| Identifier | HPI103461 |
| Interaction | p53 <==> HBx |
| Role & State | RS:0000002,activity; RS:0000074,inhibitor; |
| Interaction Type | IT:0000371,interaction; IT:0000271,express; IT:0000227,bind; IT:0000076,inhibition; IT:0000099,formation; IT:0000174,repress; IT:0000128,phosphorylation; IT:0000353,phosphorylate; IT:0000262,react; IT:0000266,disruption; IT:0000089,addition; IT:0000068,transcription; IT:0000085,synthesis; IT:0000114,activation; IT:0000026,interact; IT:0000372,treatment; |
| Biological Process | BP:0031099,regeneration; BP:0019835,cytolysis; BP:0016049,cell growth; BP:0071897,DNA synthesis; BP:0040007,growth; BP:0016446,mutation; BP:0006281,DNA repair; BP:0032502,development; BP:0006915,apoptosis; |
| Biological Function | BF:0016563,transcriptional activity; |
| Subcelluar Location | SCL:0000002,intracellular; |
| Detection Method | DM:0000019,co-immunoprecipitation; DM:0000019,immunoprecipitation; |
| Reference | 10190565_6, Using the p53-deficient cell line Saos-2, we demonstrated that expression of HBx also resulted in diminished overall cellular DNA repair of damage induced by both aflatoxin B1 epoxide and UVC radiation, using both the host cell reactivation and unscheduled DNA synthesis assays.
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| Reference | 10767646_1, p53 mutations and binding of p53 to hepatitis B virus (HBV) x protein (HBx) have been suggested as alternative mechanisms of development of hepatocellular carcinomas (HCCs) in man, both processes resulting in intracellular accumulation of the protein which is detectable by immunohistochemical approaches.
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| Reference | 10767646_9, In addition, p53 accumulation was also observed in some parenchymal and ductular (oval) cells in cirrhotic livers and, more frequently, in fulminant hepatitis, being independent of HBx expression, and seemingly associated with the damage and/or regeneration of liver parenchyma, perhaps merely reflecting a cellular stress response.
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| Reference | 12538486_5, Because loss of p53 transcription activity can be induced by binding to hepatitis B virus X protein (HBx), we generated HBx stable transfectants from Chang liver cells and examined their susceptibility to Ad5WS1-induced cytolysis.
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| Reference | 12538486_7, Disruption of p53 transcription activity by HBx in Chang liver cells rendered them susceptible to infection with Ad5WS1.
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| Reference | 12538486_9, Our results suggest that E1B M(r) 55000-deleted adenovirus may have therapeutic potential for the treatment of HCC with loss of p53 transcription activity or with HBx expression.
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| Reference | 18294283_2, We have previously found that doxorubicin increased the p53 levels in cells containing p53-binding HBx protein and restored the p53-mediated transcriptional activity that was suppressed by HBx.
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| Reference | 18294283_4, We found that six phosphorylation sites of the Serine residues of p53 were efficiently phosphorylated in HBx-expressing ChangX-34 cells, suggesting that the binding of HBx to the p53 protein does not interfere with the phosphorylation of p53 by signaling kinases.
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| Reference | 18601905_5, The anti-apoptotic Mcl-1 protein is suppressed by p53 but reactivated by HBx.
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| Reference | 19375220_2, While the inhibition of p53 by HBx is well known, the effect of p53 on HBx function has not been well studied.
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| Reference | 21438026_3, This was experimentally addressed through co-immunoprecipitation assays examining the interaction between WtHBx and MutHBx proteins with p53, reporter assays determining the impact of the HBx proteins on p53-mediated gene transcription, and clonogenic survival assays evaluating the effect of HBx on cell growth in lines of varying p53-expression status.
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| Reference | 8521383_5, First, inhibition of apoptosis may be a consequence of the failure of p53, in the presence of HBx, to upregulate genes, such as p21WAF1, Bax, or Fas, that are involved in the apoptotic pathway.
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| Reference | 8521383_9, Because the HBx gene is frequently integrated into the genome of hepatocellular carcinoma cells, inhibition of p53-mediated apoptosis by HBx may provide a clonal selective advantage for hepatocytes expressing this integrated viral gene during the early stages of human liver carcinogenesis.
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| Reference | 9405677_2, Recognizing the importance of p53-mediated apoptosis for maintaining homeostasis and preventing neoplastic transformation, here we further examine the physical interaction between HBx and p53 as well as the functional consequences of this association.
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| Reference | 9677410_9, At the same time, the results indicate that p53 plays a defensive role against HBV by transcriptionally repressing the HBV core promoter through liver-specific enhancer II and HBx is required to counteract this inhibitory function of p53.
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