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• W1967051008 endingPage "93" @default.
• W1967051008 startingPage "81" @default.
• W1967051008 abstract "In response to oncogenic insults, normal human cells execute a defense response that culminates in cellular suicide, apoptosis. Normal human diploid fibroblasts expressing the human papillomavirus type 16 (HPV-16) E7 oncoprotein are predisposed to apoptosis when they are deprived of growth factors. Even though a dominant negative p53 mutant abrogates the cell death response, it is not accompanied by p53 phosphorylation, the DNA binding capacity of p53 remains unaltered, and no activation of common p53-dependent transcriptional targets is observed. Expression of two insulin-like growth factor-1 binding proteins, IGFBP-2 and -5, is increased presumably in response to enhanced NF-kappaB activity in HPV-16 E7-expressing serum-starved cells. Phosphorylation of AKT, an important modulator of IGF-1 survival signaling, is lower in serum-starved E7-expressing cells, and exogenously added IGF-1 can partially inhibit the cell death response. This suggests that IGFBP-2 and -5 may limit IGF-1 availability thus decreasing survival signaling. Caspase 3 but not caspase 8 is activated in serum-starved HPV-16 E7-expressing cells. Caspase inhibition affects nuclear DNA fragmentation, but cell death is not inhibited. Although mitochondria play important roles in caspase-dependent as well as -independent forms of cell death, there is no evidence for cytochrome c release and thus for mitochondrial permeabilization in growth factor deprived HPV-16 E7-expressing cells." @default.
• W1967051008 created "2016-06-24" @default.
• W1967051008 creator A5001039737 @default.
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• W1967051008 date "2004-02-01" @default.
• W1967051008 modified "2023-09-24" @default.
• W1967051008 title "Molecular pathways executing the “trophic sentinel” response in HPV-16 E7-expressing normal human diploid fibroblasts upon growth factor deprivation" @default.
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• W1967051008 doi "https://doi.org/10.1016/j.virol.2003.11.008" @default.
• W1967051008 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/14967490" @default.
• W1967051008 hasPublicationYear "2004" @default.
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