Here in-vivo transcription studies reveal that FNR occupies the hlyE promoter more frequently than CRP , providing a mechanism for the moderate upregulation of hlyE expression in response to two distinct environmental signals .
Here in-vivo transcription studies reveal that FNR occupies the hlyE promoter more frequently than CRP , providing a mechanism for the moderate upregulation of hlyE expression in response to glucose-starvation .
Here in-vivo transcription studies reveal that FNR occupies the hlyE promoter more frequently than CRP , providing a mechanism for the moderate upregulation of hlyE expression in response to oxygen .
Thus , CRP enhances hlyE expression in response to FNR enhances hlyE expression in response to oxygen starvation .
Thus , CRP enhances hlyE expression in response to glucose-starvation enhances hlyE expression in response to oxygen starvation .
Previous studies have shown that CRP contribute to hlyE expression when E. coli is grown on a solid medium .
Thus , we concluded that CRP all contribute towards the regulation of hlyE expression .
Footprinting studies have shown that CRP activate hlyE expression from the same site centered 61.5 bp upstream of the SlyA-associated transcription start site .
CRP are known to activate hlyE expression
This reciprocity of transcriptional efficiency provides a mechanism for the moderate upregulation of hlyE expression in response to two distinct environmental signals rather than , for the much larger degree of upregulation when CRP act synergistically by binding at different sites within the ansB promoter .
This reciprocity of binding site recognition provides a mechanism for the moderate upregulation of hlyE expression in response to two distinct environmental signals rather than , for the much larger degree of upregulation when CRP act synergistically by binding at different sites within the ansB promoter .
This reciprocity of transcriptional efficiency provides a mechanism for the moderate upregulation of hlyE expression in response to glucose-starvation rather than , for the much larger degree of upregulation when CRP act synergistically by binding at different sites within the ansB promoter .
This reciprocity of transcriptional efficiency provides a mechanism for the moderate upregulation of hlyE expression in response to oxygen rather than , for the much larger degree of upregulation when CRP act synergistically by binding at different sites within the ansB promoter .
This reciprocity of binding site recognition provides a mechanism for the moderate upregulation of hlyE expression in response to glucose-starvation rather than , for the much larger degree of upregulation when CRP act synergistically by binding at different sites within the ansB promoter .
This reciprocity of binding site recognition provides a mechanism for the moderate upregulation of hlyE expression in response to oxygen rather than , for the much larger degree of upregulation when CRP act synergistically by binding at different sites within the ansB promoter .
On the other hand , the transcriptional regulator Crp , previously described as an activator of hlyE transcription in Escherichia coli , is involved in transcriptional repression of hlyE in S. Typhi .
The Crp regulator is involved in transcriptional repression of S. Typhi hlyE Crp is a transcriptional regulator previously reported to be an activator of hlyE transcription in E. coli .
CRP is a transcriptional regulator previously reported as an activator of the hlyE transcription in E. coli .