Expanding the prion concept to cancer biology: dominant-negative effect of aggregates of mutant p53 tumour suppressor.

摘要: p53 is a key protein that participates in cell-cycle control, and its malfunction can lead to cancer. This tumour suppressor has three main domains; the N-terminal transactivation domain, CTD (C-terminal domain) core domain (p53C) constitutes sequence-specific DBD (DNA-binding region). Most mutations related cancer development are found DBD. Aggregation of into amyloid oligomers fibrils been shown. Moreover, aggregates both mutant WT (wild-type) forms were detected tissues. We propose if aggregation occurred, it would be crucial aspect development, as lose functions an aggregated state. Mutant also exert dominant-negative regulatory effect on p53. Herein, we discuss light fact amyloid-like convert more species, leading gain function addition loss function. In summary, results obtained last decade indicate may have characteristics common with amyloidogenic prion diseases.