2019
DOI: 10.1111/apha.13426
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Estimation of p70S6K Thr389 and 4E‐BP1 Thr37/46 phosphorylation support dependency of tension per se in a dose‐response relationship for downstream mTORC1 signalling

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Cited by 7 publications
(8 citation statements)
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“…This suggests that signalling for translation initiation is independent of excitation, Ca 2+ ‐release and active actin‐myosin interaction. This finding is in agreement with recent data from our lab showing that activation of signalling for translation initiation is dependent on tension development per se in a dose‐response manner 36,37 …”
Section: Discussionsupporting
confidence: 93%
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“…This suggests that signalling for translation initiation is independent of excitation, Ca 2+ ‐release and active actin‐myosin interaction. This finding is in agreement with recent data from our lab showing that activation of signalling for translation initiation is dependent on tension development per se in a dose‐response manner 36,37 …”
Section: Discussionsupporting
confidence: 93%
“…35 In another recent study by ourselves, we employed an ex vivo approach and observed similar increases in mTORC1 signalling in response to eccentric contractions (ECC) and passive stretching (PAS) when peak tension and tension-time-integral was equalized. 36,37 In addition, we observed a dose-response relationship between increases in mTORC1 signalling and peak tension during PAS. Collectively, these data suggest that increased tension development is an important independent factor for the initiation of the anabolic process in skeletal muscle.…”
Section: Introductionmentioning
confidence: 64%
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“…As another variety of regulatory molecules in the upstream of autophagy, mTORC1 can suppress the initial formation of autophagic vesicles by inhibiting ATG13 ( Odle et al, 2020 ). In addition to inhibiting autophagy, mTORC1 also regulates the growth and proliferation of cells through two different types of downstream molecule, namely, P70S6K and 4E-BP1 ( Rindom et al, 2020 ). In our previous study, it was demonstrated that ASPP2 can regulate liver regeneration and hepatocyte proliferation through mTORC1 pathway ( Shi et al, 2018 ), despite the lack of clarity on whether ASPP2 could regulate autophagy and apoptosis through mTORC1 pathway.…”
Section: Introductionmentioning
confidence: 99%