Antisense targeting of E6AP elevates p53 in HPV-infected cells but not in normal cells
نویسندگان
چکیده
منابع مشابه
Normal cells, but not cancer cells, survive severe Plk1 depletion.
We previously reported the phenotype of depletion of polo-like kinase 1 (Plk1) using RNA interference (RNAi) and showed that p53 is stabilized in Plk1-depleted cancer cells. In this study, we further analyzed the Plk1 depletion-induced phenotype in both cancer cells and primary cells. The vector-based RNAi approach was used to evaluate the role of the p53 pathway in Plk1 depletion-induced apopt...
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During proinflammatory reactions such as endotoxemia, ischemia-reperfusion and immune reactions, excessive amounts of cytokines and prostanoids are released resulting in liver injury. In the liver, Kupffer cells are the primary source of cytokines and prostanoids. Obliteration of Kupffer cells prevents experimentally-induced liver damage, suggesting a major role for Kupffer in the pathogenesis ...
متن کاملInitial mechanistic studies of antisense targeting in cells.
UNLABELLED The continued development of antisense targeting will require a better understanding of the mechanism. METHODS We performed initial studies of the mechanism of intracellular antisense targeting through measurements of in situ transcription, immunofluorescence, reverse transcription polymerase chain reaction (RT-PCR), 32P-labeled uridine-5'-triphosphate (alpha-32P-UTP) incorporation...
متن کاملHypoxia induces p53 accumulation through MDM2 down-regulation and inhibition of E6-mediated degradation.
Hypoxia, a result of DNA-damaging agents such as ionizing radiation, induces the nuclear accumulation of the p53 tumor suppressor protein. However, unlike the effect in ionizing radiation, hypoxia readily induces the nuclear accumulation of p53 in HPV E6-infected cells. In HPV-infected cells, a key regulator of p53 protein levels is the E6 oncoprotein. In association with the endogenous cellula...
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ژورنال
عنوان ژورنال: Oncogene
سال: 1997
ISSN: 0950-9232,1476-5594
DOI: 10.1038/sj.onc.1200872