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Mitochondria and mitochondrial function can be downstream targets of oxidative stress which impairs their function, and they themselves can produce reactive oxygen species and induce oxidative stress in the cell (Zorov et al. [2006]).
Interestingly, our own data indicate that these factors could be downstream targets of mitochondrial activity.
Interestingly, western-blot analysis revealed that PPARδ is strongly expressed in quadriceps muscle extracts from transgenic mice thus suggesting that PPARδ could be downstream targets of mitochondrial activity.
The basic-helix I domain of Twist1 family members contain Akt substrate consensus motif and may be downstream targets of Akt signaling.
Stat3 and Stat5 transcription factors have been widely implicated in the pathogenesis of tumors [64], [65] and are known to be downstream targets of K-Ras [27], [44], [48] [50].
In addition, we found that PGC-1α and PPARδ, two major regulators of muscle phenotype were up regulated in p43 transgenic mice suggesting that these proteins could be downstream targets of mitochondrial activity.
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There was downregulation of SMAD3 and SMAD5, which are downstream targets of TGF beta.
Moreover, we showed that p70S6K and elF4E, both are downstream targets of mTOR, are activated (Fig. 2A and D).
Several genes are related to epigenetic regulation, including Jmjd1a and Jmjd2c which are downstream targets of Oct4 [21], [21].
These genetic analyses support the idea that fzy-1 and APC/C are downstream targets of bub-1 in C. elegans.
Because the intracellular level of Ca2+ is highly regulated and compartmentalized, transient alterations in Ca2+ concentration are excellent signals, and are downstream targets of G-protein coupled receptors (GPCRs), ion channels and transporters, all important examples of therapeutic targets [1].
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