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Both these pathways have been associated with AS through genetic studies [ 36, 37].
Both these pathways have been shown to play a role in normal mouse spermatogonial stem cell renewal (44, 45).
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Both of these pathways have been implicated in dental caries.
Both of these pathways have been associated with cardiac hypertrophy.
Proteins from both of these pathways have already been implicated as possible cancer therapeutic targets.
Both of these pathways have well-known roles in cancer progression.
Both of these pathways have been shown to participate to some degree in the regulation of lipid metabolism.
Both of these pathways have been shown to reduce though not prevent polyposis in the Apc Min/+ mouse (Fujishita et al., 2008; Musteanu et al., 2010).
While both of these pathways have been shown to be inhibited by ATO in some tumor types [ 47, 48], the ability of this compound to affect them in gliomas is less clear.
These results support that a systems biology (pathway) approach will provide additional insight into the genetic etiology of PD and that these pathways have both biological and statistical support to be important in PD.
For example, the protein ubiquitination, mTOR signaling, mitochondrial function, and the Nrf2 pathways are altered by both DR and Rapa, and these pathways have been proposed to be important in aging.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com