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1. |
Data show that the mDRA-6-induced apoptosis was repressed by 77.9% by Caspase-8 inhibitor ZIF, 54.2% by Caspase-3 inhibitor ZDF, and 8.7% by Caspase-9 inhibitor ZLF, but was not repressed by Caspase-10 inhibitor ZAF. |
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2. |
The caspase-9-cleaved form of Sema7A reveals abundant caspase-9-activated cells in 2-year-old (aged) but not in 2-month-old (young) mice. |
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3. |
Polymorphism in Caspase 9-1263 was observed to play a protective role in susceptibility to BC risk. Caspase 9 gene variants were also associated with reduced risk of NMBIC stages. |
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4. |
Our results suggest that the presence of the G/G genotype represents a higher risk factor in our MS population and a differential production of CASP-9 might be a contributory factor in determining the severity of MS. |
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5. |
Data suggest that in the absence of its ligand Shh the dependence receptor Patched serves as the anchor for a caspase-activating complex that includes DRAL, and caspase-9. |
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6. |
The oxidative modification of caspase-9 by reactive oxygen species can mediate its interaction with apoptotic protease-activating factor 1, and can promote its formation of disulfide-linked complexes. |
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7. |
Observational study of gene-disease association and gene-gene interaction. (HuGE Navigator) |
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8. |
Study confirms the association between CASP9 gene and non-small cell lung cancer oncogenesis, rs1052576 which locates in exon 5 of CASP9 gene is associated with NSCLC. |
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9. |
Clinical trial of gene-disease association, gene-environment interaction, and pharmacogenomic / toxicogenomic. (HuGE Navigator) |
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10. |
Extracellular adenosine induces apoptosis in Caco-2 cells by activating caspase-9 and the downstream effector caspase caspase-3 in association with mitochondrial damage via A(2a) adenosine receptors. |
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11. |
Results describe the immunohistochemical distribution of caspase 3, 9 and Bax in intracranial U87 glioblastoma xenografts, and show that xenografts contain cells positive for caspase-3, caspase-9, and Bax. |
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12. |
DYRK1A regulates caspase-9-mediated apoptosis during retina development |
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13. |
Observational study of gene-disease association, gene-environment interaction, and pharmacogenomic / toxicogenomic. (HuGE Navigator) |
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14. |
Regulation of apoptosis through inhibitory phosphorylation of caspase 9 may play a role in the function of DYRK1A during development and in pathogenesis. |
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15. |
an apoptotic inhibitory complex comprised of DR5, FADD, caspase-8, and c-FLIP(L) exists in MCF-7 cells, and the absence of c-FLIP(L) from this complex induces DR5- and FADD-mediated caspase-8 activation in the death inducing signaling complex |
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16. |
the simultaneous downregulation of uPAR and MMP-9 induces apoptosome-mediated apoptosis through FADD-associated protein RIP and caspase 9 |
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17. |
Caspase-3 and caspase-7 exhibit differential activity toward multiple substrate proteins, including Bid, XIAP, gelsolin, caspase-6, and cochaperone p23. |
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18. |
These results illustrate that JEV infection triggers caspase cascades involving the initiators caspase-8 and -9, probably through FADD-independent but mitochondrion-dependent pathways. |
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19. |
Western blotting suggests that vinorelbine cleaves caspase-3, -9 and -8 and reduces the amount of mitochondrial cytochrome c. |
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20. |
Melatonin maintains mitochondrial membrane potential and attenuates activation of initiator (casp-9) and effector caspases (casp-3/casp-7) and PARP in UVR-exposed HaCaT keratinocytes |
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21. |
It is concluded that P. aeruginosa can induce apoptosis with an up-regulated expression of Bax and a down-regulated expression of Bcl-2, which resulted in increased levels of cytochrome c release and increased caspase-3 and -9 in human U937 cells. |
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22. |
Enteropathogenic Escherichia coli induced apoptosis in T84 intestinal epithelial cells via induction of caspases-3, -8, and -9. |
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23. |
characterization of the caspase 9 signaling cascade; data provide novel insights into the ordering of a caspase signaling network downstream of caspase-9 in intact cells during apoptosis |
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24. |
the induction of apoptosis through the inhibition of endogenous FGF signaling is caspase-9 pathway- dependent |
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25. |
Arg(10) in the D domain of caspase-9 interacts with Asp(160) in the TTCD motif of ERK2. Differences in the TTCD motif in other MAPK family members could account for the selective recognition of caspase-9 by ERK1/2 |
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26. |
Results indicate that miR-1 and miR-133 are involved in regulating cell fate, and that post-transcriptional repression of HSP60 and HSP70 by miR-1 and of caspase-9 by miR-133 contributes significantly to their opposing actions. |
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27. |
Observational study of gene-disease association. (HuGE Navigator) |
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28. |
Observational study of gene-environment interaction and pharmacogenomic / toxicogenomic. (HuGE Navigator) |
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29. |
a caspase-9 signaling cascade induces feedback disruption of the mitochondrion through cleavage of anti-apoptotic Bcl-2, Bcl-xL, and Mcl-1 |
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30. |
Bortezomib induced apoptosis of EBV lymphoblastoid cell lines (LCLs) by inducing cleavage of caspases 8 and 9 |
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31. |
RGDS directly binds and activates caspases 8 and 9, inhibits chemotaxis, and induces apoptosis of HUVECs with a mechanism independent from its antiadhesive effect. |
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32. |
caspase-3, -8, and -9 activity is enhanced by safrole oxidase in lung cancer cells |
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33. |
results suggest that ML-IAP might regulate apoptosis by sequestering Smac and preventing it from antagonizing XIAP-mediated inhibition of caspases, rather than by direct inhibition of caspases |
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34. |
ILP2 is an unstable protein, and cannot inhibit caspase 9 in a physiological way on its own; possibly ILP2 requires assistance from unidentified cellular factors to be an effective inhibitor of apoptosis in vivo |
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35. |
These results provide evidence for a novel type 1 IFN-mediated pathway that regulates apoptosis of T cells through a mitochondrial-dependent and caspase-dependent and independent pathway. |
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36. |
caspase-9 redistribution is a regulated process and requires the activity of a caspase other than the caspase-9- this is required to control the activity of caspase-9 |
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37. |
AMF regulates expression of Apaf-1 and caspase-9 genes via a complex signaling pathway and indirectly regulates formation of the apoptosome. |
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38. |
Results suggest that CASP-9 promoter polymorphisms affect CASP-9 expression and contribute to genetic susceptibility to lung cancer. |
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39. |
Caspase-9-deficient cells reveal strongly impaired apoptosis, caspase activation, and mitochondrial membrane depolarization upon CD95 triggering. |
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40. |
Data suggest that the expression levels of caspase 9 or caspase 9S do not play a major role in determining vulnerability to apoptosis in human astrocytoma cells. |
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41. |
the antiapoptotic property of Hualpha-Syn in neuronal cell lines is associated with the attenuation of caspase-3 activity without affecting the caspase-9 activity |
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42. |
processing and activation upon dsRNA-dependent protein kinase expression |
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43. |
OGG1 targeted to mitochondria reduces the activation of caspase-9 |
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44. |
Caspase-9 is not only required for DeltaPsi(M) loss but also for caspase-2 activation, suggesting that these two events are downstream of the apoptosome |
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45. |
inhibition of caspase-9 activity represents another mechanism of acquired cisplatin resistance |
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46. |
CASP 9 by itself can activate caspase 7 in the absence of the caspase 3-dependent pathway in TNF-alpha-induced apoptosis |
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47. |
S-nitrosation regulates activation of endogenous procaspase-9 in HT-29 cells |
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48. |
Pro-CASP9 moved from the nucleus to the mitochondria of U937 cells during TPA-induced differentiation. |
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49. |
Dopamine[DA] neurons were labeled and transduced with dominant negative Casp9. Progressive DA neuron lesion was induced by striatal 6-OHDA injection.Inhibiting apoptosis at caspase-9 is protective in vitro, but not in vivo. |
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50. |
procaspase-9 is dimerized and processed by redox stress in mitochondria |
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51. |
TGF-beta is involved in the physiological loss of gastric epithelial cells by activating apoptosis mediated by Smad7, Bim, and caspase-9 |
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52. |
Caspase-9 is activated in oxidized low-density lipoprotein (ox-LDL) induces apoptosis in endothelial cells. |
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53. |
These data suggest that increased proneness to caspase activation in lymphocytes could reflect an ongoing systemic response in neurodegenerative disease with pathogenetic implications. |
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54. |
caspase-9 is activated by reactive oxygen species (ROS) without involvement of cytochrome c release in hypoxic injury |
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55. |
Protein kinase A regulates caspase-9 activation by Apaf-1 downstream of cytochrome c |
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56. |
phosphorylation of caspase-9 at Thr125 sets the threshold for activation of the intrinsic apoptotic pathway during the cell cycle |
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57. |
Down-regulation of caspase-9 is involved during serum-factor dependent phagocytosis of platelets by monocytes. |
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58. |
A novel human caspase-9 splice variant containing only the CARD domain was cloned. |
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59. |
Endogenously expressed XIAP bound active forms of both caspase-9 and caspase-3. However, downregulation of XIAP were unable to induce caspase-9 activity, indicating that it is not a major determinant in blocking caspase-9 in NSCLC cells. |
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60. |
Results demonstrate that cleavage by caspase 3 does not activate caspase 9, but enhances apoptosis by alleviating XIAP inhibition of the apical caspase. |
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61. |
regulation of alternative splicing in lung adenocarcinoma cells by de novo ceramide |
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62. |
caspase-9 binds to NAIP in an ATP-dependent manner |
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63. |
activation by an alternative mechanism virally infected cells beside the well characterized pathways via death receptors or mitochondrial cytochrome c release |
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64. |
Presentation of nitric oxide regulates monocyte survival through effects on this enzyme and caspase-3 activation. |
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65. |
caspase 9 acts as a focal point for multiple protein kinase signaling pathways that regulate apoptosis |
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66. |
These results indicate that resveratrol seems to exert its growth-inhibitory/apoptotic effect on the breast cancer cell line MCF7 via the Akt-caspase-9 pathway. |
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67. |
caspase-9 activation in human disease can play a prominent role in localized cellular degenerative processes without causing nuclear or cell death. |
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68. |
Low-dose 5-aza-2'-deoxycytidine (DAC) induced enhancement of apoptosis mediated by Adenovirus-p53 infection, and ectopic overexpression of procaspase-9. |
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69. |
required for Parvovirus B19 virus-induced apoptosis in primary hepatocytes and hepatocellular carcinoma cell line HepG2 |
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70. |
Adenovirus encoding HIV-1 Vpr activates caspase 9 and induces apoptotic cell death in both p53 positive and negative human tumor cell lines. |
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71. |
identified SRp30a as an RNA trans-acting factor that functions as a major regulator of caspase-9 pre-mRNA processing and is required for ceramide to mediate the alternative splicing of caspase-9 |
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72. |
Blood values increased in untreated Parkinson disease patientes. |
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73. |
These data indicate that the caspase-9 gene is rarely mutated in gastric, colorectal and lung adenocarcinomas, and suggest that caspase-9 gene mutation may not contribute to the pathogenesis of these cancers. |
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74. |
caspase-3 and caspase-9 activation has critical roles in hypoxia/reoxygenation induced apoptosis |
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75. |
caspases-3 and caspase-9 play novel roles in transcription by regulating polycomb protein function through direct cleaving of Ring1B. |
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76. |
single amino acid substitutions at the dimer interface abrogate the activity of caspases-8 and -9 |
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77. |
Role for caspase-9 mediated cleavage of Raf-1 in the negative feedback regulation of hematopoietic cell apoptosis induced by growth factor withdrawal. |
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78. |
BCR-signal causes Bax translocation, followed by mitochondrial depolarization, and cytC release; subsequent caspase-9 activation can account for events further downstream |
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79. |
Thrombin is able to induce activation of caspases 3 and 9 in human platelets and significantly increases the amount in the cytoskeleton of the active forms of both caspases and the procaspases 3 and 9. |
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80. |
Caspase-9 at chromosome 1 reveal rare allelic variants in neuroblastoma tumors |
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81. |
aggregation of multiple procaspase-9 molecules can induce their activation independent of the apoptosome |
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82. |
Apollon binds to, ubiquitinates and facilitates proteasomal degradation of SMAC and caspase-9, results suggesting that Apollon has an essential function in preventing SMAC-induced apoptosis |
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83. |
blocks apocytochrome c activation and Bax-induced apoptosis |
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84. |
Gossypol induced complete cytochrome c release from mitochondria amd increased caspases-3 and -9 activity in large cell lymphoma cells. |
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85. |
BMPs promote apoptotic cell death in normal human pulmonary artery smooth muscle cells (PASMCs) by activation of caspases-3, -8, and -9, cytochrome c release, and downregulation of Bcl-2 |
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86. |
Activation of caspase-9 is required for UV-induced apoptosis of human keratinocytes |
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87. |
caspase 9 is not critical for ultraviolet ray-induced apoptosis in tumor cells |
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88. |
the functional apoptosome complex in apoptotic cells consists primarily of Apaf-1 and processed caspase-9 |
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89. |
Smac-induced apoptosis proceeds via a pathway mediated by caspase-9 that can be inhibited by zLEHD-fmk and overexpression of XIAP protein. |
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90. |
caspase-9 autoprocessing is regulated by c-Abl in the apoptotic response to genotoxic stress. |