IndraLab

Statements

RPS6KB1 phosphorylates IRS1 on S639. 7 / 11
2 | 7 2
reach
"Together, this may suggest that T-cad upregulation in SHR might be a characteristic feature of hypertensive and insulin resistant VSMC phenotype.Attenuation of insulin signaling is achieved through a [MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
24815187
reach
"P70S6K phosphorylates IRS-1 on S312 and/or S636 and S639."
23006971
reach
"When mTORC1 is activated, S6K1 could directly phosphorylate IRS1 (S307 and S636/S639) and promote its degradation, which subsequently blunts PI3K-AKT activation and its downstream effects such as glucose uptake, glycogen accumulation, etc. [2,3]."
30011848
reach
"P70S6K can phosphorylate IRS-1 on S312 and/or S636 and S639."
24931005
reach
"mTOR and its downstream effector S6K1 suppress IRS1 activity by directly phosphorylating IRS1 at Ser636 and Ser639 and Ser307, respectively, which leads to desensitization of insulin signaling."
18949383
reach
"It has been reported that S6K1 can directly phosphorylate IRS1 at S307 and S636/S639, which abolishes the adaptor function of IRS1, leading to its insensitivity to upstream stimuli [38]."
35879299
reach
"In addition, when mTORC1 is activated, S6K1 could directly phosphorylate Insulin receptor substrate 1 (IRS1; S307 and S636 and S639) and promote its degradation, which subsequently blunts phosphoinositide 3-kinase (PI3K)-AKT activation and its downstream effects such as glucose uptake and glycogen accumulation."
33574765