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Western blot analysis of extracts from PANC1, using AMPK alpha Antibody. The lane on the left was treated with blocking peptide....
Fig. 1. LDHA and AMPK were up-regulated synchronously in breast cancer. A. Expression levels of LDHA, AMPK and pAMPK were assessed by Western blot (above) and gray image scanning (below) in eight different breast cancer cell lines, including four NTNBC cell lines and four TNBC cell lines. GAPDH was used as a loading control. B. Expression levels of LDHA and AMPK were determined by qRT-PCR (above). The differences between TNBC and NTNBC cell lines were analyzed (below). GAPDH was used as an internal control. C. Expression levels of LDHA, AMPK and pAMPK were assessed by Western blot (above) and gray image scanning (below) in eight different breast cancer tissues, including four NTNBC tissues and four TNBC tissues. GAPDH was used as a loading control. D. Expression levels of LDHA and AMPK were determined by qRT-PCR (above). The diffe...
Fig. 2. The expression of LDHA and AMPK showed a positive correlation in breast cancer. A. The expression of LDHA and AMPK were detected by IHC using breast cancer TMAs of 112 patients. Representative IHC images of four staining degrees (no-weak-medium-strong) of LDHA and AMPK expression under a microscope were showed (400). B. The correlation between LDHA and AMPK expression scores of 112 breast cancer patients was analyzed and a positive correlation between them was showed....
Fig. 4. Myostatin regulated translation elongation through AMP. C2C12 myotubes were treated with various concentration recombinant myostatin (0, 0.01,0.1, 1, 2, 3 µg/ml) for 48 h andthen lysed and cellular extracts were analyzed by Western blot with anti-AMPK(A)....
Fig. 4. |Myostatin regulated translation elongation through AMPK.C2C12 myotubes were treated with various concentration recombinant myostatin (0, 0.01,429 0.1, 1, 2, 3 µg/ml) for 48 h andthen lysed and cellular extracts were analyzed by Western blot with 430 anti-AMPK(A)....
Fig. 5| AA treatment activated the AMPK and inhibited PI3K/AKT signaling pathway. The cells were treated with or without AA (5 μM) for 3 days. aRepresentative western blot of p-AMPK, AMPK, p-PI3K, PI3K, p-AKT, and AKT. GAPDH was served as a loading control....
Fig. 5 AA treatment activated the AMPK and inhibited PI3K/AKT signaling pathway. The cells were treated with or without AA (5 μM) for 3 days. a Representative western blot of p-AMPK, AMPK, p-PI3K, PI3K, p-AKT, and AKT. GAPDH was served as a loading control. b Relative protein expression of p-AMPK/AMPK, p-PI3K/PI3K, and p-AKT/AKT. Unpaired t test, *P < 0.05, ***P < 0.001. Each experiment was repeated three times (p-AMPK, phosphorylated AMP-activated protein kinase; AMPK, AMP-activated protein kinase; p-PI3K, phosphorylated phosphoinositide-3 kinase; PI3K, phosphoinositide-3 kinase; p-AKT, phosphorylated protein kinase B; AKT, protein kinase B)...
FIGURE 6 AMPK is a critical upstream regulator of FoxO1 and TFEB. A and B, Gastrodin activated AMPK in the foam cells. A, Representative blots of AMPK and p‐AMPK in macrophages. B, Immunofluorescence analysis of p‐AMPK in macrophages. C and D, The inhibition of AMPK activity decreased the phosphorylation of FoxO1 and nuclear translocation of TFEB. Macrophages were treated with CC (10μM) for 1 h. The phosphorylation level of FoxO1 was analysed by Western blotting C, and nuclear translocation of TFEB was determined by immunofluorescence D. *P < .05; **P < .01. Results are presented as mean ± SD of three independent experiments. The value represents fold of vehicle. CC, Dorsomorphin dihydrochloride...

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