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Comment
. 2022 Aug 9;7(1):277.
doi: 10.1038/s41392-022-01111-x.

Targeting folliculin to selectively inhibit mTORC1: a promising strategy for treating nonalcoholic fatty liver disease

Yan Ling  1 , Yanpeng Li  2 , Liang Li  3
Affiliations
Comment

Targeting folliculin to selectively inhibit mTORC1: a promising strategy for treating nonalcoholic fatty liver disease

Yan Ling et al. Signal Transduct Target Ther. .
No abstract available

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Conflict of interest statement

The authors declare no competing interests.

Figures

Fig. 1
Fig. 1
Canonical and noncanonical mTORC1 signaling based on substrate recruitment and phosphorylation distinctions. mTORC1 is a signaling hub that integrates numerous upstream inputs, including nutrients, growth factors, and metabolic intermediates. Rags is needed for the physical recruitment of mTORC1 to the lysosomal membrane, which is required for mTORC1 activation. The action of mTORC1 on its canonical substrates S6K and 4E-BP1 is regulated by the binding of growth factors and their receptors, which promote the activity of PI3K-Akt-TSC-Rheb signaling axis to activate mTORC1. Instead, the phosphorylation of TFE3 is controlled by FLCN-RagC/D-mTORC1 signaling axis. S6K and 4E-BP1 both have a TOS motif, whereas TFE3 has a Rag-binding region in its structure. This is the mechanism underlying the distinct phosphorylation behaviors of these two mTORC1 substrate classes. GF growth factor, P phosphorylation, GTP guanosine triphosphate, GDP guanosine diphosphate, TOS TOR signaling motif, RBR Rag-binding region
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References

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