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phosphor ampk p ampk  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc phosphor ampk p ampk
    Effects of <t>AMPK</t> on decidualization. A and B HESCs were pretreated with 8-Br-cAMP and MPA for three days, followed by treatment with various concentrations of testosterone (0.001–100 μM) for an additional two days. AMPK ( A ) and SIRT1 ( B ) mRNA levels were further measured using real-time PCR. Statistical significance is denoted by * p < 0.05. C HESCs were treated with 8-Br-cAMP and MPA for 1–5 days, and AMPK and SIRT1 mRNA levels were further measured using real-time PCR. D -I HESCs were pretreated with 8-Br-cAMP and MPA for three days, followed by treatment with Dorsomorphin (5 μM) or A-769662 (20 μM) alone or combining Dorsomorphin/A-769662 with testosterone (100 μM) for an additional two days. IGFBP1 ( D ) and PRL ( E ) mRNA levels were further measured using real-time PCR. IGFBP1 protein ( F ) that was released into the medium was measured using ELISA. PDK4 ( G ) and SIRT1 ( H ) mRNA levels were further measured using real-time PCR. Statistical significance is denoted by * p < 0.05, ** p < 0.01. I Proteins of <t>p-AMPK,</t> SIRT1, and PDK4 were measured using Western blot analysis. Quantitative analysis of p-AMPK (J), SIRT1 (K), and PDK4 (L) protein expression levels were showed in histogram. a represents the treated cells vs. non-decidualized cells. b represents the treated cells vs. decidualized cells without other treatments. Statistical significance is denoted by * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001
    Phosphor Ampk P Ampk, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Decreased AMPK/SIRT1/PDK4 induced by androgen excess inhibits human endometrial stromal cell decidualization in PCOS"

    Article Title: Decreased AMPK/SIRT1/PDK4 induced by androgen excess inhibits human endometrial stromal cell decidualization in PCOS

    Journal: Cellular and Molecular Life Sciences: CMLS

    doi: 10.1007/s00018-024-05362-5

    Effects of AMPK on decidualization. A and B HESCs were pretreated with 8-Br-cAMP and MPA for three days, followed by treatment with various concentrations of testosterone (0.001–100 μM) for an additional two days. AMPK ( A ) and SIRT1 ( B ) mRNA levels were further measured using real-time PCR. Statistical significance is denoted by * p < 0.05. C HESCs were treated with 8-Br-cAMP and MPA for 1–5 days, and AMPK and SIRT1 mRNA levels were further measured using real-time PCR. D -I HESCs were pretreated with 8-Br-cAMP and MPA for three days, followed by treatment with Dorsomorphin (5 μM) or A-769662 (20 μM) alone or combining Dorsomorphin/A-769662 with testosterone (100 μM) for an additional two days. IGFBP1 ( D ) and PRL ( E ) mRNA levels were further measured using real-time PCR. IGFBP1 protein ( F ) that was released into the medium was measured using ELISA. PDK4 ( G ) and SIRT1 ( H ) mRNA levels were further measured using real-time PCR. Statistical significance is denoted by * p < 0.05, ** p < 0.01. I Proteins of p-AMPK, SIRT1, and PDK4 were measured using Western blot analysis. Quantitative analysis of p-AMPK (J), SIRT1 (K), and PDK4 (L) protein expression levels were showed in histogram. a represents the treated cells vs. non-decidualized cells. b represents the treated cells vs. decidualized cells without other treatments. Statistical significance is denoted by * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001
    Figure Legend Snippet: Effects of AMPK on decidualization. A and B HESCs were pretreated with 8-Br-cAMP and MPA for three days, followed by treatment with various concentrations of testosterone (0.001–100 μM) for an additional two days. AMPK ( A ) and SIRT1 ( B ) mRNA levels were further measured using real-time PCR. Statistical significance is denoted by * p < 0.05. C HESCs were treated with 8-Br-cAMP and MPA for 1–5 days, and AMPK and SIRT1 mRNA levels were further measured using real-time PCR. D -I HESCs were pretreated with 8-Br-cAMP and MPA for three days, followed by treatment with Dorsomorphin (5 μM) or A-769662 (20 μM) alone or combining Dorsomorphin/A-769662 with testosterone (100 μM) for an additional two days. IGFBP1 ( D ) and PRL ( E ) mRNA levels were further measured using real-time PCR. IGFBP1 protein ( F ) that was released into the medium was measured using ELISA. PDK4 ( G ) and SIRT1 ( H ) mRNA levels were further measured using real-time PCR. Statistical significance is denoted by * p < 0.05, ** p < 0.01. I Proteins of p-AMPK, SIRT1, and PDK4 were measured using Western blot analysis. Quantitative analysis of p-AMPK (J), SIRT1 (K), and PDK4 (L) protein expression levels were showed in histogram. a represents the treated cells vs. non-decidualized cells. b represents the treated cells vs. decidualized cells without other treatments. Statistical significance is denoted by * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

    Techniques Used: Real-time Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay, Western Blot, Expressing

    Androgen excess regulates decidualization via the AR/AMPK/SIRT1/PDK4 pathway. PDK4 levels were induced during decidualization. PDK4 expression decreased in the endometrium of PCOS patients. Androgen excess regulates decidualization via the AR/AMPK/SIRT1/PDK4 pathway
    Figure Legend Snippet: Androgen excess regulates decidualization via the AR/AMPK/SIRT1/PDK4 pathway. PDK4 levels were induced during decidualization. PDK4 expression decreased in the endometrium of PCOS patients. Androgen excess regulates decidualization via the AR/AMPK/SIRT1/PDK4 pathway

    Techniques Used: Expressing



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    Effects of <t>AMPK</t> on decidualization. A and B HESCs were pretreated with 8-Br-cAMP and MPA for three days, followed by treatment with various concentrations of testosterone (0.001–100 μM) for an additional two days. AMPK ( A ) and SIRT1 ( B ) mRNA levels were further measured using real-time PCR. Statistical significance is denoted by * p < 0.05. C HESCs were treated with 8-Br-cAMP and MPA for 1–5 days, and AMPK and SIRT1 mRNA levels were further measured using real-time PCR. D -I HESCs were pretreated with 8-Br-cAMP and MPA for three days, followed by treatment with Dorsomorphin (5 μM) or A-769662 (20 μM) alone or combining Dorsomorphin/A-769662 with testosterone (100 μM) for an additional two days. IGFBP1 ( D ) and PRL ( E ) mRNA levels were further measured using real-time PCR. IGFBP1 protein ( F ) that was released into the medium was measured using ELISA. PDK4 ( G ) and SIRT1 ( H ) mRNA levels were further measured using real-time PCR. Statistical significance is denoted by * p < 0.05, ** p < 0.01. I Proteins of <t>p-AMPK,</t> SIRT1, and PDK4 were measured using Western blot analysis. Quantitative analysis of p-AMPK (J), SIRT1 (K), and PDK4 (L) protein expression levels were showed in histogram. a represents the treated cells vs. non-decidualized cells. b represents the treated cells vs. decidualized cells without other treatments. Statistical significance is denoted by * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001
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    Effects of AMPK on decidualization. A and B HESCs were pretreated with 8-Br-cAMP and MPA for three days, followed by treatment with various concentrations of testosterone (0.001–100 μM) for an additional two days. AMPK ( A ) and SIRT1 ( B ) mRNA levels were further measured using real-time PCR. Statistical significance is denoted by * p < 0.05. C HESCs were treated with 8-Br-cAMP and MPA for 1–5 days, and AMPK and SIRT1 mRNA levels were further measured using real-time PCR. D -I HESCs were pretreated with 8-Br-cAMP and MPA for three days, followed by treatment with Dorsomorphin (5 μM) or A-769662 (20 μM) alone or combining Dorsomorphin/A-769662 with testosterone (100 μM) for an additional two days. IGFBP1 ( D ) and PRL ( E ) mRNA levels were further measured using real-time PCR. IGFBP1 protein ( F ) that was released into the medium was measured using ELISA. PDK4 ( G ) and SIRT1 ( H ) mRNA levels were further measured using real-time PCR. Statistical significance is denoted by * p < 0.05, ** p < 0.01. I Proteins of p-AMPK, SIRT1, and PDK4 were measured using Western blot analysis. Quantitative analysis of p-AMPK (J), SIRT1 (K), and PDK4 (L) protein expression levels were showed in histogram. a represents the treated cells vs. non-decidualized cells. b represents the treated cells vs. decidualized cells without other treatments. Statistical significance is denoted by * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

    Journal: Cellular and Molecular Life Sciences: CMLS

    Article Title: Decreased AMPK/SIRT1/PDK4 induced by androgen excess inhibits human endometrial stromal cell decidualization in PCOS

    doi: 10.1007/s00018-024-05362-5

    Figure Lengend Snippet: Effects of AMPK on decidualization. A and B HESCs were pretreated with 8-Br-cAMP and MPA for three days, followed by treatment with various concentrations of testosterone (0.001–100 μM) for an additional two days. AMPK ( A ) and SIRT1 ( B ) mRNA levels were further measured using real-time PCR. Statistical significance is denoted by * p < 0.05. C HESCs were treated with 8-Br-cAMP and MPA for 1–5 days, and AMPK and SIRT1 mRNA levels were further measured using real-time PCR. D -I HESCs were pretreated with 8-Br-cAMP and MPA for three days, followed by treatment with Dorsomorphin (5 μM) or A-769662 (20 μM) alone or combining Dorsomorphin/A-769662 with testosterone (100 μM) for an additional two days. IGFBP1 ( D ) and PRL ( E ) mRNA levels were further measured using real-time PCR. IGFBP1 protein ( F ) that was released into the medium was measured using ELISA. PDK4 ( G ) and SIRT1 ( H ) mRNA levels were further measured using real-time PCR. Statistical significance is denoted by * p < 0.05, ** p < 0.01. I Proteins of p-AMPK, SIRT1, and PDK4 were measured using Western blot analysis. Quantitative analysis of p-AMPK (J), SIRT1 (K), and PDK4 (L) protein expression levels were showed in histogram. a represents the treated cells vs. non-decidualized cells. b represents the treated cells vs. decidualized cells without other treatments. Statistical significance is denoted by * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

    Article Snippet: The proteins were resolved to perform a western blot analysis on the Protein Simple Wes™ Western Blot machine (ProteinSimple, USA) with antibodies against the proteins of interest, including PDK4 (1:200, Abgent, AP7041B), AR (1:100, Invitrogen, AN1-15), phosphor-AMPK (p-AMPK) (1:200, cell signaling technology, 2535S), SIRT1 (1:100, cell signaling technology, 8469S) using a standard procedure, and the expression of each protein was normalized to the expression of Vinculin in the corresponding sample.

    Techniques: Real-time Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay, Western Blot, Expressing

    Androgen excess regulates decidualization via the AR/AMPK/SIRT1/PDK4 pathway. PDK4 levels were induced during decidualization. PDK4 expression decreased in the endometrium of PCOS patients. Androgen excess regulates decidualization via the AR/AMPK/SIRT1/PDK4 pathway

    Journal: Cellular and Molecular Life Sciences: CMLS

    Article Title: Decreased AMPK/SIRT1/PDK4 induced by androgen excess inhibits human endometrial stromal cell decidualization in PCOS

    doi: 10.1007/s00018-024-05362-5

    Figure Lengend Snippet: Androgen excess regulates decidualization via the AR/AMPK/SIRT1/PDK4 pathway. PDK4 levels were induced during decidualization. PDK4 expression decreased in the endometrium of PCOS patients. Androgen excess regulates decidualization via the AR/AMPK/SIRT1/PDK4 pathway

    Article Snippet: The proteins were resolved to perform a western blot analysis on the Protein Simple Wes™ Western Blot machine (ProteinSimple, USA) with antibodies against the proteins of interest, including PDK4 (1:200, Abgent, AP7041B), AR (1:100, Invitrogen, AN1-15), phosphor-AMPK (p-AMPK) (1:200, cell signaling technology, 2535S), SIRT1 (1:100, cell signaling technology, 8469S) using a standard procedure, and the expression of each protein was normalized to the expression of Vinculin in the corresponding sample.

    Techniques: Expressing

    The hypothesis that ISKNV triggered ROS-mediated stress signals both modulate the autophagic flux pathway and anti-oxidants response on enhancement of viral replication in fish cells. The ISKNV shows a novel approach, using ROS-mediated stress response that can either activate the AMPK/mTOR autophagy signaling pathway via phosphorylation or induce the oxidative defense stress signal in the early replication stages in fish cells. The ISKNV-induced AMPK/mTOR autophagy signaling pathway is primed by ROS-mediated stress signals on either phosphorylation of AMPK on threonine 172 or suppresses phosphorylation of mTOR on serine 1448 for autophagy induction. On the other hand, the oxidative stress response also upregulates the stress transcriptional factor Nrf2 and antioxidant enzymes such as Cu/MnSOD (SOD1) and ZnSOD (SOD2), which are correlated with metabolized ROS, such as superoxide, for the recovery of biological functions in proteins. Thus, ISKNV induced ROS-mediated AMPK/mTOR autophagy pathway on enhanced viral replication that can be inhibited by treatment with antioxidants NAC, which provides a novel strategy for viral control.

    Journal: Viruses

    Article Title: ISKNV Triggers AMPK/mTOR-Mediated Autophagy Signaling through Oxidative Stress, Inducing Antioxidant Enzyme Expression and Enhancing Viral Replication in GF-1 Cells

    doi: 10.3390/v16060914

    Figure Lengend Snippet: The hypothesis that ISKNV triggered ROS-mediated stress signals both modulate the autophagic flux pathway and anti-oxidants response on enhancement of viral replication in fish cells. The ISKNV shows a novel approach, using ROS-mediated stress response that can either activate the AMPK/mTOR autophagy signaling pathway via phosphorylation or induce the oxidative defense stress signal in the early replication stages in fish cells. The ISKNV-induced AMPK/mTOR autophagy signaling pathway is primed by ROS-mediated stress signals on either phosphorylation of AMPK on threonine 172 or suppresses phosphorylation of mTOR on serine 1448 for autophagy induction. On the other hand, the oxidative stress response also upregulates the stress transcriptional factor Nrf2 and antioxidant enzymes such as Cu/MnSOD (SOD1) and ZnSOD (SOD2), which are correlated with metabolized ROS, such as superoxide, for the recovery of biological functions in proteins. Thus, ISKNV induced ROS-mediated AMPK/mTOR autophagy pathway on enhanced viral replication that can be inhibited by treatment with antioxidants NAC, which provides a novel strategy for viral control.

    Article Snippet: The blots were incubated with (self-made) polyclonal antibodies against MCP, LC3B (GTX127375, GeneTex, San Antonio, TX, USA), MTOR (2972, Cell Signaling Technology, Inc., Danvers, MA, USA), phospho-mTOR (Ser 2448) (2971, Cell Signaling Technology, Inc., Danvers, MA, USA), AMPK (H1213, Santa Cruz, Dallas, TK, USA), phosphor-AMPK (Thr 172) (Bo314, Santa Cruz Dallas, TK, USA), Nrf2 (011356, Enzo Life Sciences, Farmingdale, NY, USA), CAT (sc-27103, Santa Cruz, Dallas, TK, USA), Cu/SOD (206504, CAYMAN CHEMICAL, Ann Arbor, MI, USA), Mn/SOD (TX 116093, GeneTex, San Antonio, TX, USA) and ACTB/ß-actin, followed by peroxidase-labeled goat antirabbit conjugate (1:7500) (MAB1501, Calbiochem, San Diego, CA, USA).

    Techniques: Control