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In addition, experience in human trials has shown that induction of capsid-specific CD8+ T cell responses can lead to clearance of AAV vector-transduced cells3,5,6,17.
Previous studies have shown that induction of cadherin-mediated cell-cell adhesion leads to tight junction formation, and that blocking cadherin-mediated cell-cell adhesion inhibits tight junction assembly.
Experimental studies have shown that induction of vasoconstriction provoked rapid normalization of the vascular tone due to in part reflex activation of the trigeminal nerve.
We have previously shown that induction of AKT activity by vGPCR promotes mTOR activation in neighboring cells [19].
We have shown that induction of GRP78/Bip and reduction of CHOP following pretreatment with Yokukansan or Senkyu reduces cell toxicity caused by ER stress.
To that end, it has been shown that induction of autophagy results in selective degradation of catalase, leading to accumulation of mitochondrial ROS and ultimately cell death[27].
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It was therefore pertinent to show that induction of eIF4E protects cells against apoptosis.
On the contrary, Firestein et al. showed that induction of SIRT1 suppresses intestinal tumorigenesis and colon cancer growth.
Mosieniak et al. showed that induction of cellular senescence was accompanied by autophagy in colon cancer cells with an increase in Beclin-1 and p62/SQSTM1 protein levels.
Furthermore, we show that induction of the inositol 1,4,5-trisphosphate receptor type 1 is controlled by the calcium/calcineurin/NF-ATc pathway.
Although the role of Drosophila phagocytes in the activation of other immune tissues has not been clear, we show that induction of the antibacterial-peptide gene Defensin in the fat body during infection requires blood-cell contributions.
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