2000
DOI: 10.1002/1098-2744(200011)29:3<179::aid-mc7>3.0.co;2-k
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Downregulation of p53 by sustained JNK activation during apoptosis
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Cited by 23 publications
(17 citation statements)
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Abstract
Smart CitationsHow this paper cites the one you are viewing
“…In fact, p53 and JNK can form a complex, and JNK is a regulator of p53 stability (13)(14)(15)(16). In one study, sustained activation of JNK1 down-regulated p53 expression during apoptosis (16), similar to our findings.…”
Section: Discussion
supporting
confidence: 89%
Abstract
Smart CitationsHow this paper cites the one you are viewing
“…In fact, p53 and JNK can form a complex, and JNK is a regulator of p53 stability (13)(14)(15)(16). In one study, sustained activation of JNK1 down-regulated p53 expression during apoptosis (16), similar to our findings.…”
Section: Discussion
supporting
confidence: 89%
Abstract
Smart CitationsHow this paper cites the one you are viewing
“…Recent work by Girnius and Davis [41] demonstrated that JNK can promote the apoptosis of exfoliated epithelial cells. In this study, compared with the IC group, MAPK8 was upregulated in the IS and IR groups, though more so in the former than in the latter, which indicated that JNK might participate in intestinal cell damage caused by C. perfringens type C. Continuous activation of JNK1 during intestinal cell apoptosis can elicit a marked decrease in the expression of TP53 [39], which is consistent with the changed expression levels of JNK and TP53 in our study here.…”
Section: Discussion
supporting
confidence: 88%
Abstract
Smart CitationsHow this paper cites the one you are viewing
“…Recently [26], the poly(ADP-ribose) polymerase-1, involved in the DNA-damage repair, was shown to be cleaved by caspase 3 and subsequently generate fragments that induce apoptosis. Mechanisms involved in the proteolytic cleavage need to be extensively investigated : autoproteolysis of p53 has been shown, but an effect of caspase 3, a cysteine protease, has also been suggested [27]. However, we showed that the Z-VAD(OMe)fluoromethylketone caspase inhibitor had no effect on the p40…”
Section: Lack Of Caspase Involvement In the P40 Induction
mentioning
confidence: 76%
Abstract
Smart CitationsHow this paper cites the one you are viewing
“…In fact, p53 and JNK can form a complex, and JNK is a regulator of p53 stability (13)(14)(15)(16). In one study, sustained activation of JNK1 down-regulated p53 expression during apoptosis (16), similar to our findings.…”
Section: Discussion
supporting
confidence: 89%
Abstract
Smart CitationsHow this paper cites the one you are viewing
“…Recent work by Girnius and Davis [41] demonstrated that JNK can promote the apoptosis of exfoliated epithelial cells. In this study, compared with the IC group, MAPK8 was upregulated in the IS and IR groups, though more so in the former than in the latter, which indicated that JNK might participate in intestinal cell damage caused by C. perfringens type C. Continuous activation of JNK1 during intestinal cell apoptosis can elicit a marked decrease in the expression of TP53 [39], which is consistent with the changed expression levels of JNK and TP53 in our study here.…”
Section: Discussion
supporting
confidence: 88%
Abstract
Smart CitationsHow this paper cites the one you are viewing
“…Recently [26], the poly(ADP-ribose) polymerase-1, involved in the DNA-damage repair, was shown to be cleaved by caspase 3 and subsequently generate fragments that induce apoptosis. Mechanisms involved in the proteolytic cleavage need to be extensively investigated : autoproteolysis of p53 has been shown, but an effect of caspase 3, a cysteine protease, has also been suggested [27]. However, we showed that the Z-VAD(OMe)fluoromethylketone caspase inhibitor had no effect on the p40…”
Section: Lack Of Caspase Involvement In the P40 Induction
mentioning
confidence: 76%
Abstract
Smart CitationsHow this paper cites the one you are viewing
“…In fact, p53 and JNK can form a complex, and JNK is a regulator of p53 stability (13)(14)(15)(16). In one study, sustained activation of JNK1 down-regulated p53 expression during apoptosis (16), similar to our findings.…”
Section: Discussion
supporting
confidence: 89%
Abstract
Smart CitationsHow this paper cites the one you are viewing
“…Recent work by Girnius and Davis [41] demonstrated that JNK can promote the apoptosis of exfoliated epithelial cells. In this study, compared with the IC group, MAPK8 was upregulated in the IS and IR groups, though more so in the former than in the latter, which indicated that JNK might participate in intestinal cell damage caused by C. perfringens type C. Continuous activation of JNK1 during intestinal cell apoptosis can elicit a marked decrease in the expression of TP53 [39], which is consistent with the changed expression levels of JNK and TP53 in our study here.…”
Section: Discussion
supporting
confidence: 88%
Abstract
Smart CitationsHow this paper cites the one you are viewing
“…Recently [26], the poly(ADP-ribose) polymerase-1, involved in the DNA-damage repair, was shown to be cleaved by caspase 3 and subsequently generate fragments that induce apoptosis. Mechanisms involved in the proteolytic cleavage need to be extensively investigated : autoproteolysis of p53 has been shown, but an effect of caspase 3, a cysteine protease, has also been suggested [27]. However, we showed that the Z-VAD(OMe)fluoromethylketone caspase inhibitor had no effect on the p40…”
Section: Lack Of Caspase Involvement In the P40 Induction
mentioning
confidence: 76%