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Collectively, these data might indicate that the diminished ROS buffering of GSH-deficient cells leads to an increased activation of the mTOR pathway which could drive to the MZB-like properties of Gclc -deficient FoB
Sndergrd, S
Interestingly, the GH loop undergoes major structural rearrangements in the 135S cell entry intermediate of PV suggesting the possibility that the mutations also play a role during expansion or uncoating [26]
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