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These findings along with studies of the competition between E. coli SSB and the RecA recombinase protein demonstrate how SSB bound in its different modes might regulate accessibility to ssDNA of other genome maintenance proteins.
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It still remains to be determined how the switch between the two modes might be regulated, and which mechanism is most significant in vivo.
The autosomal dominant mode of inheritance of each of these distinct syndromes suggested that the underlying genes might regulate critical aspects of vascular morphogenesis.
Our observations raise the possibility that the microscopic changes in ssDNA-binding modes observed for SSB cause macroscopic condensation (or de-condensation) of the nucleoprotein fiber that, in turn, might regulate access to ssDNA.
How E1A might regulate this activity is unknown.
It was indicated that d6 might regulate osteoclasts activity through RANKL/RANK/NFATc1 pathway.
These results indicate that EMD might regulate certain gene expression during periodontal tissue regeneration.
Results suggest that lncRNAs might regulate cell proliferation.
Therefore, 08SG2/OsBAK1 might regulate grain length through GS3.
These results reminded us that Notch signaling might regulate monocyte-derived macrophages recruitment for renal fibrogenesis.
Our cellular analysis suggested that OsLAP6/OsPKS1 might regulate pollen exine formation by affecting bacula elongation.
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