Sentence examples for latent origin from inspiring English sources

OriP, the latent origin of Epstein-Barr virus (EBV), consists of two essential elements: the dyad symmetry (DS) and the family of repeats (FR).

Interestingly, we have shown that USP7 stimulates the DNA binding activity of EBNA1 and is important for transcriptional activation by EBNA1 at the latent origin of EBV replication [32].

Initial genetic dissections of EBV identified one viral protein, Epstein-Barr Nuclear Antigen 1 (EBNand, and one region of the viral genome, termed latent origin of plasmid replication (oriP), as being necessary and sufficient for replication of the viral plasmid.

Hence, binding of EBNA-1 to the family-of-repeats (FR) locus in the latent origin of replication, oriP, positively regulates the expression of the Cp promoter that drives the transcription of six EBNA genes in cells expressing latency III [7], [8] while binding to specific sites in the Qp promoter is involved in the autoregulation of EBNA-1 expression in different latency types [9].

The only viral elements needed for the episomal maintenance of plasmids in human cells is the latent origin of plasmid replication, oriP, and the viral protein EBNA-1.

EBNA1 binds to the latent origin of EBV replication (OriP), which is essential for EBV genome replication and maintenance during its latency [49], [50].

The virus also employs epigenetic mechanisms, for example chromatin remodelling and demethylation of the lytic switch gene Rta (ORF50) promoter, to control its entry into the lytic phase and hyperacetylation of the latent replication origin to control latent cycle replication (Lu et al, 2006).

The common variants were apparently clustered in certain specific regions, e.g., from 6 kb to 10 kb, which is the region that encodes EBER-1, 2 (EBV-encoded RNA) and contains the OriP (the latent cycle origin of DNA replication), and from 79 kb to 83 kb, the region that encodes EBNA3 etc.

Here the interaction of the EBNA1 protein with the latent viral replication origin, oriP, is described and the possible role of cellular licensing factors in controlling replication of the EBV episome is considered.

The latter was essentially achieved by an activation of latent DNA replication origins (i.e. an increase of the number of replicon origins per unit length of DNA) and was observed immediately prior to commitment to flowering [ 84, 85].

LANAs are supposed to bind to the origin of latent viral DNA replication (oriP) and tether the viral DNA to the host's chromosome in order to allow co-replication of the viral genome with the cellular genome upon mitosis.