The regulation mechanism of c-jun and junB by human papillomavirus type 16 E5 oncoprotein
In this study, we show that HPV-16 E5 induced anchorage-independent growth in immortalized human epidermal keratinocytes and that HPV-16 E5 in human keratinocytes had higher expression of c-jun and junB; also, we investigated the role of transcriptional initiation pathways in the expression elevation. In addition, Ras-dependent pathway, as well as PKC-dependent pathway, leads to HPV-16 E5-induced c-jun gene expression.
An analysis of all possible icosahedral viral capsids is proposed. It takes into account the diversity of coat proteins and their positioning in elementary pentagonal and hexagonal configurations, leading to definite capsid size. We show that the self-organization of observed capsids during their production implies a definite composition and configuration of elementary building blocks. The exact number of different protein dimers is related to the size of a given capsid, labeled by its T -number. Simple rules determining these numbers for each value of T are deduced and certain consequences concerning the probabilities of mutations and evolution of capsid viruses are discussed.