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Deciphering physiological changes that mediate transition of Mycobacterium tuberculosis between replicating and nonreplicating states is essential to understanding how the pathogen can persist in an individual host for decades.
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The oxygen tension gradient within the stem cell niche appears to provide signaling that mediates transition of these cells from quiescence to proliferation and trigger their differentiation [ 38- 42].
On the other hand, there are observations that oxygen tension gradient within the stem cell niche appears to provide signaling that mediates transition of these cells from quiescence to proliferation and trigger their differentiation [ 38- 42, 154- 156).
This variant, for the first time, allowed to monitor the hydrogen peroxide mediated transitions of ferric KatG to compound I and back to the resting enzyme.
In particular, F2R stimulates the synthesis of interleukin 6 (IL6) a cytokine exerting strong pro-atherogenic effects that mediate the transition of the inflammatory process in the vascular wall from an acute to a chronic phase [6].
The signals that mediate the transition of a normal fibroblast into a CAF are not fully understood.
Although these stromal changes provide a means through which differences between MGUS and MM can be defined, the impact of these changes and their ability to mediate the transition of MGUS to MM is still unknown and warrants further investigation.
These signals mediating the transition of normal to reactive fibroblasts are still not completely defined.
Our cell cycle analyses demonstrated that TSPY was capable of mediating the transition of its host cells through G2/M phase at a faster pace than those lacking TSPY.
On the other hand, cyclin A has a role in mediating the transition of G1 to S and G2 to M phase of the cell cycle, since it is required for the onset of DNA replication and mitosis [ 28, 29].
It is interesting to note that GacS/ GacA and RetS/ LadS systems are proposed to be involved in mediating the transition of the P. aeruginosa phenotype from an acute to chronic phase infection [ 78].
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