PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 29111403-5 2018 Pharmacological and genetic inhibition of autophagy suppressed Cd-induced apoptosis, as evidenced by inhibition of caspase-8, caspase-3, and PARP-1 cleavage, indicating that autophagy promotes apoptosis. Cadmium 63-65 caspase 3 Mus musculus 126-135 33396178-8 2021 Inhibition of caspase with pan-caspase inhibitor, Z-VAD-FMK, prevented MC3T3-E1 subclone 14 cells from cadmium-induced reduction of Runx2, STC2, caspase 9, and accumulation of cleaved PARP and cleaved caspase 3. Cadmium 103-110 caspase 3 Mus musculus 201-210 32058163-5 2020 In addition, following cadmium exposure, the nuclear transcription factor c-jun was significantly activated, which led to increased expression of downstream gene c-jun, resulting in downstream activation of the apoptosis-related protein Caspase3 and upregulation of Cleaved-PARP, as well as inhibition of the anti-apoptosis protein Bcl-2. Cadmium 23-30 caspase 3 Mus musculus 237-245 30414103-5 2019 Cd accumulation was recorded in the cortical homogenates, accompanied by elevated levels of lipid peroxidation, nitric oxide, tumor necrosis factor-alpha, interleukin-1beta, and the pro-apoptotic mRNA Bax and caspase-3. Cadmium 0-2 caspase 3 Mus musculus 209-218 30544760-7 2018 Furthermore, Cd triggered an apoptotic cascade via upregulation of caspase-3 and Bax and downregulation of Bcl-2. Cadmium 13-15 caspase 3 Mus musculus 67-76 29111403-3 2018 Cd decreased cell viability in a dose-dependent manner; cleaved caspase-8, caspase-3, and poly (ADP-ribose) polymerase (PARP)-1; increased DNA laddering; induced CCAAT-enhancer-binding protein homologous protein (CHOP); and reduced tumor necrosis factor (TNF)-alpha expression; indicating that caspase-dependent and endoplasmic reticulum (ER)-mediated apoptosis are involved in Cd-induced immunotoxicity. Cadmium 0-2 caspase 3 Mus musculus 75-84 21620867-7 2011 Immunohistochemical analysis revealed that telmisartan significantly decreased the cadmium-induced overexpression of inducible nitric oxide synthase (iNOS), nuclear factor-kappaB (NF-kappaB), Fas ligand (FasL) and caspase-3 in renal tissue. Cadmium 83-90 caspase 3 Mus musculus 214-223 25409916-8 2016 Furthermore, the transcriptional status and the activities of Caspase 9 and Caspase 3 were increased significantly in the liver when exposed to high doses of Cd, Cr or their mixture. Cadmium 158-160 caspase 3 Mus musculus 76-85 23880315-7 2013 Although cadmium administration did not result in any visible structural changes in the placenta, increased apoptosis was detected in MT-I/II(-/-) placentas following cadmium exposure, with a significant increase in levels of both p53 and caspase 3 proteins. Cadmium 167-174 caspase 3 Mus musculus 239-248 23891603-10 2013 A significant increase in liver DNA AP sites and 8-oxo-dG levels with concomitant increase in caspase-3 was observed in CD fed and irradiated animals compared to NSD fed and irradiated mice. Cadmium 120-122 caspase 3 Mus musculus 94-103 20025959-4 2010 Greater Cd uptake was observed in C57 embryos compared to SWV and these observations of differential uptake were associated with increased alterations in expression of biomarkers of metal response (e.g. c-Casp3) and strain sensitivity. Cadmium 8-10 caspase 3 Mus musculus 205-210 21337715-7 2011 In addition, cadmium provoked germ cell apoptosis by upregulating expression of the proapoptotic proteins Bax and caspase-3 and downregulating expression of the antiapoptotic protein Bcl-XL. Cadmium 13-20 caspase 3 Mus musculus 114-123 21337715-10 2011 Additionally, quercetin protected germ cells from cadmium-induced apoptosis by downregulating the expression of Bax and caspase-3 and upregulating Bcl-XL expression. Cadmium 50-57 caspase 3 Mus musculus 120-129 16780805-7 2006 Cadmium (25 microM) induced apoptosis earliest at 6 h. Alterations in ROS and GSH preceded mitochondrial membrane depolarization and caspase-3 activation followed by apoptosis. Cadmium 0-7 caspase 3 Mus musculus 133-142 19748544-8 2009 Also, the reductions in hepatic nitric oxide and zinc ion levels, and the increases in hepatic cadmium ion concentration, and myeloperoxidase and caspase-3 activities following cadmium exposure were significantly attenuated by carnosine treatment. Cadmium 177-184 caspase 3 Mus musculus 146-155 16563667-6 2006 The early markers of apoptosis-loss in mitochondrial membrane potential and caspase-3 activation were evident as early as 1.5h by 50microM Cd. Cadmium 139-141 caspase 3 Mus musculus 76-85 16728380-10 2006 Inhibition of caspase-3 protected oxidative stress produced by cadmium, suggesting that the activation of caspase-3 also contributes to generation of reactive oxygen species (ROS). Cadmium 63-70 caspase 3 Mus musculus 14-23 16728380-10 2006 Inhibition of caspase-3 protected oxidative stress produced by cadmium, suggesting that the activation of caspase-3 also contributes to generation of reactive oxygen species (ROS). Cadmium 63-70 caspase 3 Mus musculus 106-115 15501611-8 2004 Decreased expression of pro-apoptotic genes, particularly Casp3, and DNA repair genes possibly contributes to Cd-induced carcinogenesis. Cadmium 110-112 caspase 3 Mus musculus 58-63 16728380-4 2006 Activation of caspase-3 was observed at 8 h and DNA fragmentation at 16 h in the presence of 20 microM cadmium, suggesting that caspase-3 activation is a prior step to DNA fragmentation in cadmium-induced apoptosis. Cadmium 103-110 caspase 3 Mus musculus 14-23 16728380-4 2006 Activation of caspase-3 was observed at 8 h and DNA fragmentation at 16 h in the presence of 20 microM cadmium, suggesting that caspase-3 activation is a prior step to DNA fragmentation in cadmium-induced apoptosis. Cadmium 103-110 caspase 3 Mus musculus 128-137 16728380-4 2006 Activation of caspase-3 was observed at 8 h and DNA fragmentation at 16 h in the presence of 20 microM cadmium, suggesting that caspase-3 activation is a prior step to DNA fragmentation in cadmium-induced apoptosis. Cadmium 189-196 caspase 3 Mus musculus 14-23 16728380-4 2006 Activation of caspase-3 was observed at 8 h and DNA fragmentation at 16 h in the presence of 20 microM cadmium, suggesting that caspase-3 activation is a prior step to DNA fragmentation in cadmium-induced apoptosis. Cadmium 189-196 caspase 3 Mus musculus 128-137 16728380-5 2006 Inhibitors of caspase-3, -8, -9, and a general caspase inhibitor suppressed cadmium-induced caspase-3 activation and apoptosis indicating the importance of caspase-3 in cadmium-induced toxicity in these cells. Cadmium 76-83 caspase 3 Mus musculus 14-31 16728380-5 2006 Inhibitors of caspase-3, -8, -9, and a general caspase inhibitor suppressed cadmium-induced caspase-3 activation and apoptosis indicating the importance of caspase-3 in cadmium-induced toxicity in these cells. Cadmium 76-83 caspase 3 Mus musculus 14-23 16728380-5 2006 Inhibitors of caspase-3, -8, -9, and a general caspase inhibitor suppressed cadmium-induced caspase-3 activation and apoptosis indicating the importance of caspase-3 in cadmium-induced toxicity in these cells. Cadmium 76-83 caspase 3 Mus musculus 92-101 16728380-5 2006 Inhibitors of caspase-3, -8, -9, and a general caspase inhibitor suppressed cadmium-induced caspase-3 activation and apoptosis indicating the importance of caspase-3 in cadmium-induced toxicity in these cells. Cadmium 169-176 caspase 3 Mus musculus 14-31 16728380-5 2006 Inhibitors of caspase-3, -8, -9, and a general caspase inhibitor suppressed cadmium-induced caspase-3 activation and apoptosis indicating the importance of caspase-3 in cadmium-induced toxicity in these cells. Cadmium 169-176 caspase 3 Mus musculus 14-23 16728380-5 2006 Inhibitors of caspase-3, -8, -9, and a general caspase inhibitor suppressed cadmium-induced caspase-3 activation and apoptosis indicating the importance of caspase-3 in cadmium-induced toxicity in these cells. Cadmium 169-176 caspase 3 Mus musculus 92-101 16413650-4 2006 The early stage markers of apoptosis, i.e. decreased mitochondrial membrane potential and caspase-3 activation were observed as early as 1.5 h by the highest dose of Cd (50 microM). Cadmium 166-168 caspase 3 Mus musculus 90-99 11181107-6 2001 Moreover, Cd exposure led to a rapid and sustained intracellular calcium (Ca2+) elevation, followed by caspase-3 activation and PARP cleavage, all of which preceded the characteristic DNA fragmentation. Cadmium 10-12 caspase 3 Mus musculus 103-112 11181107-8 2001 It is believed that intracellular Ca2+ elevation may trigger caspase-3 activation either through mitochondria or through activation of Ca2+-dependent protease in Cd-treated thymocytes. Cadmium 162-164 caspase 3 Mus musculus 61-70 10966523-10 2000 Six months of Cd exposure to MT-null animals resulted in greater increases in renal caspase-3 activity, an indicator of apoptosis, than to WT mice. Cadmium 14-16 caspase 3 Mus musculus 84-93