Analysis of c-Myc domains involved in stimulating SV40 replication.
We have demonstrated previously that overproduction of c-Myc, N-Myc and, to a lesser extent, L-Myc facilitates the replication of simian virus 40 (SV40)-based vectors in human lymphoid cells. Using a series of c-myc deletion mutants, we investigated which c-Myc regions are important in stimulating SV40 replication. The ability of c-Myc to promote SV40 replication was significantly reduced by deletions in the second exon domain, formerly shown to be crucial for c-Myc's transforming capacity. The c-myc mutants with a disrupted basic region (b) or leucine zipper (Zip) motif were also unable to stimulate SV40 replication. These regions are implicated in protein-DNA and protein-protein interactions, respectively, suggesting that the c-Myc protein might be associated with the DNA-protein replication complex. We present data obtained from gel mobility shift assays and from an immunocomplex-binding assay substantiating this hypothesis.
Classon
M
M
Department of Tumor Biology, Karolinska Institute, Stockholm, Sweden.
Wennborg
A
A
Henriksson
M
M
Klein
G
G
D001483:Base Sequence; D015152:Blotting, Northern; D015153:Blotting, Western; D004279:DNA, Viral; D005455:Fluorescent Antibody Technique; D016259:Genes, myc; D006801:Humans; D008969:Molecular Sequence Data; D016271:Proto-Oncogene Proteins c-myc / Q000235:genetics / Q000502:physiology*; D015183:Restriction Mapping; D017384:Sequence Deletion; D013539:Simian virus 40 / Q000235:genetics / Q000502:physiology*; D013329:Structure-Activity Relationship; D014407:Tumor Cells, Cultured; D014779:Virus Replication / Q000502:physiology*
D004279:DNA, Viral; D016271:Proto-Oncogene Proteins c-myc