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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 18493 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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    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 3918 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc anti 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
    Anti P Akt Ser473, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 859 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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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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    Abcam anti 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
    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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    Cell Signaling Technology Inc phospho akt p akt
    The <t>miR-630/YAP1/ERK</t> feedback loop may be responsible for gefitinib resistance in EGFR-mutated lung adenocarcinoma cells. (A) The cell lysates of PC9 and PC9GR were evaluated for the expression of YAP1, Bcl-2, Slug, and IGF1R by real-time PCR. (B) MiR-630 inhibitor were transfected into PC9 cells. MiR-630 mimic was transfected into low PC9GR cells. After 48 h, the cells lysates were evaluated for the expression of YAP1, Bcl-2, Slug, and IGF1R by real-time PCR. (C) PC9 cells were transfected with the indicated combination of miR-630 inhibitor, shYAP1, shBcl-2, and shSlug for 24 h. PC9GR cells were transfected with the indicated combination of miR-630 mimic, YAP1, Bcl-2, and Slug overexpression plasmids for 24 h. These cells were treated with 0.1% DMSO or 10 μM of gefitinib for 24 h and were subjected to annexin-V and PI staining, followed by a flow cytometry analysis. The percentages of apoptotic cells in the annexin V+/PI- population plus annexin-V+/PI+ are summarized. (D) PC9 cells were transfected with the indicated combination of miR-630 inhibitor and shYAP1 for 48 h. PC9GR cells were transfected with the indicated combination of miR-630 mimic and YAP1 overexpression plasmids for 48 h. The cells lysates were evaluated for expression of <t>p-AKT,</t> total AKT, p-ERK, total ERK and β-actin by western blotting. (E) YAP1-overexpressing PC9 and PC9GR cells were treated with 10 μM AZD6244 for 5 h. The cell lysates were evaluated for the expression of YAP1, p-ERK, total ERK and β-actin by western blotting. MiR-630 expression of these cells were evaluated by real-time PCR. P value was calculated by the Student's t -test. The significant differences in experimental groups were compared to vehicle or indicated treatment (*P
    Phospho Akt P Akt, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 338 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Abcam anti pan akt phospho t308 antibody
    The <t>miR-630/YAP1/ERK</t> feedback loop may be responsible for gefitinib resistance in EGFR-mutated lung adenocarcinoma cells. (A) The cell lysates of PC9 and PC9GR were evaluated for the expression of YAP1, Bcl-2, Slug, and IGF1R by real-time PCR. (B) MiR-630 inhibitor were transfected into PC9 cells. MiR-630 mimic was transfected into low PC9GR cells. After 48 h, the cells lysates were evaluated for the expression of YAP1, Bcl-2, Slug, and IGF1R by real-time PCR. (C) PC9 cells were transfected with the indicated combination of miR-630 inhibitor, shYAP1, shBcl-2, and shSlug for 24 h. PC9GR cells were transfected with the indicated combination of miR-630 mimic, YAP1, Bcl-2, and Slug overexpression plasmids for 24 h. These cells were treated with 0.1% DMSO or 10 μM of gefitinib for 24 h and were subjected to annexin-V and PI staining, followed by a flow cytometry analysis. The percentages of apoptotic cells in the annexin V+/PI- population plus annexin-V+/PI+ are summarized. (D) PC9 cells were transfected with the indicated combination of miR-630 inhibitor and shYAP1 for 48 h. PC9GR cells were transfected with the indicated combination of miR-630 mimic and YAP1 overexpression plasmids for 48 h. The cells lysates were evaluated for expression of <t>p-AKT,</t> total AKT, p-ERK, total ERK and β-actin by western blotting. (E) YAP1-overexpressing PC9 and PC9GR cells were treated with 10 μM AZD6244 for 5 h. The cell lysates were evaluated for the expression of YAP1, p-ERK, total ERK and β-actin by western blotting. MiR-630 expression of these cells were evaluated by real-time PCR. P value was calculated by the Student's t -test. The significant differences in experimental groups were compared to vehicle or indicated treatment (*P
    Anti Pan Akt Phospho T308 Antibody, supplied by Abcam, used in various techniques. Bioz Stars score: 95/100, based on 205 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc anti phosphorylated p akt
    The <t>miR-630/YAP1/ERK</t> feedback loop may be responsible for gefitinib resistance in EGFR-mutated lung adenocarcinoma cells. (A) The cell lysates of PC9 and PC9GR were evaluated for the expression of YAP1, Bcl-2, Slug, and IGF1R by real-time PCR. (B) MiR-630 inhibitor were transfected into PC9 cells. MiR-630 mimic was transfected into low PC9GR cells. After 48 h, the cells lysates were evaluated for the expression of YAP1, Bcl-2, Slug, and IGF1R by real-time PCR. (C) PC9 cells were transfected with the indicated combination of miR-630 inhibitor, shYAP1, shBcl-2, and shSlug for 24 h. PC9GR cells were transfected with the indicated combination of miR-630 mimic, YAP1, Bcl-2, and Slug overexpression plasmids for 24 h. These cells were treated with 0.1% DMSO or 10 μM of gefitinib for 24 h and were subjected to annexin-V and PI staining, followed by a flow cytometry analysis. The percentages of apoptotic cells in the annexin V+/PI- population plus annexin-V+/PI+ are summarized. (D) PC9 cells were transfected with the indicated combination of miR-630 inhibitor and shYAP1 for 48 h. PC9GR cells were transfected with the indicated combination of miR-630 mimic and YAP1 overexpression plasmids for 48 h. The cells lysates were evaluated for expression of <t>p-AKT,</t> total AKT, p-ERK, total ERK and β-actin by western blotting. (E) YAP1-overexpressing PC9 and PC9GR cells were treated with 10 μM AZD6244 for 5 h. The cell lysates were evaluated for the expression of YAP1, p-ERK, total ERK and β-actin by western blotting. MiR-630 expression of these cells were evaluated by real-time PCR. P value was calculated by the Student's t -test. The significant differences in experimental groups were compared to vehicle or indicated treatment (*P
    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
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    Abcam anti akt1 phospho s473 antibody ep2109y
    The <t>miR-630/YAP1/ERK</t> feedback loop may be responsible for gefitinib resistance in EGFR-mutated lung adenocarcinoma cells. (A) The cell lysates of PC9 and PC9GR were evaluated for the expression of YAP1, Bcl-2, Slug, and IGF1R by real-time PCR. (B) MiR-630 inhibitor were transfected into PC9 cells. MiR-630 mimic was transfected into low PC9GR cells. After 48 h, the cells lysates were evaluated for the expression of YAP1, Bcl-2, Slug, and IGF1R by real-time PCR. (C) PC9 cells were transfected with the indicated combination of miR-630 inhibitor, shYAP1, shBcl-2, and shSlug for 24 h. PC9GR cells were transfected with the indicated combination of miR-630 mimic, YAP1, Bcl-2, and Slug overexpression plasmids for 24 h. These cells were treated with 0.1% DMSO or 10 μM of gefitinib for 24 h and were subjected to annexin-V and PI staining, followed by a flow cytometry analysis. The percentages of apoptotic cells in the annexin V+/PI- population plus annexin-V+/PI+ are summarized. (D) PC9 cells were transfected with the indicated combination of miR-630 inhibitor and shYAP1 for 48 h. PC9GR cells were transfected with the indicated combination of miR-630 mimic and YAP1 overexpression plasmids for 48 h. The cells lysates were evaluated for expression of <t>p-AKT,</t> total AKT, p-ERK, total ERK and β-actin by western blotting. (E) YAP1-overexpressing PC9 and PC9GR cells were treated with 10 μM AZD6244 for 5 h. The cell lysates were evaluated for the expression of YAP1, p-ERK, total ERK and β-actin by western blotting. MiR-630 expression of these cells were evaluated by real-time PCR. P value was calculated by the Student's t -test. The significant differences in experimental groups were compared to vehicle or indicated treatment (*P
    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
    Average 99 stars, based on 134 article reviews
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    Cell Signaling Technology Inc anti phospho p akt
    The <t>miR-630/YAP1/ERK</t> feedback loop may be responsible for gefitinib resistance in EGFR-mutated lung adenocarcinoma cells. (A) The cell lysates of PC9 and PC9GR were evaluated for the expression of YAP1, Bcl-2, Slug, and IGF1R by real-time PCR. (B) MiR-630 inhibitor were transfected into PC9 cells. MiR-630 mimic was transfected into low PC9GR cells. After 48 h, the cells lysates were evaluated for the expression of YAP1, Bcl-2, Slug, and IGF1R by real-time PCR. (C) PC9 cells were transfected with the indicated combination of miR-630 inhibitor, shYAP1, shBcl-2, and shSlug for 24 h. PC9GR cells were transfected with the indicated combination of miR-630 mimic, YAP1, Bcl-2, and Slug overexpression plasmids for 24 h. These cells were treated with 0.1% DMSO or 10 μM of gefitinib for 24 h and were subjected to annexin-V and PI staining, followed by a flow cytometry analysis. The percentages of apoptotic cells in the annexin V+/PI- population plus annexin-V+/PI+ are summarized. (D) PC9 cells were transfected with the indicated combination of miR-630 inhibitor and shYAP1 for 48 h. PC9GR cells were transfected with the indicated combination of miR-630 mimic and YAP1 overexpression plasmids for 48 h. The cells lysates were evaluated for expression of <t>p-AKT,</t> total AKT, p-ERK, total ERK and β-actin by western blotting. (E) YAP1-overexpressing PC9 and PC9GR cells were treated with 10 μM AZD6244 for 5 h. The cell lysates were evaluated for the expression of YAP1, p-ERK, total ERK and β-actin by western blotting. MiR-630 expression of these cells were evaluated by real-time PCR. P value was calculated by the Student's t -test. The significant differences in experimental groups were compared to vehicle or indicated treatment (*P
    Anti Phospho P Akt, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 80 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc rabbit anti p akt antibody
    The <t>miR-630/YAP1/ERK</t> feedback loop may be responsible for gefitinib resistance in EGFR-mutated lung adenocarcinoma cells. (A) The cell lysates of PC9 and PC9GR were evaluated for the expression of YAP1, Bcl-2, Slug, and IGF1R by real-time PCR. (B) MiR-630 inhibitor were transfected into PC9 cells. MiR-630 mimic was transfected into low PC9GR cells. After 48 h, the cells lysates were evaluated for the expression of YAP1, Bcl-2, Slug, and IGF1R by real-time PCR. (C) PC9 cells were transfected with the indicated combination of miR-630 inhibitor, shYAP1, shBcl-2, and shSlug for 24 h. PC9GR cells were transfected with the indicated combination of miR-630 mimic, YAP1, Bcl-2, and Slug overexpression plasmids for 24 h. These cells were treated with 0.1% DMSO or 10 μM of gefitinib for 24 h and were subjected to annexin-V and PI staining, followed by a flow cytometry analysis. The percentages of apoptotic cells in the annexin V+/PI- population plus annexin-V+/PI+ are summarized. (D) PC9 cells were transfected with the indicated combination of miR-630 inhibitor and shYAP1 for 48 h. PC9GR cells were transfected with the indicated combination of miR-630 mimic and YAP1 overexpression plasmids for 48 h. The cells lysates were evaluated for expression of <t>p-AKT,</t> total AKT, p-ERK, total ERK and β-actin by western blotting. (E) YAP1-overexpressing PC9 and PC9GR cells were treated with 10 μM AZD6244 for 5 h. The cell lysates were evaluated for the expression of YAP1, p-ERK, total ERK and β-actin by western blotting. MiR-630 expression of these cells were evaluated by real-time PCR. P value was calculated by the Student's t -test. The significant differences in experimental groups were compared to vehicle or indicated treatment (*P
    Rabbit Anti P Akt Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 88/100, based on 83 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Santa Cruz Biotechnology p akt1 2 3 antibody
    The <t>miR-630/YAP1/ERK</t> feedback loop may be responsible for gefitinib resistance in EGFR-mutated lung adenocarcinoma cells. (A) The cell lysates of PC9 and PC9GR were evaluated for the expression of YAP1, Bcl-2, Slug, and IGF1R by real-time PCR. (B) MiR-630 inhibitor were transfected into PC9 cells. MiR-630 mimic was transfected into low PC9GR cells. After 48 h, the cells lysates were evaluated for the expression of YAP1, Bcl-2, Slug, and IGF1R by real-time PCR. (C) PC9 cells were transfected with the indicated combination of miR-630 inhibitor, shYAP1, shBcl-2, and shSlug for 24 h. PC9GR cells were transfected with the indicated combination of miR-630 mimic, YAP1, Bcl-2, and Slug overexpression plasmids for 24 h. These cells were treated with 0.1% DMSO or 10 μM of gefitinib for 24 h and were subjected to annexin-V and PI staining, followed by a flow cytometry analysis. The percentages of apoptotic cells in the annexin V+/PI- population plus annexin-V+/PI+ are summarized. (D) PC9 cells were transfected with the indicated combination of miR-630 inhibitor and shYAP1 for 48 h. PC9GR cells were transfected with the indicated combination of miR-630 mimic and YAP1 overexpression plasmids for 48 h. The cells lysates were evaluated for expression of <t>p-AKT,</t> total AKT, p-ERK, total ERK and β-actin by western blotting. (E) YAP1-overexpressing PC9 and PC9GR cells were treated with 10 μM AZD6244 for 5 h. The cell lysates were evaluated for the expression of YAP1, p-ERK, total ERK and β-actin by western blotting. MiR-630 expression of these cells were evaluated by real-time PCR. P value was calculated by the Student's t -test. The significant differences in experimental groups were compared to vehicle or indicated treatment (*P
    P Akt1 2 3 Antibody, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 88/100, based on 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    N/A
    The serine threonine protein kinase AKT1 is catalytically inactive in serum starved primary and immortalized fibroblasts Survival factors can suppress apoptosis in a transcription independent manner by activating the serine
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    Image Search Results


    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

    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

    The miR-630/YAP1/ERK feedback loop may be responsible for gefitinib resistance in EGFR-mutated lung adenocarcinoma cells. (A) The cell lysates of PC9 and PC9GR were evaluated for the expression of YAP1, Bcl-2, Slug, and IGF1R by real-time PCR. (B) MiR-630 inhibitor were transfected into PC9 cells. MiR-630 mimic was transfected into low PC9GR cells. After 48 h, the cells lysates were evaluated for the expression of YAP1, Bcl-2, Slug, and IGF1R by real-time PCR. (C) PC9 cells were transfected with the indicated combination of miR-630 inhibitor, shYAP1, shBcl-2, and shSlug for 24 h. PC9GR cells were transfected with the indicated combination of miR-630 mimic, YAP1, Bcl-2, and Slug overexpression plasmids for 24 h. These cells were treated with 0.1% DMSO or 10 μM of gefitinib for 24 h and were subjected to annexin-V and PI staining, followed by a flow cytometry analysis. The percentages of apoptotic cells in the annexin V+/PI- population plus annexin-V+/PI+ are summarized. (D) PC9 cells were transfected with the indicated combination of miR-630 inhibitor and shYAP1 for 48 h. PC9GR cells were transfected with the indicated combination of miR-630 mimic and YAP1 overexpression plasmids for 48 h. The cells lysates were evaluated for expression of p-AKT, total AKT, p-ERK, total ERK and β-actin by western blotting. (E) YAP1-overexpressing PC9 and PC9GR cells were treated with 10 μM AZD6244 for 5 h. The cell lysates were evaluated for the expression of YAP1, p-ERK, total ERK and β-actin by western blotting. MiR-630 expression of these cells were evaluated by real-time PCR. P value was calculated by the Student's t -test. The significant differences in experimental groups were compared to vehicle or indicated treatment (*P

    Journal: Theranostics

    Article Title: A low microRNA-630 expression confers resistance to tyrosine kinase inhibitors in EGFR-mutated lung adenocarcinomas via miR-630/YAP1/ERK feedback loop

    doi: 10.7150/thno.22048

    Figure Lengend Snippet: The miR-630/YAP1/ERK feedback loop may be responsible for gefitinib resistance in EGFR-mutated lung adenocarcinoma cells. (A) The cell lysates of PC9 and PC9GR were evaluated for the expression of YAP1, Bcl-2, Slug, and IGF1R by real-time PCR. (B) MiR-630 inhibitor were transfected into PC9 cells. MiR-630 mimic was transfected into low PC9GR cells. After 48 h, the cells lysates were evaluated for the expression of YAP1, Bcl-2, Slug, and IGF1R by real-time PCR. (C) PC9 cells were transfected with the indicated combination of miR-630 inhibitor, shYAP1, shBcl-2, and shSlug for 24 h. PC9GR cells were transfected with the indicated combination of miR-630 mimic, YAP1, Bcl-2, and Slug overexpression plasmids for 24 h. These cells were treated with 0.1% DMSO or 10 μM of gefitinib for 24 h and were subjected to annexin-V and PI staining, followed by a flow cytometry analysis. The percentages of apoptotic cells in the annexin V+/PI- population plus annexin-V+/PI+ are summarized. (D) PC9 cells were transfected with the indicated combination of miR-630 inhibitor and shYAP1 for 48 h. PC9GR cells were transfected with the indicated combination of miR-630 mimic and YAP1 overexpression plasmids for 48 h. The cells lysates were evaluated for expression of p-AKT, total AKT, p-ERK, total ERK and β-actin by western blotting. (E) YAP1-overexpressing PC9 and PC9GR cells were treated with 10 μM AZD6244 for 5 h. The cell lysates were evaluated for the expression of YAP1, p-ERK, total ERK and β-actin by western blotting. MiR-630 expression of these cells were evaluated by real-time PCR. P value was calculated by the Student's t -test. The significant differences in experimental groups were compared to vehicle or indicated treatment (*P

    Article Snippet: Anti-phospho-AKT (p-AKT), Anti-AKT, anti-total ERK, and anti-phospho-ERK (p-ERK) antibodies were obtained from Cell Signaling (Danvers, MA).

    Techniques: Expressing, Real-time Polymerase Chain Reaction, Transfection, Over Expression, Staining, Flow Cytometry, Cytometry, Western Blot