2015
DOI: 10.1016/j.bbagen.2015.01.013
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Interaction of p53 with prolyl isomerases: Healthy and unhealthy relationships

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Cited by 25 publications
(35 citation statements)
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References 197 publications
(267 reference statements)
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“…However, it remains controversial whether PIN1 acts as a tumor promoter (10,14,(18)(19)(20) or tumor suppressor (11,12,22). TP53 is one of the more than 50 critical regulatory proteins catalyzed by PIN1 (8,13). TP53 mutation is also one of the most common genetic alterations in HCC and leads to the accumulation of mutant TP53 protein that endows oncogenic activities (5,7,23).…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…However, it remains controversial whether PIN1 acts as a tumor promoter (10,14,(18)(19)(20) or tumor suppressor (11,12,22). TP53 is one of the more than 50 critical regulatory proteins catalyzed by PIN1 (8,13). TP53 mutation is also one of the most common genetic alterations in HCC and leads to the accumulation of mutant TP53 protein that endows oncogenic activities (5,7,23).…”
Section: Discussionmentioning
confidence: 99%
“…These contradictory reports regarding the function of PIN1 in oncogenesis suggest that PIN1 can either function as a conditional tumor promoter or suppressor. Among the many documented targets of PIN1-mediated prolyl-isomerization that regulate cell fate, TP53 represents the most relevant one and is frequently deregulated in cancer (8,10,13). A recent study has shown that PIN1 conveys oncogenic signals in concert with mutant TP53 protein to promote aggressiveness in breast cancer cells, and concomitant high PIN1 expression and TP53 mutation have been proposed as an independent prognostic factor of poor clinical outcome in breast cancer patients (14).…”
Section: Introductionmentioning
confidence: 99%
“…It appears that Pin1 represents a common mediator linking proapoptotic cooperative activity of the p53 family members. As a regulator of p53, Pin1 regulates many cellular responses related to cell cycle and cell death, including genotoxic response, apoptosis, and mitochondrial apoptotic function (Wulf et al, 2002;Zacchi et al, 2002;Zheng et al, 2002;Follis et al, 2015;Mantovani et al, 2015).…”
Section: Stability Of Transcription Factorsmentioning
confidence: 99%
“…Adoptive gene transfer experiments in the mouse hematopoietic system directly demonstrated that mutations at codon 58 (one of the hotspots in BL) augment the oncogenic potential of c- myc [10]. On this basis, one might hypothesize that, like Thr 58 mutation, a decrease in Pin1 activity should potentiate the oncogenic action of Myc: this putative tumor suppressive effect of Pin1 might be further reinforced by its positive action on p53 [11, 15], a key suppressor of Myc-induced lymphomagenesis [16]. …”
Section: Introductionmentioning
confidence: 99%