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  • 99
    Cell Signaling Technology Inc p akt
    P Akt, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 18348 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/p akt/product/Cell Signaling Technology Inc
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    p akt  (Abcam)
    99
    Abcam p akt
    <t>ERK/AKT</t> signaling pathway is involved in the activation of the <t>TNF/caspase-3</t> cascade within ovarian cancer cells. (A) Inhibition of ERKIR decreased caspase-3 expression levels within CAOV-3 cells compared with in the control group. (B) Inhibition of ERKIR inhibited TNF-induced CAOV-3 cell apoptosis compared with in the control group. (C) PL-PTX-induced CAOV-3 cell apoptosis was inhibited via an ERK inhibitor compared with in the control group. **P
    P Akt, supplied by Abcam, used in various techniques. Bioz Stars score: 99/100, based on 2008 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    99
    Cell Signaling Technology Inc anti p akt
    CRLF1 promotes tumorigenesis by activating the MAPK/ERK and <t>PI3K/AKT</t> pathways. a An MAPK phosphorylation antibody array revealed that <t>ERK1/2</t> and AKT (P-S473) were activated in CRLF1-overexpressing IHH-4 cells. b Western blotting assays showed changes in the levels of ERK1/2 and AKT (P-S473) in CRLF1 knockdown or CRLF1-overexpressing cells. c IHH-4-CRLF1 cells were cultured with 10 μM U0126, 10 μM MK-2206, or 10 μM U0126+10 μM MK-2206 for 24 h. Western blotting analyses were performed to evaluate the effects of these two inhibitors on phosphorylation levels of ERK1/2 and AKT. β-Actin was used as a loading control. d MTT proliferation assay results demonstrating inhibited proliferation in CRLF1-overexpressing IHH-4 cells treated with MK-2206, U0126, or MK-2206+U0126
    Anti P Akt, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 3862 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    99
    Cell Signaling Technology Inc p akt ser473
    CRLF1 promotes tumorigenesis by activating the MAPK/ERK and <t>PI3K/AKT</t> pathways. a An MAPK phosphorylation antibody array revealed that <t>ERK1/2</t> and AKT (P-S473) were activated in CRLF1-overexpressing IHH-4 cells. b Western blotting assays showed changes in the levels of ERK1/2 and AKT (P-S473) in CRLF1 knockdown or CRLF1-overexpressing cells. c IHH-4-CRLF1 cells were cultured with 10 μM U0126, 10 μM MK-2206, or 10 μM U0126+10 μM MK-2206 for 24 h. Western blotting analyses were performed to evaluate the effects of these two inhibitors on phosphorylation levels of ERK1/2 and AKT. β-Actin was used as a loading control. d MTT proliferation assay results demonstrating inhibited proliferation in CRLF1-overexpressing IHH-4 cells treated with MK-2206, U0126, or MK-2206+U0126
    P Akt Ser473, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 4098 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    95
    Abcam anti p akt
    CRLF1 promotes tumorigenesis by activating the MAPK/ERK and <t>PI3K/AKT</t> pathways. a An MAPK phosphorylation antibody array revealed that <t>ERK1/2</t> and AKT (P-S473) were activated in CRLF1-overexpressing IHH-4 cells. b Western blotting assays showed changes in the levels of ERK1/2 and AKT (P-S473) in CRLF1 knockdown or CRLF1-overexpressing cells. c IHH-4-CRLF1 cells were cultured with 10 μM U0126, 10 μM MK-2206, or 10 μM U0126+10 μM MK-2206 for 24 h. Western blotting analyses were performed to evaluate the effects of these two inhibitors on phosphorylation levels of ERK1/2 and AKT. β-Actin was used as a loading control. d MTT proliferation assay results demonstrating inhibited proliferation in CRLF1-overexpressing IHH-4 cells treated with MK-2206, U0126, or MK-2206+U0126
    Anti P Akt, supplied by Abcam, used in various techniques. Bioz Stars score: 95/100, based on 652 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    99
    Cell Signaling Technology Inc phosphorylated akt p akt
    CRLF1 promotes tumorigenesis by activating the MAPK/ERK and <t>PI3K/AKT</t> pathways. a An MAPK phosphorylation antibody array revealed that <t>ERK1/2</t> and AKT (P-S473) were activated in CRLF1-overexpressing IHH-4 cells. b Western blotting assays showed changes in the levels of ERK1/2 and AKT (P-S473) in CRLF1 knockdown or CRLF1-overexpressing cells. c IHH-4-CRLF1 cells were cultured with 10 μM U0126, 10 μM MK-2206, or 10 μM U0126+10 μM MK-2206 for 24 h. Western blotting analyses were performed to evaluate the effects of these two inhibitors on phosphorylation levels of ERK1/2 and AKT. β-Actin was used as a loading control. d MTT proliferation assay results demonstrating inhibited proliferation in CRLF1-overexpressing IHH-4 cells treated with MK-2206, U0126, or MK-2206+U0126
    Phosphorylated Akt P Akt, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 625 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    99
    Abcam anti pan akt phospho t308 antibody
    CRLF1 promotes tumorigenesis by activating the MAPK/ERK and <t>PI3K/AKT</t> pathways. a An MAPK phosphorylation antibody array revealed that <t>ERK1/2</t> and AKT (P-S473) were activated in CRLF1-overexpressing IHH-4 cells. b Western blotting assays showed changes in the levels of ERK1/2 and AKT (P-S473) in CRLF1 knockdown or CRLF1-overexpressing cells. c IHH-4-CRLF1 cells were cultured with 10 μM U0126, 10 μM MK-2206, or 10 μM U0126+10 μM MK-2206 for 24 h. Western blotting analyses were performed to evaluate the effects of these two inhibitors on phosphorylation levels of ERK1/2 and AKT. β-Actin was used as a loading control. d MTT proliferation assay results demonstrating inhibited proliferation in CRLF1-overexpressing IHH-4 cells treated with MK-2206, U0126, or MK-2206+U0126
    Anti Pan Akt Phospho T308 Antibody, supplied by Abcam, used in various techniques. Bioz Stars score: 99/100, based on 205 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    99
    Cell Signaling Technology Inc anti phosphorylated p akt
    CRLF1 promotes tumorigenesis by activating the MAPK/ERK and <t>PI3K/AKT</t> pathways. a An MAPK phosphorylation antibody array revealed that <t>ERK1/2</t> and AKT (P-S473) were activated in CRLF1-overexpressing IHH-4 cells. b Western blotting assays showed changes in the levels of ERK1/2 and AKT (P-S473) in CRLF1 knockdown or CRLF1-overexpressing cells. c IHH-4-CRLF1 cells were cultured with 10 μM U0126, 10 μM MK-2206, or 10 μM U0126+10 μM MK-2206 for 24 h. Western blotting analyses were performed to evaluate the effects of these two inhibitors on phosphorylation levels of ERK1/2 and AKT. β-Actin was used as a loading control. d MTT proliferation assay results demonstrating inhibited proliferation in CRLF1-overexpressing IHH-4 cells treated with MK-2206, U0126, or MK-2206+U0126
    Anti Phosphorylated P Akt, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 136 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti phosphorylated p akt/product/Cell Signaling Technology Inc
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    pakt  (Abcam)
    99
    Abcam pakt
    CRLF1 promotes tumorigenesis by activating the MAPK/ERK and <t>PI3K/AKT</t> pathways. a An MAPK phosphorylation antibody array revealed that <t>ERK1/2</t> and AKT (P-S473) were activated in CRLF1-overexpressing IHH-4 cells. b Western blotting assays showed changes in the levels of ERK1/2 and AKT (P-S473) in CRLF1 knockdown or CRLF1-overexpressing cells. c IHH-4-CRLF1 cells were cultured with 10 μM U0126, 10 μM MK-2206, or 10 μM U0126+10 μM MK-2206 for 24 h. Western blotting analyses were performed to evaluate the effects of these two inhibitors on phosphorylation levels of ERK1/2 and AKT. β-Actin was used as a loading control. d MTT proliferation assay results demonstrating inhibited proliferation in CRLF1-overexpressing IHH-4 cells treated with MK-2206, U0126, or MK-2206+U0126
    Pakt, supplied by Abcam, used in various techniques. Bioz Stars score: 99/100, based on 305 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    99
    Abcam anti akt1 phospho s473 antibody ep2109y
    CRLF1 promotes tumorigenesis by activating the MAPK/ERK and <t>PI3K/AKT</t> pathways. a An MAPK phosphorylation antibody array revealed that <t>ERK1/2</t> and AKT (P-S473) were activated in CRLF1-overexpressing IHH-4 cells. b Western blotting assays showed changes in the levels of ERK1/2 and AKT (P-S473) in CRLF1 knockdown or CRLF1-overexpressing cells. c IHH-4-CRLF1 cells were cultured with 10 μM U0126, 10 μM MK-2206, or 10 μM U0126+10 μM MK-2206 for 24 h. Western blotting analyses were performed to evaluate the effects of these two inhibitors on phosphorylation levels of ERK1/2 and AKT. β-Actin was used as a loading control. d MTT proliferation assay results demonstrating inhibited proliferation in CRLF1-overexpressing IHH-4 cells treated with MK-2206, U0126, or MK-2206+U0126
    Anti Akt1 Phospho S473 Antibody Ep2109y, supplied by Abcam, used in various techniques. Bioz Stars score: 99/100, based on 134 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti akt1 phospho s473 antibody ep2109y/product/Abcam
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    99
    Proteintech mouse akt phospho s473 monoclonal
    CRLF1 promotes tumorigenesis by activating the MAPK/ERK and <t>PI3K/AKT</t> pathways. a An MAPK phosphorylation antibody array revealed that <t>ERK1/2</t> and AKT (P-S473) were activated in CRLF1-overexpressing IHH-4 cells. b Western blotting assays showed changes in the levels of ERK1/2 and AKT (P-S473) in CRLF1 knockdown or CRLF1-overexpressing cells. c IHH-4-CRLF1 cells were cultured with 10 μM U0126, 10 μM MK-2206, or 10 μM U0126+10 μM MK-2206 for 24 h. Western blotting analyses were performed to evaluate the effects of these two inhibitors on phosphorylation levels of ERK1/2 and AKT. β-Actin was used as a loading control. d MTT proliferation assay results demonstrating inhibited proliferation in CRLF1-overexpressing IHH-4 cells treated with MK-2206, U0126, or MK-2206+U0126
    Mouse Akt Phospho S473 Monoclonal, supplied by Proteintech, used in various techniques. Bioz Stars score: 99/100, based on 169 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mouse akt phospho s473 monoclonal/product/Proteintech
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    92
    Epitomics p akt
    Role of redox regulation in the anti-apoptotic effects of SP. Mouse corneal epithelial cells were treated with 100 μM L-BSO and 1 μM SP 2 h before the addition of glucose for 24 h. The phosphorylation of <t>Akt</t> was evaluated by Immunofluorescence staining or Western blot (A). The apoptosis was evaluated by FACS analysis followed by FITC-Annexin V/PI staining (B), and the detection of Bad, Bax, <t>AIF,</t> Ca 2+ and mitochondrial membrane potential (C). The intracellular ROS and glutathione (GSH) were detected by staining with the fluorescence probes (D) and measured by the fluorescence intensity (E). The cellular total antioxidant capacity (TAC) was measured by the ABTS assay (E).
    P Akt, supplied by Epitomics, used in various techniques. Bioz Stars score: 92/100, based on 118 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/p akt/product/Epitomics
    Average 92 stars, based on 118 article reviews
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    N/A
    Rabbit polyclonal Akt antibody
      Buy from Supplier

    Image Search Results


    ERK/AKT signaling pathway is involved in the activation of the TNF/caspase-3 cascade within ovarian cancer cells. (A) Inhibition of ERKIR decreased caspase-3 expression levels within CAOV-3 cells compared with in the control group. (B) Inhibition of ERKIR inhibited TNF-induced CAOV-3 cell apoptosis compared with in the control group. (C) PL-PTX-induced CAOV-3 cell apoptosis was inhibited via an ERK inhibitor compared with in the control group. **P

    Journal: Molecular Medicine Reports

    Article Title: Pegylated liposomal-paclitaxel induces ovarian cancer cell apoptosis via TNF-induced ERK/AKT signaling pathway

    doi: 10.3892/mmr.2018.8811

    Figure Lengend Snippet: ERK/AKT signaling pathway is involved in the activation of the TNF/caspase-3 cascade within ovarian cancer cells. (A) Inhibition of ERKIR decreased caspase-3 expression levels within CAOV-3 cells compared with in the control group. (B) Inhibition of ERKIR inhibited TNF-induced CAOV-3 cell apoptosis compared with in the control group. (C) PL-PTX-induced CAOV-3 cell apoptosis was inhibited via an ERK inhibitor compared with in the control group. **P

    Article Snippet: The primary antibodies used were against: Caspase-9 (1:1,200; ab32539), ERK (1:1,000; ab54230) and phosphorylayed (p)ERK 1/2 (phospho-Thr202/Tyr204; 1:1,000; ab214362), caspase-3 (1:1,200; ab2171), protein kinase B (AKT; 1:1,000; ab8805), p-AKT (phosphor-S473; 1:1,000; ab8932) and β-actin (1:500; ab8226; all Abcam) for 12 h at 4°C.

    Techniques: Activation Assay, Inhibition, Expressing

    CRLF1 promotes tumorigenesis by activating the MAPK/ERK and PI3K/AKT pathways. a An MAPK phosphorylation antibody array revealed that ERK1/2 and AKT (P-S473) were activated in CRLF1-overexpressing IHH-4 cells. b Western blotting assays showed changes in the levels of ERK1/2 and AKT (P-S473) in CRLF1 knockdown or CRLF1-overexpressing cells. c IHH-4-CRLF1 cells were cultured with 10 μM U0126, 10 μM MK-2206, or 10 μM U0126+10 μM MK-2206 for 24 h. Western blotting analyses were performed to evaluate the effects of these two inhibitors on phosphorylation levels of ERK1/2 and AKT. β-Actin was used as a loading control. d MTT proliferation assay results demonstrating inhibited proliferation in CRLF1-overexpressing IHH-4 cells treated with MK-2206, U0126, or MK-2206+U0126

    Journal: Cell Death & Disease

    Article Title: CRLF1 promotes malignant phenotypes of papillary thyroid carcinoma by activating the MAPK/ERK and PI3K/AKT pathways

    doi: 10.1038/s41419-018-0352-0

    Figure Lengend Snippet: CRLF1 promotes tumorigenesis by activating the MAPK/ERK and PI3K/AKT pathways. a An MAPK phosphorylation antibody array revealed that ERK1/2 and AKT (P-S473) were activated in CRLF1-overexpressing IHH-4 cells. b Western blotting assays showed changes in the levels of ERK1/2 and AKT (P-S473) in CRLF1 knockdown or CRLF1-overexpressing cells. c IHH-4-CRLF1 cells were cultured with 10 μM U0126, 10 μM MK-2206, or 10 μM U0126+10 μM MK-2206 for 24 h. Western blotting analyses were performed to evaluate the effects of these two inhibitors on phosphorylation levels of ERK1/2 and AKT. β-Actin was used as a loading control. d MTT proliferation assay results demonstrating inhibited proliferation in CRLF1-overexpressing IHH-4 cells treated with MK-2206, U0126, or MK-2206+U0126

    Article Snippet: The sections were then incubated with diluted rabbit anti-CRLF1 antibody (1:100; HPA041493, Sigma-Aldrich, USA), p-ERK1/2 antibody (1:400; #4370, Cell Signaling Technology, USA), or p-AKT antibody (1:100; #4060, Cell Signaling Technology, USA) at 4 °C overnight.

    Techniques: Ab Array, Western Blot, Cell Culture, MTT Assay, Proliferation Assay

    Role of redox regulation in the anti-apoptotic effects of SP. Mouse corneal epithelial cells were treated with 100 μM L-BSO and 1 μM SP 2 h before the addition of glucose for 24 h. The phosphorylation of Akt was evaluated by Immunofluorescence staining or Western blot (A). The apoptosis was evaluated by FACS analysis followed by FITC-Annexin V/PI staining (B), and the detection of Bad, Bax, AIF, Ca 2+ and mitochondrial membrane potential (C). The intracellular ROS and glutathione (GSH) were detected by staining with the fluorescence probes (D) and measured by the fluorescence intensity (E). The cellular total antioxidant capacity (TAC) was measured by the ABTS assay (E).

    Journal: PLoS ONE

    Article Title: Substance P Inhibits Hyperosmotic Stress-Induced Apoptosis in Corneal Epithelial Cells through the Mechanism of Akt Activation and Reactive Oxygen Species Scavenging via the Neurokinin-1 Receptor

    doi: 10.1371/journal.pone.0149865

    Figure Lengend Snippet: Role of redox regulation in the anti-apoptotic effects of SP. Mouse corneal epithelial cells were treated with 100 μM L-BSO and 1 μM SP 2 h before the addition of glucose for 24 h. The phosphorylation of Akt was evaluated by Immunofluorescence staining or Western blot (A). The apoptosis was evaluated by FACS analysis followed by FITC-Annexin V/PI staining (B), and the detection of Bad, Bax, AIF, Ca 2+ and mitochondrial membrane potential (C). The intracellular ROS and glutathione (GSH) were detected by staining with the fluorescence probes (D) and measured by the fluorescence intensity (E). The cellular total antioxidant capacity (TAC) was measured by the ABTS assay (E).

    Article Snippet: Immunofluorescence staining Cells were fixed by 4% paraformaldehyde for 15 min, permeabilized with 0.1% Triton X-100 for 5 min and blocked with 5% bovine serum albumin (BSA) for 1 h. The samples were stained with primary antibodies against AIF (Santa Cruz Biotechnology, Santa Cruz, CA), p-Akt (pS473, Epitomics, Burlingame, CA), MnSOD, catalase, NQO1, Hmox1, Bad and Bax (abcam, Cambridge, MA) at a concentration of 1:100 overnight at 4°C, and then incubated with fluorescein-conjugated secondary antibodies (Santa Cruz Biotechnology) at 37°C for 30 min.

    Techniques: Immunofluorescence, Staining, Western Blot, FACS, Fluorescence, ABTS Assay

    Role of NK-1 receptor in the anti-apoptotic effects of SP. Mouse corneal epithelial cells were treated with 1 μM NK-1 receptor antagonist L-733,060 with 1 μM SP 2 h before the addition of glucose for 24 h. The phosphorylation of Akt was evaluated by Immunofluorescence staining or Western blot (A). The apoptosis was evaluated by FACS analysis followed by FITC-Annexin V/PI staining (B), and the detection of Bad, Bax, AIF, Ca 2+ and mitochondrial membrane potential (C). The intracellular ROS and glutathione (GSH) were detected by staining with the fluorescence probes (D) and measured by the fluorescence intensity (E). The cellular total antioxidant capacity (TAC) was measured by the ABTS assay (E).

    Journal: PLoS ONE

    Article Title: Substance P Inhibits Hyperosmotic Stress-Induced Apoptosis in Corneal Epithelial Cells through the Mechanism of Akt Activation and Reactive Oxygen Species Scavenging via the Neurokinin-1 Receptor

    doi: 10.1371/journal.pone.0149865

    Figure Lengend Snippet: Role of NK-1 receptor in the anti-apoptotic effects of SP. Mouse corneal epithelial cells were treated with 1 μM NK-1 receptor antagonist L-733,060 with 1 μM SP 2 h before the addition of glucose for 24 h. The phosphorylation of Akt was evaluated by Immunofluorescence staining or Western blot (A). The apoptosis was evaluated by FACS analysis followed by FITC-Annexin V/PI staining (B), and the detection of Bad, Bax, AIF, Ca 2+ and mitochondrial membrane potential (C). The intracellular ROS and glutathione (GSH) were detected by staining with the fluorescence probes (D) and measured by the fluorescence intensity (E). The cellular total antioxidant capacity (TAC) was measured by the ABTS assay (E).

    Article Snippet: Immunofluorescence staining Cells were fixed by 4% paraformaldehyde for 15 min, permeabilized with 0.1% Triton X-100 for 5 min and blocked with 5% bovine serum albumin (BSA) for 1 h. The samples were stained with primary antibodies against AIF (Santa Cruz Biotechnology, Santa Cruz, CA), p-Akt (pS473, Epitomics, Burlingame, CA), MnSOD, catalase, NQO1, Hmox1, Bad and Bax (abcam, Cambridge, MA) at a concentration of 1:100 overnight at 4°C, and then incubated with fluorescein-conjugated secondary antibodies (Santa Cruz Biotechnology) at 37°C for 30 min.

    Techniques: Immunofluorescence, Staining, Western Blot, FACS, Fluorescence, ABTS Assay

    Role of Akt reactivation in the anti-apoptotic effects of SP. Mouse corneal epithelial cells were treated with 40 μM Akt inhibitor V and 1 μM SP 2 h before the addition of glucose for 24 h. The phosphorylation of Akt was evaluated by Immunofluorescence staining or Western blot (A). The apoptosis was evaluated by FACS analysis followed by FITC-Annexin V/PI staining (B), and the detection of Bad, Bax, AIF, Ca 2+ and mitochondrial membrane potential (C). The intracellular ROS and glutathione (GSH) were detected by staining with the fluorescence probes (D) and measured by the fluorescence intensity (E). The cellular total antioxidant capacity (TAC) was measured by the ABTS assay (E).

    Journal: PLoS ONE

    Article Title: Substance P Inhibits Hyperosmotic Stress-Induced Apoptosis in Corneal Epithelial Cells through the Mechanism of Akt Activation and Reactive Oxygen Species Scavenging via the Neurokinin-1 Receptor

    doi: 10.1371/journal.pone.0149865

    Figure Lengend Snippet: Role of Akt reactivation in the anti-apoptotic effects of SP. Mouse corneal epithelial cells were treated with 40 μM Akt inhibitor V and 1 μM SP 2 h before the addition of glucose for 24 h. The phosphorylation of Akt was evaluated by Immunofluorescence staining or Western blot (A). The apoptosis was evaluated by FACS analysis followed by FITC-Annexin V/PI staining (B), and the detection of Bad, Bax, AIF, Ca 2+ and mitochondrial membrane potential (C). The intracellular ROS and glutathione (GSH) were detected by staining with the fluorescence probes (D) and measured by the fluorescence intensity (E). The cellular total antioxidant capacity (TAC) was measured by the ABTS assay (E).

    Article Snippet: Immunofluorescence staining Cells were fixed by 4% paraformaldehyde for 15 min, permeabilized with 0.1% Triton X-100 for 5 min and blocked with 5% bovine serum albumin (BSA) for 1 h. The samples were stained with primary antibodies against AIF (Santa Cruz Biotechnology, Santa Cruz, CA), p-Akt (pS473, Epitomics, Burlingame, CA), MnSOD, catalase, NQO1, Hmox1, Bad and Bax (abcam, Cambridge, MA) at a concentration of 1:100 overnight at 4°C, and then incubated with fluorescein-conjugated secondary antibodies (Santa Cruz Biotechnology) at 37°C for 30 min.

    Techniques: Immunofluorescence, Staining, Western Blot, FACS, Fluorescence, ABTS Assay