Insulin activates RSK (p90 ribosomal S6 kinase) to trigger a new negative feedback loop that regulates insulin signaling for glucose metabolism.
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Suppression of feedback loops mediated by PI3K/mTOR induces multiple overactivation of compensatory pathways: an unintended consequence leading to drug resistance.Hepatic MiR-291b-3p Mediated Glucose Metabolism by Directly Targeting p65 to Upregulate PTEN Expression.The p90rsk-mediated signaling of ethanol-induced cell proliferation in HepG2 cell line.Mitochondrial AKAP1 supports mTOR pathway and tumor growth.Pharmacological inhibition of S6K1 increases glucose metabolism and Akt signalling in vitro and in diet-induced obese mice.Rapamycin reverses insulin resistance (IR) in high-glucose medium without causing IR in normoglycemic medium.
P2860
Insulin activates RSK (p90 ribosomal S6 kinase) to trigger a new negative feedback loop that regulates insulin signaling for glucose metabolism.
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article científic
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article scientifique
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articolo scientifico
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artigo científico
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bilimsel makale
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scientific article published on 13 September 2013
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vedecký článok
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vetenskaplig artikel
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videnskabelig artikel
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vědecký článek
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Insulin activates RSK (p90 rib ...... naling for glucose metabolism.
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Insulin activates RSK
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type
label
Insulin activates RSK (p90 rib ...... naling for glucose metabolism.
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Insulin activates RSK
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prefLabel
Insulin activates RSK (p90 rib ...... naling for glucose metabolism.
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Insulin activates RSK
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P2093
P2860
P356
P1476
Insulin activates RSK (p90 rib ...... gnaling for glucose metabolism
@en
P2093
André Marette
Jun-Ichi Abe
Michael Shum
Nicolas Smadja-Lamère
Paul Déléris
P2860
P304
31165-31176
P356
10.1074/JBC.M113.474148
P407
P577
2013-09-13T00:00:00Z