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Recent findings suggest that ageing, like many other biological processes, is subject to regulation by pathways that may have been partially conserved throughout evolution [1], [2].
The absence of the expected negative correlation between IL-6 and SOCS-3 may be attributed to the induction of SOCS-3 by a variety of cytokines, for example, IL-10 and lipopolysaccharide, raising the issue of IL-6 regulation by pathways other than JAK/STAT.
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Through its regulation by these pathways or by other signaling entities, the intrinsic cell death pathway confers resistance to anti-HER2 treatments.
Milk protein synthesis regulation by signaling pathways in vivo is still poorly understood.
Regulation by other pathways is not taken into account and might change the in vivo expression patterns of these genes.
In vitro LC3 lipidation requires energy and is subject to regulation by the pathways modulating autophagy in vivo.
The development of physiological aging is subject to the regulation by signaling pathways, which are influenced by endogenous and exogenous factors.
In summary, quite detailed information is available on the downstream processes involved in ribosomal biosynthesis and their regulation by signaling pathways.
Taken together these examples demonstrate that key mitochondrial processes can be subject to the regulation by signaling pathways, which normally respond to extrinsic stimuli.
Interestingly, in ciNPCs and control NPCs, genes that are known to be subjected to regulation by these pathways show very similar expression patterns, which are significantly different from that in MEFs (Supplementary information, Figure S7).
This regulation involves the modulation of both PPARGC1A activity through histone deacetylase/NAD+/SIRT1 pathway and crosstalk with its transcriptional regulation by Pi3k/mTORC2/CREB pathway [ 54].
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