Some patients' cells demonstrated REP-1 mRNA levels similar to control; however, in others the mRNA levels were quite low.
The rep-typing scheme for determining plasmid types demonstrated that rep-types 2 and 9 were predominant in the ST40 strain collection but disclosed also the presence of some new plasmids [ 55, 85, 86].
This data demonstrated that Rep-ITR specificity lies outside of the ITR binding regions.
Recent work in C. elegans has demonstrated that rep-1 may prenylate specific Rabs in specific tissues, such as rab-27 which is involved in synaptic transmission, and does not participate in the prenylation of other rabs [9].
Genetic diversity of strains responsible for CBB was demonstrated by rep-PCR [ 24], AFLP [ 25] and recently by MLSA [ 26].
While it has been demonstrated that rep-PCR is comparable to RFLP and RAPD, several limitations such as poor resolution and band separation have been observed for rep-PCR (Olive and Bean 1999).
These findings demonstrate that REPs possess cellular plasticity, and suggest that the phenotypic transition of REPs to myofibroblasts, modulated by inflammatory molecules, underlies the connection between anemia and renal fibrosis in CKD.
These observations demonstrated that rBeauR-Rep-M41-Struct-2 was not pathogenic indicating that replacement of the structural and accessory genes did not restore virulence.
In summary, our observations of the parameters used to assess pathogenicity demonstrated that rBeauR-Rep-M41-Struct-2 was not pathogenic and that it had the characteristics associated with Beau-R rather than M41-CK.
Once the rep has demonstrated an aptitude for prospecting calls, the process begins anew for the next activity milestone.
Although this mutation is silent for both Rep and RepA, it could conceivably have an adverse effect on ssDNA genomic or transcribed RNA secondary structures, as has been demonstrated for other silent Rep mutations [ 67, 68].
