Titlebook: Epstein-Barr Virus and Human Disease ? 1988; Dharam V. Ablashi,Alberto Faggioni,Gary R. Pearson Book 1989 The Humana Press Inc. 1989 DNA.P

legacy

Anti EBNA-1 Protein Induced with TPAls with phorbol ester, which activates the EBV replicative life cycle, induced the production of two cellular competitors which upon competition uncoupled the binding of EBNA-1 to ori-P. Gel retardation assay, DNase I footprinting and methylation interference analysis showed that the two cellular co

BOLT

Characterization of the EBV Alkaline Exonuclease Expressed in a Recombinant Prokaryotic Systemhoma and nasopharyngeal carcinoma (NPC). One of the major constraints on studying EBV is the lack of a fully permissive tissue culture system, which has limited both the quality and quantity of EBV proteins available for analysis. However, despite this limitation the EBV genome has been shown to enc

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濃縮

VOC

Identification of the Gene Product Encoded by the ,l Repeats of the EBV Genomeomal fraction. They are polyadenylated and contain open reading frames (ORFs). These ORFs include partially homologous clusters of short tandem repeats: the .l repeats (125 bp/repeat) on the DL transcript and the .l repeats (102 bp/repeat) on the DR transcript (figure 1) (2,3,4,5,6,7,8,9).

共同給與

Anti EBNA-1 Protein Induced with TPApled the binding of EBNA-1 to ori-P. Gel retardation assay, DNase I footprinting and methylation interference analysis showed that the two cellular competitors bound specifically to the 20x 30 bp tandem repeat clusters in the EBV ori-P.

Atheroma

Dritte Hauptgruppe (B, Al, Ga, In, Tl3+), pattern of latent protein expression very similar to that in LCLs, that is, EBNAs 1–6 and LMP, are found. However, in both the BL and NPC, EBNA expression is restricted to EBNA1. (In the NPC, but not in the BL, LMP is also expressed.)

Cholagogue

entitle

油氈

https://doi.org/10.1007/0-306-47954-0for the gene encoding the EBV nuclear antigen-2 (EBNA-2) (1). We selected this promoter because of the probable importance of the gene product as a contributor to EBV cell transformation (2) and because of our work showing that the function of this promoter is down-regulated by the phorbol ester, TPA (3).