Rosales R, Vigneron M, Macchi M, Davidson I, Xiao JH, Chambon P.In vitro binding of several cell-specific and ubiquitous nuclear proteins to the GT-I motif of the SV40 enhancer. Xiao JH, Davidson I, Macchi M, Rosales R, Vigneron M, Staub A, Chambon P.One cell-specific and three ubiquitous nuclear proteins bind in vitro to overlapping motifs in the domain B1 of the SV40 enhancer. Xiao JH, Davidson I, Ferrandon D, Rosales R, Vigneron M, Macchi M, Ruffenach F, Chambon P.Cell-type specific protein binding to the enhancer of simian virus 40 in nuclear extracts. Davidson I, Fromental C, Augereau P, Wildeman A, Zenke M, Chambon P.Specific protein binding to the simian virus 40 enhancer in vitro. Wildeman AG, Zenke M, Schatz C, Wintzerith M, Grundström T, Matthes H, Takahashi K, Chambon P.The SV40 TC-II(kappa B) and the related H-2Kb enhansons exhibit different cell type specific and inducible proto-enhancer activities, but the SV40 core sequence and the AP-2 binding site have no enhanson properties. Kanno M, Fromental C, Staub A, Ruffenach F, Davidson I, Chambon P.Cooperativity and hierarchical levels of functional organization in the SV40 enhancer. Fromental C, Kanno M, Nomiyama H, Chambon P.Activation of the U2 snRNA promoter by the octamer motif defines a new class of RNA polymerase II enhancer elements. Tanaka M, Grossniklaus U, Herr W, Hernandez N.Cell-specific activity of the constituent elements of the simian virus 40 enhancer. Nomiyama H, Fromental C, Xiao JH, Chambon P.The SV40 enhancer can be dissected into multiple segments, each with a different cell type specificity. The SV40 enhancer contains two distinct levels of organization. Discrete elements within the SV40 enhancer region display different cell-specific enhancer activities. The SV40 enhancer is composed of multiple functional elements that can compensate for one another. Multiple sequence motifs are involved in SV40 enhancer function. Zenke M, Grundström T, Matthes H, Wintzerith M, Schatz C, Wildeman A, Chambon P.
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Full textįull text is available as a scanned copy of the original print version. We also show that replication-independent transcription activation by T antigen is bidirectional and involves at least in part elements to which the factor TEF-1 binds. The natural situation in the virus of having two copies of this element might represent a compromise between maximizing both T antigen expression early in infection and late gene expression after replication begins. We find that the ability of replication to lead to a shift diminishes when early-early transcription is made increasingly stronger by multimerizing the enhancer, and suggest that replication might lead to the shift by interfering with the ability of the enhancer to direct initiation to those sites. The viral transcription enhancer contains sequences important for both early and late transcription, and we therefore have carried out experiments to evaluate its role in these events.
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Replication leads to a shift in transcription from the early-early to the late and late-early cap sites, through mechanisms poorly understood. Simian virus 40 large tumor antigen is a multifunctional protein, with two of its roles being the promotion of viral DNA replication and replication-independent activation of viral transcription.