| 包装 | 价格(元) |
| 10mg | 电议 |
| 50mg | 电议 |
Preparation Method | Hela cells were serum-starved for 1 h, treated with IGF or SC 79 (4 μg/mL) for 30 min, lysed in lysis buffer, supplemented with protease inhibitors, and analyzed for phospho-Akt by Western blotting |
Reaction Conditions | SC 79 (4 μg/mL) for 30 min |
Applications | SC 79, which inhibits PH AkT-GFP plasma membrane translocation but enhances Akt phosphorylation and activation in the cytosols |
Cell lines | HsSultan and NB4 cells |
Preparation Method | SC 79(8 ug/mL) was added to HsSultan or NB4 cell medium and incubated overnight (16-20 h). |
Reaction Conditions | 8 ug/mL SC 79 for 16-20 h |
Applications | SC 79 enhances phosphorylation of all three Akt isotypes and enhances Akt activation in a variety of cell types. |
Animal models | MCAO mice |
Preparation Method | SC 79 was administered by intraperitoneal injection at a concentration of 0.04mg/g body weight. |
Dosage form | 0.04mg/g SC 79 |
Applications | SC 79 enhances Akt activity during neuronal cell death in an in vivo mouse model of ischemia, SC 79 attenuates stroke-induced neuron death. |
| 文献引用 | |
| 产品描述 | SC 79 is an activator of osmotic Akt phosphorylation in the brain and an inhibitor of AKT-PH domain translocation[1]. SC 79 enhances phosphorylation of all three Akt isotypes and enhances Akt activation in a variety of cell types[1]. Treatment of BRAT1 knockdown cells with Akt activator SC 79 can improve their proliferation and reduces mitochondrial ROS concentration[4]. In both SH-SY5Y cells and primary murine dopaminergic neurons, pre-treatment with SC 79 largely inhibited hydrogen peroxide (H2O2)-induced cell viability reduction, apoptosis and necrosis. SC 79 activated Akt in the neuronal cells, which was required for its neuroprotection against H2O2[5]. In primary murine osteoblasts and osteoblastic MC3T3-E1 cells, pretreatment with SC 79 significantly attenuated Dex-induced cell death. Further, Dex-induced mitochondrial permeability transition pore (mPTP) opening, cytochrome C release and apoptosis activation were dramatically alleviated with SC 79 pretreatment in above cells[6]. The protective role of SC 79 against H/R of hepatocytes or hepatic I/R injury is related to activation of phosphorylation of Akt, resulting in the decrease of pro-apoptotic protein of Bim, Bax, and Bad, and increase of the anti-apoptotic protein Bcl-2 and Bcl-xL induced by cell H/R and hepatic I/R injury[7]. SC 79 enhances Akt activity during neuronal cell death in an in vivo mouse model of ischemia, SC 79 attenuates stroke-induced neuron death[1]. SC 79 protects hepatocytes from apoptosis induced by agonistic anti-Fas antibody CH11 (for humans) or Jo2 (for mice) and significantly prolongs the survival of mice given a lethal dose of Jo2[2]. Akt activator SC 79 protects hepatocytes from TNF-α-induced apoptosis and protects mice from d-galactosamine (d-Gal)/lipopolysaccharide (LPS)-induced TNF-α-mediated liver injury and damage. SC 79 not only enhances the nuclear factor-κB (NF-κB) prosurvival signaling in response to TNF-α stimulation, but also increases the expression of cellular FLICE (FADD-like IL-1β-converting enzyme)-inhibitory protein L and S (FLIPL/S), which consequently inhibits the activation of procaspase-8[2]. References: |
m.cnreagent.com