IndraLab
Statements
CYLD activates apoptotic process. 61 / 66
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5
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"Moreover, exposure of CYLD knockdown HeLa cells to anti-inflammatory drugs such as sodium salicylate or prostaglandin A1, which inhibit NF-kappaB, abolished the protective knockdown of apoptosis, suggesting that loss of CYLD confers resistance to apoptosis through activation of NF-kappaB [XREF_BIBR]."
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"FCM analyses of annexin-V, APCA, and PI revealed that lentivirus-mediated inhibition of CYLD significantly prevented early and total apoptosis (LR and TR, respectively) but not late apoptosis (UR) when compared with the sh-GFP groups (Fig. 5B; LR 4.98 ± 0.94 vs. 7.15 ± 0.10, P = 0.016; UR 1.65 ± 1.14 vs. 3.51 ± 1.19, P = 0.122; TR 6.63 ± 0.21 vs. 10.67 ± 1.28, P = 0.029)."
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"Despite the previous report showing that CYLD can promote apoptosis by interfering with TNF-alpha signaling pathway XREF_BIBR, XREF_BIBR, we did not observe any differences in apoptotic rate under (1) non induced condition, (2) removal of serum, (3) when the cells were treated with TNF-alpha alone or (4) when treated with TNF-alpha together with cyclohexamide."