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- 详细信息
- 询价记录
- 文献和实验
- 技术资料
- 抗体英文名:
Akt Antibody+Phospho-Akt(Ser473) Antibody
- 规格:
50+50ul
文献
Reference Citations:
Application: WB Species:rat; Sample:rat
Fig. 7. Effect of quercetin on TrkA/AKT pathway signaling in PASMCs. (A) The expression levels of p-TrkA/TrkA and p-AKT/AKT were measured by Western blotting in PASMCs in hypoxia and treated with increasing concentrations of quercetin for 24 h. (B) Results were quantified by densitometry analysis of the bands form (A) and then normalization to GAPDH protein. (C) Effects of NGF, GW441756, and quercetin on the expression of p-TrkA/TrkA and p-AKT/AKT in PASMCs in hypoxia. (D) Densitometric quantification of the bands were shown. (E) The effect of quercetin on PASMCs migration ability under the hypoxia condition treated with or without NGF (50 μg/L). (F) Quantification of the number of cells migrating through the polycarbonate membrane of average of 3 independent experiments. (G) Quantification of the Flow cytometry analysis results to confirm the effects of quercetin on PASMCs apoptosis and (H) cell cycle under the hypoxia condition treated with NGF (50 ug/L). *Po0.05, **Po0.01 compared with control; #Po0.05, ##Po0.01 compared with hypoxia and quercetin treated groups; &Po0.05, &&Po0.01 compared with NGF treated PASMCs.
Application: WB Species:human; Sample:Not available
Fig. 4 Fucoxanthin promotes apoptosis via inhibition of PI3K/Akt/ mTOR signaling pathway in glioblastoma cells. a Cell lysates were electrophoresed and Akt, p-Akt, mTOR and p-mTOR proteins were detected by their respective specific antibodies in indicated concentrations
Application: WB Species:human; Sample:Not available
Treatment with angelicin alters the protein expression levels of PI3K, p-Akt and total Akt in HepG2 and Huh-7 cells in vitro. (A) Representative blots demonstrating PI3K, p-Akt and total Akt protein expression levels in HepG2 and Huh-7 cells, following treatment with various concentrations of angelicin. (B) PI3K blots were semi-quantified using densitometry analysis of the protein bands and normalized to GAPDH. (C) p-Akt/Akt blots were semi-quantified using densitometry analysis of the protein bands. (D) Effects of LY294002 on angelicin-induced apoptosis. Cells were treated with the PI3K inhibitor LY294002 (3 mM) for 1 h prior to treatment with angelicin. The percentage of apoptotic cells following treatment with angelicin in the presence or absence of LY294002 was assessed using Annexin V-fluorescein isothiocyanate/propidium iodide staining and flow cytometry. Data are expressed as the mean ± standard deviation of 3 independent experiments.
Application: WB Species:human; Sample:Not available
Figure 5: Effects of RLX on the expression of pAkt and apoptosis proteins
Application: WB Species:human; Sample:Not available
Fig 5. The expression of p-p65, p-AKT and Bcl-2 (protein level) in U2-OS cells treated by LY294002 or/and Estrogen receptor β (ERβ) siRNA in the presence of 10-10 M E2.
Application: WB Species:human; Sample:Not available
(b) Western bolt shown that inhibited MEK, both decrease MNK2 expression and eIF4E phosphorylation. Inhibited AKT, decreased MNK2 and eIF4E, 4EBP1 phosphorylation.
Application: WB Species:mouse; Sample:mouse
Fig. 9. Chrysin inhibits the phosphorylation of Akt and ERK1/2. The levels of Akt, p-Akt, ERK1/2 and p-ERK1/2 in protein extracts from lung tissues were analyzed with Western blot (A). The bar graph represents percent phosphorylation level compared with the control group (B and C). Densitometric data are expressed as mean ± SEM (#p b 0.05 vs. control group; *p b 0.05 vs. OVA group, n = 6).
Application: WB Species:human; Sample:Not available
Figure 5: BVD-523 synergizes with VS-5584 in AML cells. (A) BxPC-3, MIAPaCa-2, and CFPAC-1 cells were treated with vehicle control or variable concentrations of BVD-523 and VS-5584, alone or in combination, for 48 h. Viable cells were measured by MTT assays. Standard isobologram analyses of the antitumor interactions are shown. The IC50 values of each drug are plotted on the axes; the solid line represents the additive effect, while the points represent the concentrations of each drug resulting in 50% inhibition of proliferation. Points falling below the line indicate synergism whereas those above the line indicate antagonism. (B) HPAC cells were treated with vehicle control, VS, BVD-523 (BVD), or VS plus BVD for 48 h. Cells were fxed with 80% ice-cold ethanol and stained with PI for cell cycle analysis. The percentage of cells with sub-G1 DNA content are graphed as means of triplicates ± SEM from one representative experiment. ***indicates p < 0.001; combined treatment compared to individual treatments and vehicle control. Combination index (CI) values were calculated using CompuSyn software. (C) CI vs. Fa plot (combination index vs. fraction affected) for the cell death data is presented. (D) HPAC cells were treated with vehicle control or the indicated drugs for 48 h. Whole cell lysates were subjected to Western blotting and probed with the indicated antibody. The fold changes for the densitometry measurements, normalized to β-actin and then compared to no drug treatment control, are indicated.
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文献和实验米宝 这俩天做实验,极其郁闷。我做的总AKt和pAkt,大鼠脑组织,第一次跑总AKT的时候,我觉得可能是因为蛋白是提取的浓度比较好吧,出来了一条浓浓的条带,三组总AKt都出了,接下来做pAkt,就出了一个带,效果挺明显的。后来再做pAkt的时候,跑了4张膜,显影的时候,太干净了,上面什么都没有,甚至连个杂带,斑点 都没!实验是在实验员的领导下完成的,技术上基本没什么纰漏,查阅本版面有关这问题方面的介绍,有的解释说pakt降解了!一抗是用的Phospho-Akt
出来的.像前面几位战友说的那样,可以考虑加大上样量 2. 是否WB的条件不好? 可以跑其他蛋白的WB看看,如果其他蛋白质都跑出来的很好的话, 可以考虑换个抗体试一试,,但是话说回来,cell signaling的p-AKT 很好的,我也用了好几年.ser473和T308都不错的. 3. 条带弱的话,可以用 can get sinal 去提高抗体的敏感度. BTW, 我自己跑p-akt的时候, 1抗是1:1500 2抗是 1:20000 good luck
receptorr 我在做HaCaT细胞的磷酸化Akt(473)时,背景比较高,该怎么办?(即未处理组的Akt比较高) 请高手支招。 谢谢 magichunter 说得太粗略了。 receptorr 我做的细胞是HaCaT 看看加入药物后HaCaT的磷酸化Akt是否有增高, 所以希望没有加药的那一组HaCaT的磷酸化Akt水平低 但是实际做时,发现没有
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