was increased in neutrophils exhibiting characteristic phenotypes for apoptosis
Ferraro-Peyret et al., J Immunol 2002
:
In contrast, etoposide ( ETO ),
staurosporine (STS) , or IL-2 withdrawal
triggers concomitant
caspase activation, PS exposure, and DeltaPsim disruption
Terminella et al., Am J Physiol Lung Cell Mol Physiol 2002
:
STS produced a concentration- and time dependent
increase in
caspase-3 activity in pH 7.4 medium that reached a peak at 6 h
Caballero-Benítez et al., J Neurosci Res 2003
:
We found that both K5 and
STS induce the activation of
caspase-3 ... The initiator
caspase-9 was also
activated by both K5 and
STS , as well as cytochrome-c release
Gil et al., Free Radic Biol Med 2003
:
The antioxidants idebenone ( IDB ), glutathione-ethylester ( GSH/EE ), trolox, and Mn ( III ) tetrakis ( 4-benzoic acid ) porphyrin chloride ( MnTBAP ) significantly reduced
STS induced
caspase-3-like activity and intracellular ROS generation
Ohtsuka et al., Nat Cell Biol 2004
:
When ectopically expressed,
ASC interacted directly with Bax, colocalized with Bax to the mitochondria, induced cytochrome c release with a significant reduction of mitochondrial membrane potential and
resulted in the activation of
caspase-9 , -2 and -3
Schotte et al., J Biol Chem 2004
:
Rac-1 and LIM kinase-1 dominant negative mutants were shown to inhibit
caspase-1 activation
induced by overexpression of
Asc , which is a caspase-1 activating adaptor protein
Mariathasan et al., Nature 2004
(Inflammation...) :
ASC was
essential for extracellular ATP-driven activation of
caspase-1 in toll-like receptor ( TLR ) -stimulated macrophages
Hasegawa et al., J Biol Chem 2005
(Inflammation) :
ASC mediated NF-kappaB activation leading to interleukin-8 production
requires caspase-8 and is inhibited by CLARP
Yu et al., Cell Death Differ 2006
(Inflammation) :
However, both cryopyrin and two disease associated cryopyrin mutants induced ASC oligomerization and
ASC dependent
caspase-1 activation, with the disease associated mutants being more potent than the wild-type ( WT ) cryopyrin, because of increased self-oligomerization
Chen et al., J Lipid Res 2005
:
In addition, GD1b suppressed the apoptosis associated
caspase 3 activation that was
activated by
STS
Masselli et al., Oncogene 2006
:
STS has been shown to cause RB-dependent G1 arrest or apoptosis ; however, expression of PSM-RB did not prevent
caspase activation by
STS
Kanneganti et al., Nature 2006
(Inflammation) :
Cryopyrin and
ASC are
essential for
caspase-1 activation and IL-1beta and IL-18 production in response to bacterial RNA and the imidazoquinoline compounds R837 and R848
Mariathasan et al., Nature 2006
(Inflammation) :
Macrophages exposed to Gram positive Staphylococcus aureus or Listeria monocytogenes, however,
required both
ASC and cryopyrin to activate
caspase-1 and secrete IL-1beta
Zhu et al., Apoptosis 2006
:
Of note, the
STS induced marked increase in the cellular ROS level, release of cytochrome c and activation of
caspase 3 were inhibited in cultured hippocampal cells when PTEN was knocked down by a specific antisense
Ozören et al., J Immunol 2006
:
ASC , but not TLR2, is
required for
caspase-1 activation independent of NF-kappaB in Listeria infected macrophages
Sarkar et al., J Immunol 2006
:
This RIP2 induced NF-kappaB activity and
caspase-1 binding was
inhibited in a dose dependent fashion by
ASC ... These data suggest that
ASC may
direct caspase-1 away from RIP2 mediated NF-kappaB activation, toward caspase-1 mediated processing of proIL-1beta by interfering with the RIP2 caspase-1 interaction
Parsons et al., Oncogene 2006
(Cell Transformation, Neoplastic) :
Taken together, these data suggest that upregulation of
TMS1/ASC by TNFalpha and subsequent
activation of
caspase-8 could function to amplify the apoptotic signal induced by death receptors in some cell types, including breast epithelial cells
Koo et al., Br J Pharmacol 2007
:
In addition, pinusolide and 15-MPA inhibited
STS induced
caspase-3/7 activation
Silva et al., Neurobiol Dis 2007
:
Furthermore,
STS ( 100 nM ) decreased MTT reduction and
increased caspase-3 activity in rat hippocampal nerve terminals, which was prevented by SCH58261
Fernandes-Alnemri et al., Cell Death Differ 2007
(Inflammation) :
The adapter protein
ASC binds directly to caspase-1 and is
critical for
caspase-1 activation in response to a broad range of stimuli ... To elucidate the mechanism of
activation of
caspase-1 by
ASC and its exact role in macrophage pyroptosis, we performed time-lapse confocal bioimaging analysis on human THP-1 macrophages stably expressing an ASC-GFP fusion protein
Khan et al., J Biol Chem 2007
:
Both full-length type-I IP ( 3 ) R and a truncated construct corresponding to the caspase-3 cleaved `` channel-only '' fragment were able to support
staurosporine (STS) induced
caspase-3 activation and cell death even when the IP ( 3 ) R construct harbored a mutation that inactivates the pore of the Ca ( 2+ ) channel ( D2550A )
Kobara et al., J Appl Physiol 2008
(Disease Models, Animal...) :
STS ( 1 mumol/l ) caused extensive DNA fragmentation and
increased caspase-3 activity compared with a serum deprived control
Malloy et al., Endocrinology 2009
:
In the LNCaP prostate cancer cell line,
induction of apoptosis and
caspase-3/7 activities by
staurosporine (STS) abolished [ ( 3 ) H ] 1,25-dihydroxy vitamin D ( 3 ) binding and VDR protein, suggesting that the VDR may be targeted for inactivation by caspases during apoptosis
Pardossi-Piquard et al., J Neurochem 2009
:
Conversely, the depletion of NCT drastically enhances
STS induced
caspase-3 activation and p53 pathway and favored p53 nuclear translocation ... Second, NCT still reduces
STS induced
caspase-3 activation in fibroblasts lacking PS1 and PS2
Hasegawa et al., J Immunol 2009
:
ASC mediated AP-1 activation was inhibited by chemical or protein inhibitors for caspase-8, caspase-8 targeting small interfering RNA, and p38 and JNK inhibitors, but not by a caspase-1 inhibitor, caspase-9 or Fas associated death domain protein ( FADD ) dominant negative mutants, FADD- or RICK targeting small interfering RNAs, or a MEK inhibitor, indicating that the ASC induced AP-1 activation is mediated by caspase-8, p38, and JNK, but does not
require caspase-1 , caspase-9, FADD, RICK, or ERK
Lamkanfi et al., J Biol Chem 2009
(Inflammation) :
Similarly, Cryopyrin and
ASC were
required for activation of
caspase-7 in macrophages stimulated with zymosan or mannan and ATP ... These results demonstrate that the conserved fungal components zymosan and mannan
require ASC and Cryopyrin for
caspase-1 activation and IL-1beta secretion and suggest an important role for the Cryopyrin inflammasome during fungal infections
He et al., J Immunol 2010
(Chlamydia Infections...) :
TLR2 was required for induction of pro-IL-1beta, whereas the
NLRP3/ASC was
required for
caspase-1 activation and pro-IL-1beta cleavage to produce mature IL-1beta
Brodsky et al., Cell Host Microbe 2010
:
Here we demonstrate that
caspase-1 activation in response to the Yersinia type III secretion system ( T3SS )
requires the adaptor
ASC and involves both NLRP3 and NLRC4 inflammasomes
Nguyen et al., Exp Mol Med 2010
:
Both nerve growth factor (NGF) and brain derived growth factor ( BDNF ) prevent
STS induced apoptotic morphology and
caspase-3 activity by upregulating phosphorylation of the tropomyosin receptor kinase ( Trk ) receptor
Cui et al., Front Biosci (Elite Ed) 2011
:
Western blot analysis showed that
STS significantly
affected the expression of the apoptosis related genes bcl-2, bax, and
caspase-3 in a dose dependent manner in the H9C2 cell line and in chick embryos
Abdelaziz et al., Frontiers in microbiology 2011
:
Taken together, our data demonstrate that L. pneumophila infection in murine macrophages is controlled by several mechanisms : Asc independent activation of caspase-1 and
Asc dependent regulation of NF-?B and
caspase-3 activation
Guillot-Sestier et al., Neurodegener Dis 2012
:
Thus, C1 potentiates
staurosporine (STS) induced
caspase-3 activation by upregulating p53 transcription, mRNA levels and activity ... Thus, N1 inhibits
STS induced
caspase-3 activation by downregulating p53 in various cell systems and protects rat retinal ganglion cells from hypoxia induced apoptosis
Khare et al., Immunity 2012
(Bacterial Infections) :
Activation of NLRP7 promoted
ASC dependent
caspase-1 activation, IL-1ß and IL-18 maturation, and restriction of intracellular bacterial replication, but not caspase-1 independent secretion of the proinflammatory cytokines IL-6 and tumor necrosis factor-a
Zhang et al., Hypertension 2012
(Hyperhomocysteinemia...) :
Pathologically, hHcys associated albuminuria, foot process effacement of podocytes, loss of podocyte slit diaphragm molecules, and glomerulosclerosis at the late stage were significantly improved by local
ASC gene silencing or by
caspase 1
inhibition
Ren et al., Mol Med Report 2013
:
Data showed that
ASC overexpression induced by pEGFP-ASC-C2 transfection significantly
increased caspase-1 expression and interleukin (IL)-1ß and IL-6 secretion, but did not affect tumor necrosis factor (TNF)-a secretion
Kumar et al., J Virol 2013
(West Nile Fever) :
Infection of cultured bone marrow derived dendritic cells showed that
ASC was
essential for the activation of
caspase 1, a key component of inflammasome assembly
Case et al., Proc Natl Acad Sci U S A 2013
(Necrosis) :
Legionella activation of caspase-11 stimulated
activation of
caspase-1 through NLRP3 and
ASC
Kamo et al., Hepatology 2013
(Reperfusion Injury) :
We found that
ASC deficiency
inhibited caspase-1/IL-1ß signaling and led to protection against liver ischemia/reperfusion ( IR ) damage, local enhancement of antiapoptotic functions, and down-regulation of high mobility group box 1 (HMGB1) mediated, toll-like receptor 4 (TLR4)-driven inflammation ... Conclusion :
ASC mediated
caspase-1/IL-1ß signaling promotes HMGB1 to produce a TLR4 dependent inflammatory phenotype and leads to hepatocellular injury