Prior Treatment with AICAR Causes the Selective Phosphorylation of mTOR Substrates in C2C12 Cells
In this study, we tested C2C12 cells with the AMP-activated protein kinase (AMPK) stimulator AICAR and measured the changes in the metabolic pathways and signaling kinases. AICAR caused an acute increase in the phosphorylation of the AMPK target ULK1, the mTORC1 substrate S6K, and the mTORC2 target Akt. Intriguingly, prior exposure to AICAR only decreased glucose-6 phosphate dehydrogenase activity when it underwent three-hour recovery after exposure to AICAR in a bicarbonate buffer containing glucose (KHB) instead of Dulbecco's Minimum Essential Medium (DMEM). The phosphorylation of the mTORC1 target S6K was increased afte...
Source: Current Issues in Molecular Biology - October 27, 2023 Category: Molecular Biology Authors: Cass J Dedert Kazimir R Bagdady Jonathan S Fisher Source Type: research
Prior Treatment with AICAR Causes the Selective Phosphorylation of mTOR Substrates in C2C12 Cells
In this study, we tested C2C12 cells with the AMP-activated protein kinase (AMPK) stimulator AICAR and measured the changes in the metabolic pathways and signaling kinases. AICAR caused an acute increase in the phosphorylation of the AMPK target ULK1, the mTORC1 substrate S6K, and the mTORC2 target Akt. Intriguingly, prior exposure to AICAR only decreased glucose-6 phosphate dehydrogenase activity when it underwent three-hour recovery after exposure to AICAR in a bicarbonate buffer containing glucose (KHB) instead of Dulbecco's Minimum Essential Medium (DMEM). The phosphorylation of the mTORC1 target S6K was increased afte...
Source: Current Issues in Molecular Biology - October 27, 2023 Category: Molecular Biology Authors: Cass J Dedert Kazimir R Bagdady Jonathan S Fisher Source Type: research
Prior Treatment with AICAR Causes the Selective Phosphorylation of mTOR Substrates in C2C12 Cells
In this study, we tested C2C12 cells with the AMP-activated protein kinase (AMPK) stimulator AICAR and measured the changes in the metabolic pathways and signaling kinases. AICAR caused an acute increase in the phosphorylation of the AMPK target ULK1, the mTORC1 substrate S6K, and the mTORC2 target Akt. Intriguingly, prior exposure to AICAR only decreased glucose-6 phosphate dehydrogenase activity when it underwent three-hour recovery after exposure to AICAR in a bicarbonate buffer containing glucose (KHB) instead of Dulbecco's Minimum Essential Medium (DMEM). The phosphorylation of the mTORC1 target S6K was increased afte...
Source: Current Issues in Molecular Biology - October 27, 2023 Category: Molecular Biology Authors: Cass J Dedert Kazimir R Bagdady Jonathan S Fisher Source Type: research
Prior Treatment with AICAR Causes the Selective Phosphorylation of mTOR Substrates in C2C12 Cells
In this study, we tested C2C12 cells with the AMP-activated protein kinase (AMPK) stimulator AICAR and measured the changes in the metabolic pathways and signaling kinases. AICAR caused an acute increase in the phosphorylation of the AMPK target ULK1, the mTORC1 substrate S6K, and the mTORC2 target Akt. Intriguingly, prior exposure to AICAR only decreased glucose-6 phosphate dehydrogenase activity when it underwent three-hour recovery after exposure to AICAR in a bicarbonate buffer containing glucose (KHB) instead of Dulbecco's Minimum Essential Medium (DMEM). The phosphorylation of the mTORC1 target S6K was increased afte...
Source: Current Issues in Molecular Biology - October 27, 2023 Category: Molecular Biology Authors: Cass J Dedert Kazimir R Bagdady Jonathan S Fisher Source Type: research
Prior Treatment with AICAR Causes the Selective Phosphorylation of mTOR Substrates in C2C12 Cells
In this study, we tested C2C12 cells with the AMP-activated protein kinase (AMPK) stimulator AICAR and measured the changes in the metabolic pathways and signaling kinases. AICAR caused an acute increase in the phosphorylation of the AMPK target ULK1, the mTORC1 substrate S6K, and the mTORC2 target Akt. Intriguingly, prior exposure to AICAR only decreased glucose-6 phosphate dehydrogenase activity when it underwent three-hour recovery after exposure to AICAR in a bicarbonate buffer containing glucose (KHB) instead of Dulbecco's Minimum Essential Medium (DMEM). The phosphorylation of the mTORC1 target S6K was increased afte...
Source: Current Issues in Molecular Biology - October 27, 2023 Category: Molecular Biology Authors: Cass J Dedert Kazimir R Bagdady Jonathan S Fisher Source Type: research
Prior Treatment with AICAR Causes the Selective Phosphorylation of mTOR Substrates in C2C12 Cells
In this study, we tested C2C12 cells with the AMP-activated protein kinase (AMPK) stimulator AICAR and measured the changes in the metabolic pathways and signaling kinases. AICAR caused an acute increase in the phosphorylation of the AMPK target ULK1, the mTORC1 substrate S6K, and the mTORC2 target Akt. Intriguingly, prior exposure to AICAR only decreased glucose-6 phosphate dehydrogenase activity when it underwent three-hour recovery after exposure to AICAR in a bicarbonate buffer containing glucose (KHB) instead of Dulbecco's Minimum Essential Medium (DMEM). The phosphorylation of the mTORC1 target S6K was increased afte...
Source: Current Issues in Molecular Biology - October 27, 2023 Category: Molecular Biology Authors: Cass J Dedert Kazimir R Bagdady Jonathan S Fisher Source Type: research
Prior Treatment with AICAR Causes the Selective Phosphorylation of mTOR Substrates in C2C12 Cells
In this study, we tested C2C12 cells with the AMP-activated protein kinase (AMPK) stimulator AICAR and measured the changes in the metabolic pathways and signaling kinases. AICAR caused an acute increase in the phosphorylation of the AMPK target ULK1, the mTORC1 substrate S6K, and the mTORC2 target Akt. Intriguingly, prior exposure to AICAR only decreased glucose-6 phosphate dehydrogenase activity when it underwent three-hour recovery after exposure to AICAR in a bicarbonate buffer containing glucose (KHB) instead of Dulbecco's Minimum Essential Medium (DMEM). The phosphorylation of the mTORC1 target S6K was increased afte...
Source: Current Issues in Molecular Biology - October 27, 2023 Category: Molecular Biology Authors: Cass J Dedert Kazimir R Bagdady Jonathan S Fisher Source Type: research
Prior Treatment with AICAR Causes the Selective Phosphorylation of mTOR Substrates in C2C12 Cells
In this study, we tested C2C12 cells with the AMP-activated protein kinase (AMPK) stimulator AICAR and measured the changes in the metabolic pathways and signaling kinases. AICAR caused an acute increase in the phosphorylation of the AMPK target ULK1, the mTORC1 substrate S6K, and the mTORC2 target Akt. Intriguingly, prior exposure to AICAR only decreased glucose-6 phosphate dehydrogenase activity when it underwent three-hour recovery after exposure to AICAR in a bicarbonate buffer containing glucose (KHB) instead of Dulbecco's Minimum Essential Medium (DMEM). The phosphorylation of the mTORC1 target S6K was increased afte...
Source: Current Issues in Molecular Biology - October 27, 2023 Category: Molecular Biology Authors: Cass J Dedert Kazimir R Bagdady Jonathan S Fisher Source Type: research
Prior Treatment with AICAR Causes the Selective Phosphorylation of mTOR Substrates in C2C12 Cells
In this study, we tested C2C12 cells with the AMP-activated protein kinase (AMPK) stimulator AICAR and measured the changes in the metabolic pathways and signaling kinases. AICAR caused an acute increase in the phosphorylation of the AMPK target ULK1, the mTORC1 substrate S6K, and the mTORC2 target Akt. Intriguingly, prior exposure to AICAR only decreased glucose-6 phosphate dehydrogenase activity when it underwent three-hour recovery after exposure to AICAR in a bicarbonate buffer containing glucose (KHB) instead of Dulbecco's Minimum Essential Medium (DMEM). The phosphorylation of the mTORC1 target S6K was increased afte...
Source: Current Issues in Molecular Biology - October 27, 2023 Category: Molecular Biology Authors: Cass J Dedert Kazimir R Bagdady Jonathan S Fisher Source Type: research
Prior Treatment with AICAR Causes the Selective Phosphorylation of mTOR Substrates in C2C12 Cells
In this study, we tested C2C12 cells with the AMP-activated protein kinase (AMPK) stimulator AICAR and measured the changes in the metabolic pathways and signaling kinases. AICAR caused an acute increase in the phosphorylation of the AMPK target ULK1, the mTORC1 substrate S6K, and the mTORC2 target Akt. Intriguingly, prior exposure to AICAR only decreased glucose-6 phosphate dehydrogenase activity when it underwent three-hour recovery after exposure to AICAR in a bicarbonate buffer containing glucose (KHB) instead of Dulbecco's Minimum Essential Medium (DMEM). The phosphorylation of the mTORC1 target S6K was increased afte...
Source: Current Issues in Molecular Biology - October 27, 2023 Category: Molecular Biology Authors: Cass J Dedert Kazimir R Bagdady Jonathan S Fisher Source Type: research
Prior Treatment with AICAR Causes the Selective Phosphorylation of mTOR Substrates in C2C12 Cells
In this study, we tested C2C12 cells with the AMP-activated protein kinase (AMPK) stimulator AICAR and measured the changes in the metabolic pathways and signaling kinases. AICAR caused an acute increase in the phosphorylation of the AMPK target ULK1, the mTORC1 substrate S6K, and the mTORC2 target Akt. Intriguingly, prior exposure to AICAR only decreased glucose-6 phosphate dehydrogenase activity when it underwent three-hour recovery after exposure to AICAR in a bicarbonate buffer containing glucose (KHB) instead of Dulbecco's Minimum Essential Medium (DMEM). The phosphorylation of the mTORC1 target S6K was increased afte...
Source: Current Issues in Molecular Biology - October 27, 2023 Category: Molecular Biology Authors: Cass J Dedert Kazimir R Bagdady Jonathan S Fisher Source Type: research
Prior Treatment with AICAR Causes the Selective Phosphorylation of mTOR Substrates in C2C12 Cells
In this study, we tested C2C12 cells with the AMP-activated protein kinase (AMPK) stimulator AICAR and measured the changes in the metabolic pathways and signaling kinases. AICAR caused an acute increase in the phosphorylation of the AMPK target ULK1, the mTORC1 substrate S6K, and the mTORC2 target Akt. Intriguingly, prior exposure to AICAR only decreased glucose-6 phosphate dehydrogenase activity when it underwent three-hour recovery after exposure to AICAR in a bicarbonate buffer containing glucose (KHB) instead of Dulbecco's Minimum Essential Medium (DMEM). The phosphorylation of the mTORC1 target S6K was increased afte...
Source: Current Issues in Molecular Biology - October 27, 2023 Category: Molecular Biology Authors: Cass J Dedert Kazimir R Bagdady Jonathan S Fisher Source Type: research
PLK1 regulating chemoradiotherapy sensitivity of esophageal squamous cell carcinoma through pentose phosphate pathway/ferroptosis
CONCLUSION: In ESCC, down-regulation of PLK1 can inhibit PPP, and reduce the level of NADPH and GSH, thereby promoting ferroptosis and improving their sensitivity to radiotherapy and chemotherapy. Transcription factor YY1 has a positive regulatory effect on PLK1, and their expressions were positively correlated. PLK1 may be a target for predicting and enhancing the chemoradiotherapy sensitivity of ESCC.PMID:37879213 | DOI:10.1016/j.biopha.2023.115711 (Source: Biomedicine and pharmacotherapy = Biomedecine and pharmacotherapie)
Source: Biomedicine and pharmacotherapy = Biomedecine and pharmacotherapie - October 25, 2023 Category: Drugs & Pharmacology Authors: Mengnan Zhao Tao Lu Guoshu Bi Zhengyang Hu Jiaqi Liang Yunyi Bian Mingxiang Feng Cheng Zhan Source Type: research
PLK1 regulating chemoradiotherapy sensitivity of esophageal squamous cell carcinoma through pentose phosphate pathway/ferroptosis
CONCLUSION: In ESCC, down-regulation of PLK1 can inhibit PPP, and reduce the level of NADPH and GSH, thereby promoting ferroptosis and improving their sensitivity to radiotherapy and chemotherapy. Transcription factor YY1 has a positive regulatory effect on PLK1, and their expressions were positively correlated. PLK1 may be a target for predicting and enhancing the chemoradiotherapy sensitivity of ESCC.PMID:37879213 | DOI:10.1016/j.biopha.2023.115711 (Source: Biomedicine and pharmacotherapy = Biomedecine and pharmacotherapie)
Source: Biomedicine and pharmacotherapy = Biomedecine and pharmacotherapie - October 25, 2023 Category: Drugs & Pharmacology Authors: Mengnan Zhao Tao Lu Guoshu Bi Zhengyang Hu Jiaqi Liang Yunyi Bian Mingxiang Feng Cheng Zhan Source Type: research
A Novel Chinese Medicine Formula Inhibits Non-small Cell Lung Cancer by Triggering Oxidative Stress Dependent on Pentose Phosphate Pathway
Conclusion NCHF-01 can inhibit NSCLC through oxidative stress dependent on the PPP.
DOI: 10.3779/j.issn.1009-3419.2023.101.27 (Source: Chinese Journal of Lung Cancer)
Source: Chinese Journal of Lung Cancer - October 25, 2023 Category: Cancer & Oncology Source Type: research
