| Identifier | HPI103406 |
| Interaction | p53 <==> Bax |
| Role & State | RS:0000002,activity; |
| Interaction Type | IT:0000076,inhibition; IT:0000294,stimulate; IT:0000316,induce; IT:0000099,formation; IT:0000271,express; IT:0000128,phosphorylation; IT:0000089,addition; IT:0000078,regulation; IT:0000114,activation; |
| Biological Process | BP:0006915,apoptosis; BP:0008219,cell death; BP:0001836,release of cytochrome c from mitochondria; |
| Biological Function | --- |
| Subcelluar Location | SCL:0000031,mitochondrial membrane; SCL:0000003,membrane; SCL:0000014,mitochondria; |
| Detection Method | --- |
| Reference | 10403664_2, Since the mechanisms by which cellular DNA damaged by different DNA-damaging chemicals may not be the same, we studied the involvement of p53, Bcl-2 and Bax in apoptosis induced by methyl methanesulfonate (MMS) and hydrogen peroxide (H2O2).
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| Reference | 15135649_8, Antioxidants prevented the p53 phosphorylation, up-regulation of Bax and BR931-induced apoptosis.
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| Reference | 15135649_9, These results suggest that BR931 can increase generation of ROS, leading to DNA damage and p53 phosphorylation, which, in turn, induces the activation of Bax, release of cytochrome-c from mitochondria and activation of caspases, culminating in cell death.
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| Reference | 17136495_7, Apoptosis was preceded by increased generation of reactive oxygen species, and associated with p53 activation, increased expression of Bax, release of cytochrome c from mitochondria, caspases activation, decreased levels of survivin, induction of pro-apoptotic signaling (i.e JNK) and inhibition of anti-apoptotic signaling.
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| Reference | 19097688_7, ANDRO alone induces SMMC-7721 apoptosis with p53 expression, Bax conformation and caspase-3,8,9 activation.
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| Reference | 19097688_8, Surprisingly, the addition of ANDRO to 5-FU induces synergistic apoptosis, which could be corroborated to the increased caspase-8, p53 activity and the significant changes of Bax conformation in these cells, resulting in increased losses of mitochondrial membrane potential, increased release of cytochrome c, and activation of caspase-9 and caspase-3.
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| Reference | 20948430_9, Moreover, upregulation of p21, p53-upregulated modifier of apoptosis, and Bax, three p53-target gene products, and the downregulation of Bcl-2 and MDM2, were observed in NCPMF-60-treated cells.
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| Reference | 21183427_1, Apoptosis stimulating proteins of p53 (ASPP-l and ASPP-2) are a novel family of proteins that have been found to co-stimulate p53 activation of Bax (Bcl-2 associated protein X) inducing caspase-mediated apoptosis.
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