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Cited by 13 publications
(10 citation statements)
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References 8 publications
(8 reference statements)
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“…Thus, elucidation of the relevant neuronal populations, neural circuitry, and downstream signals responsible for mTORC2‐mediated changes in activity and energy balance has the potential to offer new strategies to treat obesity and extend healthspan that are complementary to existing strategies for diet modification. Moreover, our findings imply that mTOR kinase inhibitors now being explored as interventions to rejuvenate aged tissues in the elderly (Mannick et al, ), as well as mTORC2‐specific inhibitors in development for the treatment of cancers (Murray & Cameron, ), should be evaluated carefully for long‐term effects on frailty and general health.…”
Section: Resultsmentioning
confidence: 89%
“…Thus, elucidation of the relevant neuronal populations, neural circuitry, and downstream signals responsible for mTORC2‐mediated changes in activity and energy balance has the potential to offer new strategies to treat obesity and extend healthspan that are complementary to existing strategies for diet modification. Moreover, our findings imply that mTOR kinase inhibitors now being explored as interventions to rejuvenate aged tissues in the elderly (Mannick et al, ), as well as mTORC2‐specific inhibitors in development for the treatment of cancers (Murray & Cameron, ), should be evaluated carefully for long‐term effects on frailty and general health.…”
Section: Resultsmentioning
confidence: 89%
“…Alternatively, a recent study using RICTOR knockout mice indicates that Ser 474 phosphorylation is dispensable for maximal phosphorylation of AS160, PRAS40, FOXO1, and GSK3␤ in adipose tissue (23). Nevertheless, use of mTORC2 deletion or inhibition to study the role of Akt Ser 474 phosphorylation may be confounded by several factors, including the induction of compensatory mechanisms because of a chronic absence of mTORC2 (24), lack of specificity of mTORC2 inhibitors (25), and interference from other downstream actions of mTORC2 that are independent of Akt Ser 474 phosphorylation, such as other phosphorylation sites on Akt (26 -28).…”
mentioning
confidence: 99%
“…Finally, since mTORC2 participates in cancer progression, specific mTORC2 inhibitors could be of therapeutic benefit for cancer patients [ 55 ]. Compared to kinase inhibitors of mTOR, specific mTORC2 would not induce compensatory cell survival and proliferation induced by mTORC1 inhibition.…”
Section: Mtor Inhibitorsmentioning
confidence: 99%