phosphorylated p akt Search Results


90
Abmart Inc antibodies against phosphorylated (p-)akt
Effects of quercetin on the <t>phosphorylation</t> <t>of</t> <t>Akt</t> in LPS-stimulated RAW264.7 cells. (A and B) The cells were pretreated with different concentrations of quercetin (5,10 and 20 µM) for 1 h and then stimulated with LPS (1 µg/ml) for another 6 h. (A) After different treatments, the protein levels of <t>p-Akt,</t> Akt and GAPDH were determined using western blot analysis and (B) the results were statistically analyzed. (C-G) RAW264.7 cells were pretreated with quercetin (20 µM) and AKT inhibitor (MK-2206; 5 µM) for 1 h in 6-well microplates and stimulated with LPS (1 µg/ml) for 6 or 24 h. The (C) mRNA and (D and E) protein expression levels of TNF-α, IL-6 and IL-1β were analyzed using reverse transcription-quantitative PCR and western blot analysis, respectively. (D) Representative western blots and (E) quantified results. (F and G) The protein levels of p-Akt, Akt were analyzed using western blot analysis. (F) Representative western blots and (G) quantified results. ## P<0.01 vs. non-intervention group; ** P<0.01 vs. LPS alone group; & P<0.05, && P<0.01 vs. quercetin treatment group. LPS, lipopolysaccharide; p, <t>phosphorylated.</t>
Antibodies Against Phosphorylated (P )Akt, supplied by Abmart Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/antibodies against phosphorylated (p-)akt/product/Abmart Inc
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antibodies against phosphorylated (p-)akt - by Bioz Stars, 2026-02
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90
Affinity Biosciences phosphorylated (p-) akt
MiR-107 overexpression suppressed the <t>PI3K/Akt</t> signaling pathway in FaDu cells. (a) After transfection for 48 h, the protein levels of <t>p-PI3K,</t> PI3K, p-Akt, and Akt were evaluated.
Phosphorylated (P ) Akt, supplied by Affinity Biosciences, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/phosphorylated (p-) akt/product/Affinity Biosciences
Average 90 stars, based on 1 article reviews
phosphorylated (p-) akt - by Bioz Stars, 2026-02
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90
Chengdu Zen Bioscience phosphorylated (p-)akt 310021 antibody
Results of western blot analysis. (A) Representative western blots of rat chondrocytes. The average relative expression of (B) LC3II/I, (C) <t>p-AKT/AKT</t> and (D) p-mTOR/mTOR from rat chondrocytes. (E) Representative western blots of human chondrocytes. The average relative expression of (F) LC3II/I, (G) p-AKT/AKT, and (H) p-mTOR/mTOR from human chondrocytes. *P<0.05, **P<0.01, ***P<0.001 and ****P<0.0001. Con, control group; DEX, dexamethasone group (200 µM); DEX + Li, dexamethasone (200 µM) combined with lithium chloride (10 mM) group; p-AKT, <t>phosphorylated</t> AKT; p-mTOR, phosphorylated mTOR; p-, phosphorylated.
Phosphorylated (P )Akt 310021 Antibody, supplied by Chengdu Zen Bioscience, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/phosphorylated (p-)akt 310021 antibody/product/Chengdu Zen Bioscience
Average 90 stars, based on 1 article reviews
phosphorylated (p-)akt 310021 antibody - by Bioz Stars, 2026-02
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90
Abmart Inc phosphorylated akt (p-akt
Results of western blot analysis. (A) Representative western blots of rat chondrocytes. The average relative expression of (B) LC3II/I, (C) <t>p-AKT/AKT</t> and (D) p-mTOR/mTOR from rat chondrocytes. (E) Representative western blots of human chondrocytes. The average relative expression of (F) LC3II/I, (G) p-AKT/AKT, and (H) p-mTOR/mTOR from human chondrocytes. *P<0.05, **P<0.01, ***P<0.001 and ****P<0.0001. Con, control group; DEX, dexamethasone group (200 µM); DEX + Li, dexamethasone (200 µM) combined with lithium chloride (10 mM) group; p-AKT, <t>phosphorylated</t> AKT; p-mTOR, phosphorylated mTOR; p-, phosphorylated.
Phosphorylated Akt (P Akt, supplied by Abmart Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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phosphorylated akt (p-akt - by Bioz Stars, 2026-02
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90
Chengdu Zen Bioscience phosphorylated (p‑)akt
Results of western blot analysis. (A) Representative western blots of rat chondrocytes. The average relative expression of (B) LC3II/I, (C) <t>p-AKT/AKT</t> and (D) p-mTOR/mTOR from rat chondrocytes. (E) Representative western blots of human chondrocytes. The average relative expression of (F) LC3II/I, (G) p-AKT/AKT, and (H) p-mTOR/mTOR from human chondrocytes. *P<0.05, **P<0.01, ***P<0.001 and ****P<0.0001. Con, control group; DEX, dexamethasone group (200 µM); DEX + Li, dexamethasone (200 µM) combined with lithium chloride (10 mM) group; p-AKT, <t>phosphorylated</t> AKT; p-mTOR, phosphorylated mTOR; p-, phosphorylated.
Phosphorylated (P‑)Akt, supplied by Chengdu Zen Bioscience, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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phosphorylated (p‑)akt - by Bioz Stars, 2026-02
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90
Wanleibio rabbit anti-rat phosphorylated (p)-akt pab
Results of western blot analysis. (A) Representative western blots of rat chondrocytes. The average relative expression of (B) LC3II/I, (C) <t>p-AKT/AKT</t> and (D) p-mTOR/mTOR from rat chondrocytes. (E) Representative western blots of human chondrocytes. The average relative expression of (F) LC3II/I, (G) p-AKT/AKT, and (H) p-mTOR/mTOR from human chondrocytes. *P<0.05, **P<0.01, ***P<0.001 and ****P<0.0001. Con, control group; DEX, dexamethasone group (200 µM); DEX + Li, dexamethasone (200 µM) combined with lithium chloride (10 mM) group; p-AKT, <t>phosphorylated</t> AKT; p-mTOR, phosphorylated mTOR; p-, phosphorylated.
Rabbit Anti Rat Phosphorylated (P) Akt Pab, supplied by Wanleibio, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/rabbit anti-rat phosphorylated (p)-akt pab/product/Wanleibio
Average 90 stars, based on 1 article reviews
rabbit anti-rat phosphorylated (p)-akt pab - by Bioz Stars, 2026-02
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90
EnoGene Inc phosphorylated p‑akt (ser473) (cat. no. e1a0016)
Results of western blot analysis. (A) Representative western blots of rat chondrocytes. The average relative expression of (B) LC3II/I, (C) <t>p-AKT/AKT</t> and (D) p-mTOR/mTOR from rat chondrocytes. (E) Representative western blots of human chondrocytes. The average relative expression of (F) LC3II/I, (G) p-AKT/AKT, and (H) p-mTOR/mTOR from human chondrocytes. *P<0.05, **P<0.01, ***P<0.001 and ****P<0.0001. Con, control group; DEX, dexamethasone group (200 µM); DEX + Li, dexamethasone (200 µM) combined with lithium chloride (10 mM) group; p-AKT, <t>phosphorylated</t> AKT; p-mTOR, phosphorylated mTOR; p-, phosphorylated.
Phosphorylated P‑Akt (Ser473) (Cat. No. E1a0016), supplied by EnoGene Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/phosphorylated p‑akt (ser473) (cat. no. e1a0016)/product/EnoGene Inc
Average 90 stars, based on 1 article reviews
phosphorylated p‑akt (ser473) (cat. no. e1a0016) - by Bioz Stars, 2026-02
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90
Affinity Biologicals polyclonal antibodies against phosphorylated (p)-akt (af0016)
Treatment with angelicin alters the protein expression levels of PI3K, <t>p-Akt</t> 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. *P<0.05, **P<0.01 vs. the control group (0 µM angelicin); # P<0.05 vs. the DMSO group. PI3K, phosphatidylinositol-4,5-bisphosphate 3-kinase; p-, phosphorylated; DMSO, dimethyl sulfoxide; Akt, RAC-α serine/threonine-protein kinase.
Polyclonal Antibodies Against Phosphorylated (P) Akt (Af0016), supplied by Affinity Biologicals, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/polyclonal antibodies against phosphorylated (p)-akt (af0016)/product/Affinity Biologicals
Average 90 stars, based on 1 article reviews
polyclonal antibodies against phosphorylated (p)-akt (af0016) - by Bioz Stars, 2026-02
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Image Search Results


Effects of quercetin on the phosphorylation of Akt in LPS-stimulated RAW264.7 cells. (A and B) The cells were pretreated with different concentrations of quercetin (5,10 and 20 µM) for 1 h and then stimulated with LPS (1 µg/ml) for another 6 h. (A) After different treatments, the protein levels of p-Akt, Akt and GAPDH were determined using western blot analysis and (B) the results were statistically analyzed. (C-G) RAW264.7 cells were pretreated with quercetin (20 µM) and AKT inhibitor (MK-2206; 5 µM) for 1 h in 6-well microplates and stimulated with LPS (1 µg/ml) for 6 or 24 h. The (C) mRNA and (D and E) protein expression levels of TNF-α, IL-6 and IL-1β were analyzed using reverse transcription-quantitative PCR and western blot analysis, respectively. (D) Representative western blots and (E) quantified results. (F and G) The protein levels of p-Akt, Akt were analyzed using western blot analysis. (F) Representative western blots and (G) quantified results. ## P<0.01 vs. non-intervention group; ** P<0.01 vs. LPS alone group; & P<0.05, && P<0.01 vs. quercetin treatment group. LPS, lipopolysaccharide; p, phosphorylated.

Journal: Experimental and Therapeutic Medicine

Article Title: Assessing the anti-inflammatory effects of quercetin using network pharmacology and in vitro experiments

doi: 10.3892/etm.2022.11230

Figure Lengend Snippet: Effects of quercetin on the phosphorylation of Akt in LPS-stimulated RAW264.7 cells. (A and B) The cells were pretreated with different concentrations of quercetin (5,10 and 20 µM) for 1 h and then stimulated with LPS (1 µg/ml) for another 6 h. (A) After different treatments, the protein levels of p-Akt, Akt and GAPDH were determined using western blot analysis and (B) the results were statistically analyzed. (C-G) RAW264.7 cells were pretreated with quercetin (20 µM) and AKT inhibitor (MK-2206; 5 µM) for 1 h in 6-well microplates and stimulated with LPS (1 µg/ml) for 6 or 24 h. The (C) mRNA and (D and E) protein expression levels of TNF-α, IL-6 and IL-1β were analyzed using reverse transcription-quantitative PCR and western blot analysis, respectively. (D) Representative western blots and (E) quantified results. (F and G) The protein levels of p-Akt, Akt were analyzed using western blot analysis. (F) Representative western blots and (G) quantified results. ## P<0.01 vs. non-intervention group; ** P<0.01 vs. LPS alone group; & P<0.05, && P<0.01 vs. quercetin treatment group. LPS, lipopolysaccharide; p, phosphorylated.

Article Snippet: Antibodies against phosphorylated (p-)Akt (cat. no. T55561) and Akt (cat. no. T40067) were obtained from Abmart.

Techniques: Phospho-proteomics, Western Blot, Expressing, Reverse Transcription, Real-time Polymerase Chain Reaction

MiR-107 overexpression suppressed the PI3K/Akt signaling pathway in FaDu cells. (a) After transfection for 48 h, the protein levels of p-PI3K, PI3K, p-Akt, and Akt were evaluated.

Journal: Bioengineered

Article Title: Overexpression of microRNA-107 suppressed proliferation, migration, invasion, and the PI3K/Akt signaling pathway and induced apoptosis by targeting Nin one binding (NOB1) protein in a hypopharyngeal squamous cell carcinoma cell line (FaDu)

doi: 10.1080/21655979.2022.2051266

Figure Lengend Snippet: MiR-107 overexpression suppressed the PI3K/Akt signaling pathway in FaDu cells. (a) After transfection for 48 h, the protein levels of p-PI3K, PI3K, p-Akt, and Akt were evaluated.

Article Snippet: The information of antibodies used in immunoblotting was as below: cyclin D1 (A19038), cyclin-dependent kinase 4 (CDK4, A0366), caspase-3 (A19654), bcl-2 associated X (bax, A19684), bcl-2 (A0208), E-cadherin (A11492), vimentin (A19607) all from ABclonal Technology (China); matrix metalloproteinase (MMP)-2 (10373-2-AP) and MMP-9 (10375-2-AP) both from Proteintech Group, Inc. (China); phosphorylated (p-) PI3K (Tyr358, AF3242), PI3K (AF6241), p-Akt (Ser473, AF0016), Akt (AF6261), and NOB1 (DF12216) all from Affinity Biosciences; β-actin (sc-4778) from Santa Cruz (USA); goat anti-rabbit IgG (A0208) and goat anti-mouse IgG (A0216) both from Beyotime.

Techniques: Over Expression, Transfection

MiR-107 overexpression repressed cell proliferation, migration, invasion, and the PI3K/Akt signaling pathway by regulation of NOB1 in FaDu cells. Cells were co-transfected with miR-107 mimics or mimics NC and the NOB1 overexpressing plasmid or the empty vector. (a) After co-transfection for 24 h or 48 h or 72 h, CCK-8 assay was used to measure cell proliferation. (b, c) Migratory and invasive abilities of cells at 48 h post-transfection were evaluated. Wound-healing assay: scale bar = 200 μm; Transwell assay: scale bar = 100 μm. (d, e) After co-transfection for 48 h, CDK4, bax, E-cadherin, p-PI3K, PI3K, p-Akt, and Akt protein expressions were assessed. Results were presented as means ± SD (n = 3). ^ P < 0.05 and ^^ P < 0.01 versus the miR-107 mimics+vector group.

Journal: Bioengineered

Article Title: Overexpression of microRNA-107 suppressed proliferation, migration, invasion, and the PI3K/Akt signaling pathway and induced apoptosis by targeting Nin one binding (NOB1) protein in a hypopharyngeal squamous cell carcinoma cell line (FaDu)

doi: 10.1080/21655979.2022.2051266

Figure Lengend Snippet: MiR-107 overexpression repressed cell proliferation, migration, invasion, and the PI3K/Akt signaling pathway by regulation of NOB1 in FaDu cells. Cells were co-transfected with miR-107 mimics or mimics NC and the NOB1 overexpressing plasmid or the empty vector. (a) After co-transfection for 24 h or 48 h or 72 h, CCK-8 assay was used to measure cell proliferation. (b, c) Migratory and invasive abilities of cells at 48 h post-transfection were evaluated. Wound-healing assay: scale bar = 200 μm; Transwell assay: scale bar = 100 μm. (d, e) After co-transfection for 48 h, CDK4, bax, E-cadherin, p-PI3K, PI3K, p-Akt, and Akt protein expressions were assessed. Results were presented as means ± SD (n = 3). ^ P < 0.05 and ^^ P < 0.01 versus the miR-107 mimics+vector group.

Article Snippet: The information of antibodies used in immunoblotting was as below: cyclin D1 (A19038), cyclin-dependent kinase 4 (CDK4, A0366), caspase-3 (A19654), bcl-2 associated X (bax, A19684), bcl-2 (A0208), E-cadherin (A11492), vimentin (A19607) all from ABclonal Technology (China); matrix metalloproteinase (MMP)-2 (10373-2-AP) and MMP-9 (10375-2-AP) both from Proteintech Group, Inc. (China); phosphorylated (p-) PI3K (Tyr358, AF3242), PI3K (AF6241), p-Akt (Ser473, AF0016), Akt (AF6261), and NOB1 (DF12216) all from Affinity Biosciences; β-actin (sc-4778) from Santa Cruz (USA); goat anti-rabbit IgG (A0208) and goat anti-mouse IgG (A0216) both from Beyotime.

Techniques: Over Expression, Migration, Transfection, Plasmid Preparation, Cotransfection, CCK-8 Assay, Wound Healing Assay, Transwell Assay

MiR-107 overexpression reduced the tumorigenic potential of FaDu HSCC in vivo . FaDu cells transfected with LV-based miR-107 or LV-NC were subcutaneously injected into the right armpit of the mice. (a) The tumor volume was measured every 3 days when the tumor was macroscopic. (b) At day 24, the tumor was collected and weighted. (c) The tumor tissues were stained with H&E. Scale bar = 100 μm. (d) The level of miR-107 was detected by RT-qPCR. (e) The expression of NOB1 was measured via IHC assay. Scale bar = 50 μm. (f) Evaluation of NOB1, p-PI3K, PI3K, p-Akt, and Akt protein expressions. Data were expressed as means ± SD (n = 6). &&& P < 0.001 versus the LV-NC group. LV, lentivirus.

Journal: Bioengineered

Article Title: Overexpression of microRNA-107 suppressed proliferation, migration, invasion, and the PI3K/Akt signaling pathway and induced apoptosis by targeting Nin one binding (NOB1) protein in a hypopharyngeal squamous cell carcinoma cell line (FaDu)

doi: 10.1080/21655979.2022.2051266

Figure Lengend Snippet: MiR-107 overexpression reduced the tumorigenic potential of FaDu HSCC in vivo . FaDu cells transfected with LV-based miR-107 or LV-NC were subcutaneously injected into the right armpit of the mice. (a) The tumor volume was measured every 3 days when the tumor was macroscopic. (b) At day 24, the tumor was collected and weighted. (c) The tumor tissues were stained with H&E. Scale bar = 100 μm. (d) The level of miR-107 was detected by RT-qPCR. (e) The expression of NOB1 was measured via IHC assay. Scale bar = 50 μm. (f) Evaluation of NOB1, p-PI3K, PI3K, p-Akt, and Akt protein expressions. Data were expressed as means ± SD (n = 6). &&& P < 0.001 versus the LV-NC group. LV, lentivirus.

Article Snippet: The information of antibodies used in immunoblotting was as below: cyclin D1 (A19038), cyclin-dependent kinase 4 (CDK4, A0366), caspase-3 (A19654), bcl-2 associated X (bax, A19684), bcl-2 (A0208), E-cadherin (A11492), vimentin (A19607) all from ABclonal Technology (China); matrix metalloproteinase (MMP)-2 (10373-2-AP) and MMP-9 (10375-2-AP) both from Proteintech Group, Inc. (China); phosphorylated (p-) PI3K (Tyr358, AF3242), PI3K (AF6241), p-Akt (Ser473, AF0016), Akt (AF6261), and NOB1 (DF12216) all from Affinity Biosciences; β-actin (sc-4778) from Santa Cruz (USA); goat anti-rabbit IgG (A0208) and goat anti-mouse IgG (A0216) both from Beyotime.

Techniques: Over Expression, In Vivo, Transfection, Injection, Staining, Quantitative RT-PCR, Expressing

Journal: Bioengineered

Article Title: Overexpression of microRNA-107 suppressed proliferation, migration, invasion, and the PI3K/Akt signaling pathway and induced apoptosis by targeting Nin one binding (NOB1) protein in a hypopharyngeal squamous cell carcinoma cell line (FaDu)

doi: 10.1080/21655979.2022.2051266

Figure Lengend Snippet:

Article Snippet: The information of antibodies used in immunoblotting was as below: cyclin D1 (A19038), cyclin-dependent kinase 4 (CDK4, A0366), caspase-3 (A19654), bcl-2 associated X (bax, A19684), bcl-2 (A0208), E-cadherin (A11492), vimentin (A19607) all from ABclonal Technology (China); matrix metalloproteinase (MMP)-2 (10373-2-AP) and MMP-9 (10375-2-AP) both from Proteintech Group, Inc. (China); phosphorylated (p-) PI3K (Tyr358, AF3242), PI3K (AF6241), p-Akt (Ser473, AF0016), Akt (AF6261), and NOB1 (DF12216) all from Affinity Biosciences; β-actin (sc-4778) from Santa Cruz (USA); goat anti-rabbit IgG (A0208) and goat anti-mouse IgG (A0216) both from Beyotime.

Techniques: CCK-8 Assay

Results of western blot analysis. (A) Representative western blots of rat chondrocytes. The average relative expression of (B) LC3II/I, (C) p-AKT/AKT and (D) p-mTOR/mTOR from rat chondrocytes. (E) Representative western blots of human chondrocytes. The average relative expression of (F) LC3II/I, (G) p-AKT/AKT, and (H) p-mTOR/mTOR from human chondrocytes. *P<0.05, **P<0.01, ***P<0.001 and ****P<0.0001. Con, control group; DEX, dexamethasone group (200 µM); DEX + Li, dexamethasone (200 µM) combined with lithium chloride (10 mM) group; p-AKT, phosphorylated AKT; p-mTOR, phosphorylated mTOR; p-, phosphorylated.

Journal: Molecular Medicine Reports

Article Title: Lithium prevents glucocorticoid‑induced chondrocyte autophagy: An in vitro study

doi: 10.3892/mmr.2023.13070

Figure Lengend Snippet: Results of western blot analysis. (A) Representative western blots of rat chondrocytes. The average relative expression of (B) LC3II/I, (C) p-AKT/AKT and (D) p-mTOR/mTOR from rat chondrocytes. (E) Representative western blots of human chondrocytes. The average relative expression of (F) LC3II/I, (G) p-AKT/AKT, and (H) p-mTOR/mTOR from human chondrocytes. *P<0.05, **P<0.01, ***P<0.001 and ****P<0.0001. Con, control group; DEX, dexamethasone group (200 µM); DEX + Li, dexamethasone (200 µM) combined with lithium chloride (10 mM) group; p-AKT, phosphorylated AKT; p-mTOR, phosphorylated mTOR; p-, phosphorylated.

Article Snippet: Subsequently, the membranes were incubated overnight at 4°C with primary antibodies against LC3B (rabbit; 1:2,000; cat. no. ab192890; Abcam), phosphorylated (p-)AKT (rabbit; 1:1,000; cat. no. 310021; Chengdu Zen Bioscience Co., Ltd.), AKT (rabbit; 1:1,000; cat. no. 382804; Chengdu Zen Bioscience Co., Ltd.), phosphorylated mTOR (mouse; 1:1,000; cat. no. sc-293133; Santa Cruz Biotechnology, Inc.), mTOR (mouse; 1:1,000; cat. no. sc-517464; Santa Cruz Biotechnology, Inc.), and β-tubulin (rabbit; 1:2,000; cat. no. AF7011; Affinity Biosciences).

Techniques: Western Blot, Expressing, Control

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. *P<0.05, **P<0.01 vs. the control group (0 µM angelicin); # P<0.05 vs. the DMSO group. PI3K, phosphatidylinositol-4,5-bisphosphate 3-kinase; p-, phosphorylated; DMSO, dimethyl sulfoxide; Akt, RAC-α serine/threonine-protein kinase.

Journal: Molecular Medicine Reports

Article Title: Angelicin inhibits liver cancer growth in vitro and in vivo

doi: 10.3892/mmr.2017.7219

Figure Lengend Snippet: 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. *P<0.05, **P<0.01 vs. the control group (0 µM angelicin); # P<0.05 vs. the DMSO group. PI3K, phosphatidylinositol-4,5-bisphosphate 3-kinase; p-, phosphorylated; DMSO, dimethyl sulfoxide; Akt, RAC-α serine/threonine-protein kinase.

Article Snippet: Polyclonal antibodies against PI3K (AF3242), Akt (AF6261), phosphorylated (p)-Akt (AF0016), apoptosis regulator BAX (Bax; AF0083) and Bcl-2 (AF6139) were purchased from Affinity Biologicals, Inc. (Ancaster, ON, Canada); antibodies against caspase-9 (9508T), caspase-3 (9665S), cytochrome c (4272S), Ki-67 (12075) and p-vascular endothelial growth factor receptor (VEGFR) 2 (9698) were purchased from Cell Signaling Technology, Inc. (Danvers, MA, USA).

Techniques: Expressing, In Vitro, Staining, Flow Cytometry, Standard Deviation