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This increased apoptosis correlated with a down-regulation in the activation of the PI(3 K-Akt survival pathway.
The PI3K/Akt/mTOR pathway is a prototypic survival pathway that is constitutively activated in many types of cancer.
Here we studied activation of Akt cell survival pathway in a rodent model of emergency preservation and delayed resuscitation.
Several studies demonstrated that maspin inhibits the survival pathway by influencing the response to cell death in lung cancer cells [86].
We find that autophagy is a principal, and perhaps necessary, survival pathway in DCIS.
p38MAP kinase activation is also shown to activate the survival pathway in non immune cells [22].
However, we ruled out the possibility that Celastrol simply inhibited the cell survival pathway(s).
Accumulated evidence shows that Akt and its downstream targets constitute a major cell survival pathway.
This is likely due to alterations in the intracellular apoptotic or survival pathway machinery.
Rather, it implies the involvement of a TSC2-dependent but mTORC1-independent cell survival pathway.
In summary, we demonstrate that TRAIL activates the Akt survival pathway.
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