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PMID |
Sentence |
1 |
12164482
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PARP is activated at an intermediate stage of apoptosis and is then cleaved and inactivated at a late stage by apoptotic proteases, namely caspase-3/CPP-32/Yama/apopain and caspase-7.
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2 |
14679087
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Caspase 7 is a positional candidate gene for IDDM 17 in a Bedouin Arab family.
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3 |
14679087
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Caspase 7 (CASP7), an apoptosis-related cysteine protease, is one of the few known genes in this region.
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4 |
14679087
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Caspase 7 is a positional candidate gene for IDDM 17 in a Bedouin Arab family.
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5 |
14679087
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Caspase 7 (CASP7), an apoptosis-related cysteine protease, is one of the few known genes in this region.
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6 |
14708732
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The inhibitor of apoptosis protein (IAP) Survivin has an anti-apoptotic function mediated by several mechanisms; these include inhibiting caspase 3 and caspase 7.
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7 |
17196791
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The MAP family kinases, including ERK and p38 kinase, and the transcription factor c-Jun were all activated by phosphorylation after 1 h exposure to acrolein.
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8 |
17196791
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Thus, blockade of ERK and p38 inhibited chromatin condensation, caspase-7 and -9 activation as well as ICAD cleavage induced by acrolein.
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9 |
17196791
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JNK and AKT kinases seem to be implicated in survival pathways against acrolein insult, since their respective inhibitors, SP600125 and LY294002/Wortmannin switched the mode of cell death from apoptosis to total necrosis.
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10 |
17196791
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Finally, acrolein induced phosphorylation of the pro-apoptotic factor p53 which is responsible for transcription of pro-apoptotic factors such as Bax and Fas ligand.
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11 |
17196791
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These results provide new information demonstrating the implication of MAPKs and AKT in acrolein-induced apoptosis, and this information may be useful for understanding the pathogenesis of a number of tissue diseases and environmental toxicity in response to acrolein.
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12 |
23054864
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The results showed breast cancer cells respond in a diverse manner to LiCl, i.e., at lower concentrations (1, 5, and 10 mM), LiCl induces cell survival by inhibiting apoptosis through regulation of GSK-3β, caspase-2, Bax, and cleaved caspase-7 and by activating anti-apoptotic proteins (Akt, β-catenin, Bcl-2, and cyclin D1).
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