By John McPhee

ISBN-10: 0374133735

ISBN-13: 9780374133733

ISBN-10: 0374515980

ISBN-13: 9780374515980

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Together, these observations demonstrate that substantial viral mRNA export and translation can occur in the absence of E IB55kDa or E40rf6 in some host cells. This suggests that the replication and cytolytic properties of E IB-55kDa and E40rf6 mutants are determined by different genetic backgrounds in various cell lines and that non-restrictive cells compensate for E IB55kDa and E40rf6 functions irrespective of the p53 status of the host cell. At present it is unknown why EI B-55kDa and E40rf6 are required for viral replication in some host cells and not in others.

Much of this information has been reviewed in detail previously (IMPERIALE et al. 1995; LEPPARD 1997, 1998) and will be summarized only briefly here. Early studies on the Ad2/AdS replicative cycle in HeLa cells showed that at late times of infection E IB-55kDa facilitates the cytoplasmic accumulation of viral late transcripts while simultaneously inhibiting the export of most cellular mRNAs (BELTZ and FLINT 1979; BABISS et al. 1985; PILDER et al. 1986; WILLIAMS et al. 1986; LEPPARD and SHENK 1989).

Large viral inclusion bodies known as viral genome storage sites appear. which are surrounded by IGs and replicative foci comprising both single-stranded DNA accumulation sites and the peripheral replicative zone (Fig. 2; BRIDGE and PETIERSSON 1996). At this stage splicing factors are shifted back to the IGs, which become enlarged (IG clusters) and now contain late viral RNAs enriched in exon sequences (BRIDGE et al. 1996; ASPEGREN et al. 1998). Interestingly, in the same time-frame, the association of EI B-55kDa with nuclear tracks is lost.

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The curve of binding energy by John McPhee

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