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|Title:||Evidence for the involvement of a nuclear NF-κB inhibitor in global down-regulation of the major histocompatibility complex class I enhancer in adenovirus type 12-transformed cells|
|Source:||Liu, X.,Ge, R.,Ricciardi, R.P. (1996-01). Evidence for the involvement of a nuclear NF-κB inhibitor in global down-regulation of the major histocompatibility complex class I enhancer in adenovirus type 12-transformed cells. Molecular and Cellular Biology 16 (1) : 398-404. ScholarBank@NUS Repository.|
|Abstract:||Diminished expression of major histocompatibility complex class I antigens on the surface of adenovirus type 12 (Ad12)-transformed cells contributes to their high tumorigenic potential by enabling them to escape immune recognition by cytotoxic T lymphocytes. This low class I antigen expression is due to a block in class I transcription, which is mediated by Ad12 E1A. Genetic analysis has shown that the class I enhancer is the target for transcriptional down-regulation. In this study, we show that the ability of the R1 element of the class I enhancer to stimulate transcription is greatly reduced in Ad12-transformed cells. The loss of functional activity by the R1 element was attributed to loss of binding by the NF-κB p50-p65 heterodimer. NF-κB binding appears to be blocked within the nucleus rather than at the level of nuclear translocation. Significantly, NF-κB binding activity could be recovered from the nuclear extracts of Ad12-transformed cells following detergent treatment, suggesting that the block is mediated through a nuclear inhibitor present in the Ad12-transformed cells. These results, taken together with the fact that the R2 element of the class I enhancer exhibits strong binding to the transcriptional repressor COUP-TF, suggest that the class I enhancer is globally down-regulated in Ad12-transformed cells.|
|Source Title:||Molecular and Cellular Biology|
|Appears in Collections:||Staff Publications|
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