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CAS No. : 345630-40-2
MCE 国际站:SF1670
产品活性:SF1670 是一种有效的特异性的人第10号染色体缺失的磷酸酶及张力蛋白同源蛋白 (PTEN) 抑制剂。
研究领域:PI3K/Akt/mTOR | Metabolic Enzyme/Protease | Autophagy
作用靶点:PTEN | Phosphatase | Autophagy
In Vitro: SF1670 is a specific PTEN inhibitor with prolonged intracellular retention in neutrophils. SF1670 enhances PtdIns(3,4,5)P3 signaling in transplanted neutrophils. SF1670 also elevates Akt phosphorylation in murine cells. Consistent with the enhanced Akt phosphorylation, pretreatment with SF1670 also significantly augments PtdIns(3,4,5)P3 level in mouse neutrophils. SF1670-induced Akt hyperactivation is abolished in PTEN-null neutrophils, further demonstrating that this effect is mediated by specific inhibition of PTEN activity. At 500 nM fMLP stimulation, SF1670 (500 nM)–pretreated neutrophils show nearly 70% higher (maximal) superoxide production than untreated neutrophils. HCT116 cells are pre-treated with the PTEN inhibitor SF1670 (2 μM) for 24 h (untreated HCT116 cells served as control); treated cells are subsequently plated under non-adherent conditions with added MET (60 μM), Lun (2 μM), or Gen (2 μM). SF1670 binds to the PTEN active site, resulting in elevated phosphatidylinositol (3,4,5) triphosphate signaling.
In Vivo: SF1670 (3 mg/kg; i.p.) triggers postconditioning after inducing cerebral global ischaemia (17 min) and reperfusion (24 h)‐induced injury via occlusion of both carotid arteries in mice.
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