mTORC1-S6K activation in endotoxemic TNFR-null mice.PoShun, LeeAnna, S. K. WilhelmsonAnton, P. HubnerSamuel, B. ReynoldsDana, A. GallacchiTerry, T. ChiouDavid, J. Kwiatkowski
This effect was mediated via degradation of Programmed Cell Death Protein 4 (PDCD4), a tumor suppressor protein that inhibits eIF4A activity and is negatively regulated by the mTORC1/S6K pathway. Moreover, pharmacological inhibition of eIF4A was able to enhance the effects of taxol and restore ...
Metabolic pathways that contribute to adiposity and ageing are activated by the mammalian target of rapamycin complex 1 (mTORC1) and p70 ribosomal protein S6 kinase 1 (S6K1) axis1,2,3. However, known mTORC1–S6K1 targets do not account for observed loss-of-function phenotypes, suggesting that...
Conversely, administration of rPGRN decreases the susceptibility of PGRN-deficient mice to LPS-induced endotoxemic shock and augments IL-10 production by LPS-activated macrophages in a TNFR-dependent manner. Molecular analysis reveals a ... W Yan,A Ding,HJ Kim,... - 《Journal of Immunology》 ...
Les voies de signalisation mTORC1 (mammalian target of rapamycin complex 1) / S6K1 (Ribosomal protein S6 kinase 1) et mTORC2 (mammalian target of rapamycin complex 2) /Akt2 ont été décrites pour jouer un rôle majeur dans l’action de l’insuline. En effet, les souris S6K1-/- ...
Inhibition of the PI3K-Akt-mTORC1-S6K1 axis impairs downregulation of Gfi-1, a negative regulator of Th17 differentiation. Furthermore, the authors show that S6K2, a nuclear counterpart of S6K1, is induced by the PI3K-Akt-mTORC1 axis, binds RORγ, and carries RORγ into the nucleus. ...
alsoinhibitedPP2Aactivity,whilethe PP2A agonist C2 ceramide suppressed both S6K1 activation and IRS- 1 Ser636 phosphorylation upon -Syn overexpression. Thus, -Syn overexpression negatively regulated IRS-1 via mTORC1/S6K1 signaling while activation of PP2A reverses this process. These results provide ...
干细胞产业是朝阳产业
摘要 目的观察大黄泄浊方对5/6肾切除大鼠mTORC1/p70S6K信号通路蛋白的影响,进一步研究其在保护肾脏功能可能的作用机制。方法随机将90只雄性SD大鼠分为假手术组与造模组,其中假手术组15只,造模组75只。造模组大鼠采...展开更多 作者 吴振华 曹雯萱 檀淼 高飞 杨凤文 陈素枝 任美芳 袁国栋 檀金川 机构地区 ...
本研究表明在恶性神经胶质瘤的某些情况下,STAT6在表观遗传上沉默,最终通过经由mTOR-S6K-S6通路诱导HIF-1α表达来预防癌细胞死亡。STAT6敲低时mTOR激活是抑制STAT6和Rheb之间直接相互作用抑制HIF-1α翻译的结果。研究数据说明了STAT6...