mTOR/p70S6K signaling distinguishes routine, maintenance-level autophagy from autophagic cell death during influenza A infection.

@article{Datan2014mTORp70S6KSD,
  title={mTOR/p70S6K signaling distinguishes routine, maintenance-level autophagy from autophagic cell death during influenza A infection.},
  author={Emmanuel Datan and Alireza Shirazian and Shawna Benjamin and Demetrius Matassov and Antonella Tinari and Walter Malorni and Richard A. Lockshin and Adolfo Garc{\'i}a-Sastre and Z Zakeri},
  journal={Virology},
  year={2014},
  volume={452-453},
  pages={175-190}
}
Autophagy, a stress response activated in influenza A virus infection helps the cell avoid apoptosis. However, in the absence of apoptosis infected cells undergo vastly expanded autophagy and nevertheless die in the presence of necrostatin but not of autophagy inhibitors. Combinations of inhibitors indicate that the controls of protective and lethal autophagy are different. Infection that triggers apoptosis also triggers canonical autophagy signaling exhibiting transient PI3K and mTORC1… CONTINUE READING

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mTOR / p70S6 K signaling distinguishes routine , maintenance - level autophagy from autophagic cell death during influenza A infection .
mTOR / p70S6 K signaling distinguishes routine , maintenance - level autophagy from autophagic cell death during influenza A infection .
mTOR / p70S6 K signaling distinguishes routine , maintenance - level autophagy from autophagic cell death during influenza A infection .
Autophagy , a stress response activated in influenza A virus infection helps the cell avoid apoptosis .
However , in the absence of apoptosis infected cells undergo vastly expanded autophagy and nevertheless die in the presence of necrostatin but not of autophagy inhibitors .
Inhibition of mTORC2/p70S6 K , unlike that of PI3K / mTORC1 , blocks expanded autophagy in the absence of apoptosis but not moderate autophagy .
However , in the absence of apoptosis infected cells undergo vastly expanded autophagy and nevertheless die in the presence of necrostatin but not of autophagy inhibitors .
Inhibition of mTORC2/p70S6 K , unlike that of PI3K / mTORC1 , blocks expanded autophagy in the absence of apoptosis but not moderate autophagy .
Infection that triggers apoptosis also triggers canonical autophagy signaling exhibiting transient PI3 K and mTORC1 activity .
However , in the absence of apoptosis infected cells undergo vastly expanded autophagy and nevertheless die in the presence of necrostatin but not of autophagy inhibitors .
However , in the absence of apoptosis infected cells undergo vastly expanded autophagy and nevertheless die in the presence of necrostatin but not of autophagy inhibitors .
Autophagy , a stress response activated in influenza A virus infection helps the cell avoid apoptosis .
Infection that triggers apoptosis also triggers canonical autophagy signaling exhibiting transient PI3 K and mTORC1 activity .
Inhibition of mTORC2/p70S6 K , unlike that of PI3K / mTORC1 , blocks expanded autophagy in the absence of apoptosis but not moderate autophagy .
Inhibition of mTORC2/p70S6 K , unlike that of PI3K / mTORC1 , blocks expanded autophagy in the absence of apoptosis but not moderate autophagy .
mTOR / p70S6 K signaling distinguishes routine , maintenance - level autophagy from autophagic cell death during influenza A infection .
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