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A new p38 MAP kinase-regulated transcriptional
coactivator that simulates p53-dependent apoptosis
這是 EMBO journal在2007的文章
摘要：
The p38 mitogen-activated protein kinase(MAPK)
signaling pathway plays an important role in stress-induced
cell-fate decisions by orchestrating responsed thay go from
cell-cycle arrest to apoptosis. We have identified a new p38
MAPK-regulated protein theat we named p18-hamlet, which becomes
stabilized and accumulates in response to certain genotoxic stresses
such as UV or cisplatin treatment.
Overexpression of p18-hamlet is sufficient to induce apoptosis, wherease
its downregulation reduced the apoptotic response to these DNA damage-
inducing agents. We show that p18-hamlet interacts with p53 and stimulates
the transcription of several proapoptotic p53 target genes such as PUMA
and NOXA. This correlates with enhanced p18-hamlet-induced recruitment of
p53 to the promoters.
In proliferating cells, low steady-state levels of p18-hamlet are probably
maintained by a p53-dependent negative feedback loop. Therefore, p18-hamlet
is a new cell-fate regulator that links the p38 MAPK and p53 pathways
and contributes to the establishment of p53-regulated stress responses.
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