PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 29417442-12 2018 The combination of DAPT and ATRA effectively increased the proportion of apoptotic cells and the level of caspase 3/7 activities compared to single treatment. Tretinoin 28-32 caspase 3 Homo sapiens 106-115 29417442-13 2018 Moreover, augmented caspase-3 up-regulation and bcl-2 down-regulation were found following combined application of DAPT and ATRA. Tretinoin 124-128 caspase 3 Homo sapiens 20-29 27720952-8 2016 RA covalently bound to the Thr2 residue in Rho-GDIbeta (5kDa), which is the second product resulting from the cleavage of Rho-GDIbeta (28kDa) by caspase-3. Tretinoin 0-2 caspase 3 Homo sapiens 145-154 26953980-4 2017 In the present study, 24S-OHC was found to induce apoptosis as determined by caspase-3 activation in all-trans-retinoic acid (atRA)-treated SH-SY5Y cells in which expression of caspase-8 was induced. Tretinoin 105-124 caspase 3 Homo sapiens 77-86 26953980-4 2017 In the present study, 24S-OHC was found to induce apoptosis as determined by caspase-3 activation in all-trans-retinoic acid (atRA)-treated SH-SY5Y cells in which expression of caspase-8 was induced. Tretinoin 126-130 caspase 3 Homo sapiens 77-86 26173116-5 2015 We could show that in WERI-Rb1 cells RA/BMP-4 mediated cell death is at least partially caspase-dependent, whereby RA and BMP-4 additively increased (i) Apaf-1 mRNA levels, (ii) caspase-9 cleavage activity and (iii) the number of activated, cleaved caspase-3 positive cells. Tretinoin 37-39 caspase 3 Homo sapiens 249-258 25683251-8 2015 In the combination treatment using ATRA and sorafenib, increased apoptosis, followed by the activation of p38 MAPK and JNK, the upregulation and translocation of Bax to mitochondria, and the activation of caspase-3, was observed. Tretinoin 35-39 caspase 3 Homo sapiens 205-214 24406248-5 2014 ATRA treatment caused decreased Mcl-1, caspase-3 activation, and PARP cleavage following the inactivation of phosphatidylinositol 3-kinase/AKT and the activation of GSK-3beta. Tretinoin 0-4 caspase 3 Homo sapiens 39-48 22659417-4 2012 In addition, LMP1 suppressed ATRA-mediated activation of Caspase 9, Caspase 3, and PARP but not Caspase 8 in Ad-AH cells, suggesting that LMP1 acts by blocking the activation of intrinsic apoptosis pathway by ATRA. Tretinoin 29-33 caspase 3 Homo sapiens 68-77 23693014-13 2013 We also found that treatment with ATRA induces cell survival, which is inhibited by 15e or over-expression of an inactive form of Akt, through a subsequent increase in the levels of the active form of caspase-3. Tretinoin 34-38 caspase 3 Homo sapiens 201-210 23023919-6 2012 In conclusion, downregulation of the PHB gene may inhibit apoptosis of NB4-R1 cells, and it is speculated that this was at least partly due to the downregulation of caspase-3, and PHB may be a novel target for gene therapy for retinoic acid-resistant acute promyelocytic leukemia. Tretinoin 227-240 caspase 3 Homo sapiens 165-174 19267404-4 2009 Caspase-3 colocalized and interacted with AFP in the cytoplasm of Bel 7402 cells, and translocated into nuclei in association with the occurrence of apoptosis while cells were under cotreatment with all-trans retinoic acid (ATRA) or TRAIL. Tretinoin 209-222 caspase 3 Homo sapiens 0-9 23304206-6 2012 Furthermore, RA-triggered caspase 3 activation and following Cdk5 over-activation were destroyed by treatments of both CP and Cdk5 knockdown. Tretinoin 13-15 caspase 3 Homo sapiens 26-35 20559758-4 2010 EA activated the caspase-3 pathway and enhanced the expressions of myeloid differentiation markers (CD11b, MRP-14 protein, granulocytic morphology) induced by ATRA treatment. Tretinoin 159-163 caspase 3 Homo sapiens 17-26 19467017-12 2009 Caspase-3 activity was increased upon exposure to RGZ in both U266 and RPMI-8226 cells while combination of RGZ and ATRA brought out more effective activation of caspase-3. Tretinoin 116-120 caspase 3 Homo sapiens 162-171 19557639-7 2009 Consequently, it has been shown that, in RA-treated Molt3 cells, upregulation of p21 due to RA accompanies caspase 3/PARP activation which precedes the occurrence of apoptosis. Tretinoin 41-43 caspase 3 Homo sapiens 107-116 19267404-4 2009 Caspase-3 colocalized and interacted with AFP in the cytoplasm of Bel 7402 cells, and translocated into nuclei in association with the occurrence of apoptosis while cells were under cotreatment with all-trans retinoic acid (ATRA) or TRAIL. Tretinoin 224-228 caspase 3 Homo sapiens 0-9 19731824-8 2009 Caspase-3 activity increased substantially with the increase of RGZ concentration and the addition of RGZ + ATRA in the culture medium showed similar synergism effect on caspase-3 activation (P < 0.01). Tretinoin 108-112 caspase 3 Homo sapiens 0-9 19731824-8 2009 Caspase-3 activity increased substantially with the increase of RGZ concentration and the addition of RGZ + ATRA in the culture medium showed similar synergism effect on caspase-3 activation (P < 0.01). Tretinoin 108-112 caspase 3 Homo sapiens 170-179 19112091-7 2009 RA-induced cell death was accompanied by enhanced cleavage of procaspase-3, -6, and -8, as well as enhanced cleavage of DNA fragmentation factor 45. Tretinoin 0-2 caspase 3 Homo sapiens 62-86 19017957-6 2008 RA-induced eosinophil survival appears to be associated with down-regulation of caspase 3 and inhibition of its enzymatic activity. Tretinoin 0-2 caspase 3 Homo sapiens 80-89 19764350-10 2009 In addition, our results also indicated that Cdk5 activity was involved in RA-induced HeLa apoptosis by detecting cleavages of caspase-3 and its substrate, PARP (poly (ADP-ribose) polymerases) Interestingly, the nuclear localizations of Cdk5 and p35 proteins were increased by RA treatment, which, again, suggests the involvement of Cdk5 and p35 in RA-induced apoptotic effects. Tretinoin 75-77 caspase 3 Homo sapiens 127-136 16568081-5 2006 ATRA-mediated apoptosis in CHP134 and NB-39-nu cells was associated with a significant activation of caspase-9 and caspase-3 as well as cytoplasmic release of cytochrome c from mitochondria in a p53-independent manner. Tretinoin 0-4 caspase 3 Homo sapiens 115-124 17531122-13 2007 CONCLUSIONS: Berbamine induces caspase-3-dependent apoptosis of leukemia NB4 cells via survivin-mediated pathway, suggesting that berbamine may be a novel potential agent against APL with a mechanism distinct from that of all-trans retinoic acid (ATRA) and arsenic trioxide (ATO). Tretinoin 232-245 caspase 3 Homo sapiens 31-40 17531122-13 2007 CONCLUSIONS: Berbamine induces caspase-3-dependent apoptosis of leukemia NB4 cells via survivin-mediated pathway, suggesting that berbamine may be a novel potential agent against APL with a mechanism distinct from that of all-trans retinoic acid (ATRA) and arsenic trioxide (ATO). Tretinoin 247-251 caspase 3 Homo sapiens 31-40 17616812-8 2007 Combination of ATRA and IFN-gamma showed more efficacy than IFN-gamma alone in causing apoptosis that occurred due to increases in Bax:Bcl-2 ratio, mitochondrial release of cytochrome c, and caspase-3 activity. Tretinoin 15-19 caspase 3 Homo sapiens 191-200 15374966-4 2004 In contrast, when the cells were treated with 1 micromol/L ATRA for 6 days and subsequently irradiated with different doses of UVB, they underwent massive apoptosis as assessed by morphology, expression of activated caspase-3, and DNA fragmentation. Tretinoin 59-63 caspase 3 Homo sapiens 216-225 16765349-4 2006 Upregulated p21 by RA accompanies caspase-3 activation and precedes the occurrence of apoptosis. Tretinoin 19-21 caspase 3 Homo sapiens 34-43 15976015-8 2005 Treatment with the TPA/ATRA combination resulted in a substantially decreased ratio of the percentage of mitotic cells to the percentage of caspase-3-positive cells in the tumors compared with tumors from the vehicle-treated control animals. Tretinoin 23-27 caspase 3 Homo sapiens 140-149 15908778-13 2005 Caspase 3-like activity was induced by the apoptotic concentrations of atRA at late time points. Tretinoin 71-75 caspase 3 Homo sapiens 0-9 15273718-5 2004 We found that RA+GF induce apoptosis, as shown by an increase in fragmented DNA, Annexin-V-positive cells and caspase-3 activation. Tretinoin 14-16 caspase 3 Homo sapiens 110-119 15374966-6 2004 Analysis by real-time PCR and Western blot revealed that ATRA treatment strongly increased the mRNA and protein expression of p53 and caspase-3, -6, -7, and -9, which are key regulators of apoptosis. Tretinoin 57-61 caspase 3 Homo sapiens 134-159 15159275-14 2004 These findings suggest not only that AF induces caspase-3-dependent apoptosis via a mechanism involving ROS, but also that the combined treatment with AF and ATRA induces differentiation of NB4 cells. Tretinoin 158-162 caspase 3 Homo sapiens 48-57 14502257-13 2003 CONCLUSION: These results suggest that the RA-induced apoptotic signals were transduced via downregulation of Bcl-xL and the decrease in the mitochondrial membrane function leading to caspase-3 activation. Tretinoin 43-45 caspase 3 Homo sapiens 184-193 12970919-9 2003 The inhibition of telomerase activity and the activation of Caspase-3 may be the key steps through which ATRA inhibits the proliferation of SMMC-7721 cell line. Tretinoin 105-109 caspase 3 Homo sapiens 60-69 12592339-4 2003 We observed that induction of granulocytic differentiation by retinoic acid led to robust activation of the executioner protease caspase-3, and early onset of apoptosis. Tretinoin 62-75 caspase 3 Homo sapiens 129-138 15135888-3 2004 Exposure of retinoic acid-differentiated human SH-SY5Y neuroblastoma cells to 270 microM hydrogen peroxide caused activation of caspase 3 and significant neuronal death. Tretinoin 12-25 caspase 3 Homo sapiens 128-137 14519626-0 2003 All-trans-retinoic acid-induced apoptosis in human medulloblastoma: activation of caspase-3/poly(ADP-ribose) polymerase 1 pathway. Tretinoin 0-23 caspase 3 Homo sapiens 82-121 14519626-7 2003 We also demonstrate that the ATRA-induced decrease in cell viability was due to increased cell death by apoptosis, which was accompanied by a 20-fold induction of caspase-3 activity in the most sensitive cell line, D458. Tretinoin 29-33 caspase 3 Homo sapiens 163-172 14519626-9 2003 Furthermore, ATRA-induced cell death in D283, D425, and D458 cells was accompanied by activation of caspase-3, a key executioner of apoptosis. Tretinoin 13-17 caspase 3 Homo sapiens 100-109 14519626-11 2003 Pretreatment with a specific caspase-3 inhibitor, DEVD-CHO, significantly reduced ATRA-induced apoptotic cell death. Tretinoin 82-86 caspase 3 Homo sapiens 29-38 14519626-12 2003 Thus, we demonstrate for the first time that low concentrations of ATRA inhibit MB cell proliferation and induce apoptotic cell death in part by activating caspase-3/poly(ADP-ribose) polymerase 1 effector pathway, and we show that retinoic acids and novel retinoids are potential antitumor agents in MB therapy. Tretinoin 67-71 caspase 3 Homo sapiens 156-195 14519626-12 2003 Thus, we demonstrate for the first time that low concentrations of ATRA inhibit MB cell proliferation and induce apoptotic cell death in part by activating caspase-3/poly(ADP-ribose) polymerase 1 effector pathway, and we show that retinoic acids and novel retinoids are potential antitumor agents in MB therapy. Tretinoin 231-245 caspase 3 Homo sapiens 156-195 12970919-7 2003 Besides, ATRA could inhibit the activity of telomerase, promote the expression of Caspase-3 and its activation. Tretinoin 9-13 caspase 3 Homo sapiens 82-91 12594055-6 2003 Likewise, retinoic acid inhibited caspase 3 activity in BEAS-2B cells and A549 cells induced by elastase, as well as proteolytic activity of elastase. Tretinoin 10-23 caspase 3 Homo sapiens 34-43 12594055-8 2003 These findings suggest that retinoic acid may inhibit elastase-induced lung epithelial cell injury partly through the inhibition of proteolytic activity of elastase and through the inhibition of caspase 3 activity by elastase. Tretinoin 28-41 caspase 3 Homo sapiens 195-204 12446691-10 2003 Interestingly, the cytosolic calcium chelator BAPTA-AM and K-201 protected RA-treated chondrocytes from undergoing apoptotic changes, as indicated by higher bcl-2 gene expression, reduced caspase-3 activity, and the percentage of TUNEL-positive cells. Tretinoin 75-77 caspase 3 Homo sapiens 188-197 10208436-0 1999 Synergistic effects of retinoic acid and 8-Cl-cAMP on apoptosis require caspase-3 activation in human ovarian cancer cells. Tretinoin 23-36 caspase 3 Homo sapiens 72-81 11602619-7 2001 Retinoic acid also inhibited cell proliferation and, after prolonged treatment, increased caspase-3 activity and induced cell death in ACTH-secreting cells. Tretinoin 0-13 caspase 3 Homo sapiens 90-99 12445205-5 2002 By contrast, the expression of the caspases 3 and 8, which are both activated during conventional apoptosis, was increased and unchanged, respectively, after retinoic acid treatment. Tretinoin 158-171 caspase 3 Homo sapiens 35-51 12445205-6 2002 In addition to inhibition of differentiation in skin equivalents, retinoic acid treatment led to keratinocyte apoptosis and activation of caspase-3, both of which were undetectable in differentiated control skin equivalents. Tretinoin 66-79 caspase 3 Homo sapiens 138-147 12431242-4 2002 Caspase-3 activation was shown to be a prerequisite for ATRA-induced apoptosis, which was inhibited by the pan-caspase inhibitor Z-VAD-FMK and the caspase-9 inhibitor Z-LEHD-FMK. Tretinoin 56-60 caspase 3 Homo sapiens 0-9 9125129-0 1997 Wortmannin enhances CPP32-like activity during neuronal differentiation of P19 embryonal carcinoma cells induced by retinoic acid. Tretinoin 116-129 caspase 3 Homo sapiens 20-25 9125129-2 1997 Two CPP32-like proteases, CPP32 and Mch-3, are expressed in untreated and retinoic acid-treated P19 EC cells. Tretinoin 74-87 caspase 3 Homo sapiens 4-9 9125129-2 1997 Two CPP32-like proteases, CPP32 and Mch-3, are expressed in untreated and retinoic acid-treated P19 EC cells. Tretinoin 74-87 caspase 3 Homo sapiens 26-31 9125129-5 1997 Wortmannin, PI-3K inhibitor, enhances the CPP32-like activity of the retinoic acid-treated P19 EC cells. Tretinoin 69-82 caspase 3 Homo sapiens 42-47 9276475-8 1997 De novo caspase expression was responsible for the development of spontaneous apoptosis, since specific inhibitors of ICE (YVAD-CMK) and CPP32 (DEVD-CHO), inhibited retinoic acid induced spontaneous apoptosis. Tretinoin 165-178 caspase 3 Homo sapiens 137-142 33726556-8 2022 NAC and salubrinal inhibited an increase in VEGF-A, CHOP and caspase-3 caused by ATRA in ARPE-19 cells. Tretinoin 81-85 caspase 3 Homo sapiens 61-70