PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 16418768-0 2005 The augmentation of TNFalpha-induced cell death in murine L929 fibrosarcoma by the pan-caspase inhibitor Z-VAD-fmk through pre-mitochondrial and MAPK-dependent pathways. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 105-114 tumor necrosis factor Mus musculus 20-28 18931327-5 2009 In C57Bl/6 mice, acute smoke-mediated increases in inflammatory cells, serum IL-1beta, and serum TNF-alpha were blocked by z-VAD-fmk, a pan-caspase inhibitor, or z-WEHD-fmk, a caspase-1 (IL-1-converting enzyme, [ICE]) inhibitor. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 123-132 tumor necrosis factor Mus musculus 97-106 18191813-8 2008 The TNFalpha/zVAD-induced release of AA from C12 and L929-cPLA(2)alpha-siRNA cells was pyrrophenone-insensitive, but inhibited by treatment with butylated hydroxyanisole (BHA, an antioxidant). benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 13-17 tumor necrosis factor Mus musculus 4-12 18191813-9 2008 Treatment with dithiothreitol, which inactivates secretory PLA(2) activity, decreased the amount of AA released by TNFalpha/zVAD. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 124-128 tumor necrosis factor Mus musculus 115-123 16537794-9 2006 Importantly, upon z-VAD-fmk treatment, J774A.1 macrophages overexpressed and secreted several chemokines and cytokines, including tumor necrosis factor (TNF) alpha. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 18-27 tumor necrosis factor Mus musculus 130-163 17206708-11 2007 Apoptosis was induced in lamina propria macrophages after treatment with anti-TNF, and it was abrogated through short-term pretreatment with Z-VAD-FMK. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 141-150 tumor necrosis factor Mus musculus 78-81 16874073-7 2006 z-VAD-fmk-treated J774A.1 macrophages overexpress and secrete several chemokines and cytokines, including TNFalpha. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 0-9 tumor necrosis factor Mus musculus 106-114 16420519-8 2006 RESULTS: Pretreatment with Z-VAD-fmk prevented liver injury and hepatocyte apoptosis induced by either GalN/TNF-alpha or alphaFas. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 27-36 tumor necrosis factor Mus musculus 108-117 16418768-1 2005 We investigated the mechanism of the pan-caspase inhibitor z-VAD-fmk"s augmentation of TNFalpha-induced L929 cell death and found this mechanism differs from that of TNFalpha-induced L929 cell death. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 59-68 tumor necrosis factor Mus musculus 87-95 16418768-2 2005 In the presence of 20 ng/ml TNFalpha, z-VAD-fmk initiated apoptosis and necrosis in the majority of L929 cells as measured by an agarose gel electrophoresis and lactate dehydrogenase(LDH)activity based assay. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 38-47 tumor necrosis factor Mus musculus 28-36 16418768-7 2005 These results indicate that in the presence of TNFalpha, z-VAD-fmk further augments cell death which requires the mitochondrial permeability transition and the JNK activation. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 57-66 tumor necrosis factor Mus musculus 47-55 16418769-4 2005 The pan-caspase inhibitor (z-VAD-fmk), caspase-8 inhibitor (z-IETD-fmk) and caspase-3 inhibitor (z-DEVD-fmk) augmented oridonin-and TNFalpha-induced cell death. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 27-36 tumor necrosis factor Mus musculus 132-140 10534346-5 1999 Consistently, the broad-spectrum caspase inhibitor, benzoyloxycarbonyl-val-ala-asp-fluoromethylketone (zVADfmk), prevented TNF-mediated hepatotoxicity in all GalN-dependent models, but failed to protect against Con A. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 103-110 tumor necrosis factor Mus musculus 123-126 12126645-5 2002 Injection of the caspases inhibitor ZVAD-fmk decreased TNF-induced generation of microparticles and thrombocytopenia, indicating a causal role of caspases in platelet fragmentation. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 36-44 tumor necrosis factor Mus musculus 55-58 10988295-6 2000 The striking synergistic effect of the caspase inhibitor benzyloxycarbonyl-Val-Ala-Asp(OMe)-fluoromethylketone on TNF-induced necrosis was also observed with receptors solely containing the DD. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 57-110 tumor necrosis factor Mus musculus 114-117 12652297-3 2003 General caspase inhibition by the protease inhibitor zVAD-fmk exacerbated TNF toxicity by enhancing oxidative stress and mitochondrial damage, resulting in hyperacute hemodynamic collapse, kidney failure and death. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 53-61 tumor necrosis factor Mus musculus 74-77 11361017-9 2001 In the absence of FADD deficiency, TNF-induced apoptosis was zVAD-sensitive and FB-insensitive. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 61-65 tumor necrosis factor Mus musculus 35-38 10827087-4 2000 Here, we report that in NIH3T3 cells, apoptosis in response TNF and cycloheximide is not inhibited by the broad spectrum caspase inhibitor benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone (zVAD. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 190-194 tumor necrosis factor Mus musculus 60-63 10827087-6 2000 Moreover, treatment with zVAD.fmk sensitizes the cells to the cytotoxic action of TNF. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 25-29 tumor necrosis factor Mus musculus 82-85 10827087-12 2000 This hypothesis is further strengthened by the observation that arresting the cells in the G(1) phase of the cell cycle inhibited TNF/zVAD.fmk-induced cell death, whereas blocking them in the G(2)/M phase augmented it. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 134-138 tumor necrosis factor Mus musculus 130-133 10455154-7 1999 We confirmed that the broad spectrum caspase inhibitor benzyloxycarbonyl-Val-Ala-Asp(OMe)-fluoromethylketone markedly increased the susceptibility of L929 cells to TNF, and further demonstrated that E6 enhanced this susceptibility, which again correlated with increased ROS accumulation. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 55-108 tumor necrosis factor Mus musculus 164-167 10425195-4 1999 TNF induces caspase activity in both settings, and the broad spectrum caspase inhibitor zVAD-fmk inhibits this activity and blocks both TNF-induced apoptosis and necrosis. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 88-96 tumor necrosis factor Mus musculus 136-139 10212002-0 1999 TNF-induced enterocyte apoptosis and detachment in mice: induction of caspases and prevention by a caspase inhibitor, ZVAD-fmk. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 118-126 tumor necrosis factor Mus musculus 0-3 10373464-6 1999 Furthermore, Bcl-2 can cooperate with the caspase inhibitor zVAD-fmk in a dose-dependent manner to block TNFalpha-induced cell death. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 60-68 tumor necrosis factor Mus musculus 105-113 10373464-7 1999 Overexpression of Bcl-2 results in a 10-fold decrease in the amount of zVAD-fmk required to inhibit TNFalpha-induced apoptosis. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 71-79 tumor necrosis factor Mus musculus 100-108 9565639-5 1998 zVAD-fmk and zD-fmk, two broad-spectrum inhibitors of caspases, also rendered the cells more sensitive, since the half-maximal dose for TNF-mediated necrosis decreased by a factor of 1,000. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 0-8 tumor necrosis factor Mus musculus 136-139 9565639-6 1998 The presence of zVAD-fmk also resulted in a more rapid increase of TNF-mediated production of oxygen radicals. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 16-24 tumor necrosis factor Mus musculus 67-70 9565639-7 1998 zVAD-fmk-dependent sensitization of TNF cytotoxicity could be completely inhibited by the oxygen radical scavenger butylated hydroxyanisole. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 0-8 tumor necrosis factor Mus musculus 36-39 29337003-3 2018 Here, we discover that MLFs are highly susceptible to undergo necroptosis in a ROS-dependent manner upon exposure to a prototypic death receptor-mediated necroptotic stimulus, i.e. cotreatment with tumor necrosis factor (TNF)alpha, Smac mimetic and the caspase inhibitor zVAD.fmk (TSZ). benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 271-275 tumor necrosis factor Mus musculus 198-219 32460187-8 2020 Triad3A and necroptosis were triggered in mouse microglia cells treated with oxygen and glucose deprivation (OGD), and in TNFalpha-incubated mouse hippocampal neuronal cells treated with Z-VAD-fmk, known as a pan-caspase inhibitor. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 187-196 tumor necrosis factor Mus musculus 122-130 29337003-3 2018 Here, we discover that MLFs are highly susceptible to undergo necroptosis in a ROS-dependent manner upon exposure to a prototypic death receptor-mediated necroptotic stimulus, i.e. cotreatment with tumor necrosis factor (TNF)alpha, Smac mimetic and the caspase inhibitor zVAD.fmk (TSZ). benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 271-275 tumor necrosis factor Mus musculus 221-230 29664014-6 2018 We show that TNF administration damaged the liver vascular endothelium and induced phosphorylated mixed lineage kinase domain-like (phospho-MLKL) reactivity in endothelial cells isolated from TNF/zVAD-treated WT, but not Ripk1D138N/D138N, mice. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 196-200 tumor necrosis factor Mus musculus 13-16 27605011-6 2016 Primary hepatocytes isolated from RIPK1-knockdown mice were sensitized to TNF-induced cell death that was completely inhibited by adding zVAD.fmk. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 137-145 tumor necrosis factor Mus musculus 74-77 28770700-4 2018 In the mouse hepatocyte cell line, TIB-73 cells, TNF-alpha/cycloheximide (T/C) induced RIP1/3 binding only when caspase activity was suppressed by the caspase-specific inhibitor z-VAD-fmk (zVAD). benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 178-187 tumor necrosis factor Mus musculus 49-58 28770700-4 2018 In the mouse hepatocyte cell line, TIB-73 cells, TNF-alpha/cycloheximide (T/C) induced RIP1/3 binding only when caspase activity was suppressed by the caspase-specific inhibitor z-VAD-fmk (zVAD). benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 189-193 tumor necrosis factor Mus musculus 49-58 29170425-4 2017 In this study, TNFalpha activated caspase pathway and induced cell death in RIP3 knockdown L929 cells, and the RIP3-independent cell death had been blocked by Z-VAD-FMK (pan-caspase inhibitor) or caspase 8 knockdown, demonstrating that RIP3 knockdown switched TNFalpha-induced necroptosis to caspase-dependent apoptosis. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 159-168 tumor necrosis factor Mus musculus 15-23 29170425-4 2017 In this study, TNFalpha activated caspase pathway and induced cell death in RIP3 knockdown L929 cells, and the RIP3-independent cell death had been blocked by Z-VAD-FMK (pan-caspase inhibitor) or caspase 8 knockdown, demonstrating that RIP3 knockdown switched TNFalpha-induced necroptosis to caspase-dependent apoptosis. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 159-168 tumor necrosis factor Mus musculus 260-268 27616656-3 2016 We found that TNF-alpha/ActD-induced apoptosis was completely blocked by a general caspase inhibitor ZVAD-fmk at 24 hours but hepatocytes still died by necrosis at 48 hours. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 101-109 tumor necrosis factor Mus musculus 14-23 27616656-5 2016 Inhibition of receptor-interacting protein kinase (RIP)1 by necrostatin 1 partially inhibited TNF-alpha/ZVAD-induced necrosis in primary hepatocytes. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 104-108 tumor necrosis factor Mus musculus 94-103 24577082-8 2014 TNFalpha/zVAD treatment induced cell death within 4 h. Cell death was preceded by RIPK1-RIPK3-pAkt assembly, and phosphorylation of Thr-308 and Thr473 of AKT and its direct substrate glycogen synthase kinase-3beta, as well as mTOR and its direct substrate S6 ribosomal protein (S6), suggesting activation of Akt/mTOR pathways. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 9-13 tumor necrosis factor Mus musculus 0-8 25898986-5 2015 Although exogenously added polyI:C alone marginally induced necroptosis in CT26 cells, a combined regimen of polyI:C and zVAD induced approximately 50% CT26 necroptosis in vitro without secondary effects of TNFalpha or type I IFNs. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 121-125 tumor necrosis factor Mus musculus 207-215 24751948-3 2014 It was also reported that zVAD can induce a small amount of TNF production, which was shown to be required for zVAD-induced L929 cell death, arguing for the contribution of autophagy in the zVAD-induced L929 cell death. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 26-30 tumor necrosis factor Mus musculus 60-63 24751948-3 2014 It was also reported that zVAD can induce a small amount of TNF production, which was shown to be required for zVAD-induced L929 cell death, arguing for the contribution of autophagy in the zVAD-induced L929 cell death. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 111-115 tumor necrosis factor Mus musculus 60-63 24751948-3 2014 It was also reported that zVAD can induce a small amount of TNF production, which was shown to be required for zVAD-induced L929 cell death, arguing for the contribution of autophagy in the zVAD-induced L929 cell death. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 111-115 tumor necrosis factor Mus musculus 60-63 24751948-7 2014 By the use of small hairpin RNAs and chemical inhibitors, we further demonstrated that zVAD-induced autophagy requires not only RIP1, RIP3, PI3KC3 and Beclin-1, but also RGS19 and GNAI3, and this autophagy is required for zVAD-induced TNF production. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 87-91 tumor necrosis factor Mus musculus 235-238 24751948-8 2014 Collectively, our data suggest that zVAD-induced L929 cell death is a synergistic result of autophagy, caspase inhibition and autocrine effect of TNF. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 36-40 tumor necrosis factor Mus musculus 146-149 25398540-3 2015 However, comparing the TNFalpha-induced cell death in these two cell lines, we found that, unlike the L929-N cells that show typical RIP3-dependent necrosis, TNFalpha-induced cell death in L929-A cells is pan-caspase inhibitor Z-VAD-FMK (Z-VAD)-sensitive, which does not depend on RIP3. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 227-236 tumor necrosis factor Mus musculus 158-166 23941769-2 2013 Here, we demonstrated that pan-caspase inhibitor z-VAD-fmk (zVAD) exacerbated TNFalpha-induced necroptosis and autophagy in murine fibrosarcoma L929 cells. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 49-58 tumor necrosis factor Mus musculus 78-86 23941769-2 2013 Here, we demonstrated that pan-caspase inhibitor z-VAD-fmk (zVAD) exacerbated TNFalpha-induced necroptosis and autophagy in murine fibrosarcoma L929 cells. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 60-64 tumor necrosis factor Mus musculus 78-86 23941769-3 2013 And the RIP-1 inhibitor necrostatin-1 inhibited TNFalpha+zVAD-induced necroptosis and autophagy. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 57-61 tumor necrosis factor Mus musculus 48-56 23941769-10 2013 In addition, caspase-6 activation induced by TNFalpha administration was inhibited by zVAD. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 86-90 tumor necrosis factor Mus musculus 45-53 22371307-3 2012 In the lethal mouse model of TNFalpha-mediated shock, addition of the pan-caspase inhibitor zVAD-fmk (zVAD) accelerates time to death. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 92-100 tumor necrosis factor Mus musculus 29-37 23000518-4 2012 Moreover, pan-caspase inhibitor z-VAD-fmk (zVAD) increased RIP1 expression and exacerbated TNFalpha-induced mitochondrial dysfunction and ROS production, indicating that RIP1 led to mitochondrial dysfunction and ROS production. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 32-41 tumor necrosis factor Mus musculus 91-99 23000518-4 2012 Moreover, pan-caspase inhibitor z-VAD-fmk (zVAD) increased RIP1 expression and exacerbated TNFalpha-induced mitochondrial dysfunction and ROS production, indicating that RIP1 led to mitochondrial dysfunction and ROS production. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 43-47 tumor necrosis factor Mus musculus 91-99 22371307-3 2012 In the lethal mouse model of TNFalpha-mediated shock, addition of the pan-caspase inhibitor zVAD-fmk (zVAD) accelerates time to death. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 92-96 tumor necrosis factor Mus musculus 29-37 22027097-5 2011 The pan-caspase inhibitor z-VAD-fmk (zVAD) exacerbated TNFalpha-induced necroptosis and autophagy. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 26-35 tumor necrosis factor Mus musculus 55-63 20539307-0 2011 zVAD-induced necroptosis in L929 cells depends on autocrine production of TNFalpha mediated by the PKC-MAPKs-AP-1 pathway. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 0-4 tumor necrosis factor Mus musculus 74-82 20539307-3 2011 In this study, we provided clear evidence that zVAD-induced necroptosis in L929 cells and such cell death is dependent on autocrine production of tumor necrosis factor-alpha (TNFalpha) at the transcriptional level. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 47-51 tumor necrosis factor Mus musculus 146-173 20539307-3 2011 In this study, we provided clear evidence that zVAD-induced necroptosis in L929 cells and such cell death is dependent on autocrine production of tumor necrosis factor-alpha (TNFalpha) at the transcriptional level. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 47-51 tumor necrosis factor Mus musculus 175-183 20539307-4 2011 More importantly, we identified that activating protein-1 (AP-1), but not nuclear factor kappa-B, is the transcription factor controlling zVAD-induced TNFalpha transcription. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 138-142 tumor necrosis factor Mus musculus 151-159 20539307-6 2011 Finally, we found that protein kinase C is the important upstream signaling molecule in mediating zVAD-induced activation of MAPKs and AP-1, and subsequent autocrine production of TNFalpha and cell death. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 98-102 tumor necrosis factor Mus musculus 180-188 22027097-5 2011 The pan-caspase inhibitor z-VAD-fmk (zVAD) exacerbated TNFalpha-induced necroptosis and autophagy. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 37-41 tumor necrosis factor Mus musculus 55-63 22027097-6 2011 Combined treatment with TNFalpha and zVAD further decreased the expressions of p-p38 and NF-kappaB compared with TNFalpha alone treatment. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 37-41 tumor necrosis factor Mus musculus 113-121 20702393-7 2010 Moreover, under TNF-alpha stimulation, degradation of Nucling was recovered by pan-caspase inhibitor zVAD-fmk. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 101-109 tumor necrosis factor Mus musculus 16-25