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AKT Phosphorylation - DOAJ

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Last Updated: 13 May 2022

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TNFα Mediated IL-6 Secretion Is Regulated by JAK/STAT Pathway but Not by MEK Phosphorylation and AKT Phosphorylation in U266 Multiple Myeloma Cells

IL-6 and TNF were both significantly elevated in the bone marrow aspirate samples of patients with active multiple myeloma patients with active multiple myeloma in comparison to those with normal controls. In addition, MM patients with advanced chronic disease had significantly higher IL-6 and TNF levels than those with MM in stagnation phase. However, the exact mechanisms involved in signaling pathways by which TNF promotes IL-6 secretion from MM cells are still unknown.

Source link: https://doi.org/10.1155/2013/580135


COX-2 activation is associated with Akt phosphorylation and poor survival in ER-negative, HER2-positive breast cancer

Here, we investigated the relationship of COX-2 with breast cancer survival and how this relationship is influenced by tumor estrogen and HER2 receptor status, as well as Akt pathway activation. To determine the connection between COX-2 and disease-specific survival, Kaplan-Meier's survival and multivariable Cox proportional hazards regression analyses were used. COX-2 was also highly associated with breast cancer outcome in ER-negative [Hazard ratio = 2. 72; 95% confidence interval, 1. 36-5. 41], comparing high versus low COX-2] and HER2 overexpressing breast cancer. Notably, COX-2 expression in the ER-negative and HER2-positive tumors corresponded strongly with increased phosphorylation of Akt and of the two Akt targets, BAD at Ser136 and caspase-9 at Ser196. In the ER-negative and HER2-positive breast cancer subtype, the findings show that COX-2-specific inhibitors and inhibitors of the Akt pathway may act synergistically as anticancer drugs.

Source link: https://doi.org/10.1186/1471-2407-10-626


Astaxanthin Suppresses PM2.5-Induced Neuroinflammation by Regulating Akt Phosphorylation in BV-2 Microglial Cells

Air pollution has emerged as one of the most significant problems for human health, and it has been found to be particularly worrying for neural and cognitive health. We found that exposure to PM2. 5 can cause neuroinflammation, the expression of proinflammatory M1, and disease-associated microglia signature markers in microglial cells, as well as the prevention of neurotoxic effects of this exposure via anti-inflammatory properties. In the present research, Diesel particulate matter was used as a fine particulate matter 2. 5. With different amounts of PM2. 5, cultured glial cells and BV-2 microglial cells were treated, cultured rat glial cells and BV-2 microglial cells were treated, and subsequent expression of various inflammatory mediators and signaling pathways were determined using qRT-PCR and Western blot. Following PM2. 5 therapy, however, the mRNA expression of IL-10 and arginase-1 decreased. Our findings reveal that PM2. 5 exposure reformulates microglia by proinflammatory M1 and DAM phenotype, contributing to neurotoxicity, as well as the fact that astaxanthin therapy can reduce neurotoxicity by blocking migration to the proinflammatory M1 and DAM phenotypes. These results show that PM2. 5 exposure in the microglial cells may cause brain damage, as well as the fact that astaxanthin can have a potential beneficial effect on PM2. 5 exposure of the brain.

Source link: https://doi.org/10.3390/ijms21197227


Nik-related kinase regulates trophoblast proliferation and placental development by modulating AKT phosphorylation.

A recent report using Nrk-null mice showed the importance of Nrk in optimal placental growth, but the molecular mechanism remains unknown. We found that differentiated trophoblasts from murine embryonic stem cells endogenously expressed Nrk and that Nrk disruption promoted differentiation of differentiated trophoblasts in this study. Moreover, we reported that AKT phosphorylation in Ser473 was downregulated in Nrk-null trophoblasts, and that AKT phosphorylation inhibition at AKT phosphorylation in null trophoblasts stopped the increased proliferation observed in differentiated Nek-null trophoblasts. In vivo, AKT phosphorylation was also confirmed in a larger Nrk-null placentas, implying that proper AKT control by Nrk was also crucial for normal placental growth. In addition, our comprehensive review of AKT isoforms in newly established trophoblast stem cells revealed that various degrees of upregulation of AKT phosphorylation were observed in Nrk-null TSCs relying on AKT isoforms.

Source link: https://doi.org/10.1371/journal.pone.0171503


Screening of Inhibitory Effects of Polyphenols on Akt-Phosphorylation in Endothelial Cells and Determination of Structure-Activity Features

Polyphenols have beneficial effects in type 2 diabetes mellitus. This study sought to determine the effects of structurally different polyphenols on Akt-phosphorylation in endothelial cells and to identify structure-activity features. The effects of 44 polyphenols on pAkt Ser473 were determined by a comprehensive examination by ELISA. Immunoblotting revealed a strong positive and statistically significant relationship between the tested polyphenols' mean inhibitory activities on both Akt-residues Ser473 and Thr308. Interestingly, the physical features boosting the compounds' antioxidant activity differed from those supporting structural features. The present study is the first to quantitatively measure the effect of polyphenols from nine distinct structural subclasses on pAkt in endothelial cells. The proposed molecular mechanism of action of polyphenols implicating Akt-inhibition contributes to understanding their effects on the cell level.

Source link: https://doi.org/10.3390/biom9060219


Inhibition of p70S6K does not mimic the enhancement of Akt phosphorylation by rapamycin

It has been estimated that the mTOR complex 1/p70S6K axis represses upstream PI3K/Akt signaling by phosphorylation of IRS-1 and its subsequent degradation. While this has not been tested, one potential and current model that explains Akt initiation by mTOR inhibitor rapamycin is the relief of mTORC1/p70S6K-mediated feedback inhibition of IRS-1/PI3K/Akt signaling, according to a research-based study. Inhibition or forced activation of p70S6K did not have an effect on the ability of rapamycin to raise Akt phosphorylation. Our results indicate that Akt stimulation by rapamycin or mTORC1 inhibition is unlikely as a result of the release of p70S6K-mediated feedback inhibition of IRS-1/PI3K/Akt signaling by p70S6K-mediated feedback inhibition.

Source link: https://doi.org/10.1016/j.heliyon.2017.e00378


CXCR4 Antagonist AMD3100 Reverses the Resistance to Tamoxifen in Breast Cancer via Inhibiting AKT Phosphorylation

In this research, we investigated the role of CXC chemokine receptor type 4 in tamoxifen-treated breast cancer and tamoxifen resistance. High expression of CXCR4 was found to be correlated with reduced overall survival and cancer-specific survival in tamoxifen-treated breast cancer, according to the Gene Expression Omnibus database. In vitro and in vivo, the reversal effect of AMD3100 on tamoxifen resistance was also confirmed. CXCR4's review revealed that it was a promising prognostic biomarker for tamoxifen-treated breast cancer, and that a combination of AMD3100 and tamoxifen could be a more effective therapeutic strategy for the treatment of tamoxifen resistance.

Source link: https://doi.org/10.1016/j.omto.2020.06.009


HDAC6 Mediates Poly (I:C)-Induced TBK1 and Akt Phosphorylation in Macrophages

We investigated the potential role of HDAC6 in macrophage anti-viral responses by looking at poly -induced IFN- and IL-10 production in mouse bone marrow-derived macrophages in the present study. Our results showed that HDAC6 deletion raised poly -induced INF- expression in macrophages by up-regulating TBK1 production and removing the inhibitory control of GSK-3. Our findings show that HDAC6 modulates IFN- and IL-10 macrophage production in macrophages by its control of TBK1, GSK-3, and Akt signaling. HDAC6 may act as a suppressor of anti-viral innate immune responses in macrophages.

Source link: https://doi.org/10.3389/fimmu.2020.01776


MK-2206 co-treatment with 5-fluorouracil or doxorubicin enhances chemosensitivity and apoptosis in gastric cancer by attenuation of Akt phosphorylation

Cell viability and colony formation assays revealed that MK-2206 effectively stopped cell proliferation of SGC-7901 and MKN45 cells. Assay by flow cytometry assay, MK-2206 treatment in SGC-7901 cells caused apoptosis in SGC-7901 cells. MK-2206 and doxorubicin were 0. 59 in SGC-7901 cells and 0. 57 in MKN45 cells, respectively, although 5-fluorouracil was 0. 70 in SGC-7901 cells and 0. 73 in MKN45 cells, indicating that MK-2206 could combine with doxorubicin or 5-FU to reduce cell growth in MKN45 cells. In addition, a small dose of MK-2206 co-therapy with doxorubicin or 5-FU was sufficient for complete inhibition of chemotherapeutic deposition of phosphorylated Akt expression and significant rise in pro-apoptosis activity by the activation of caspase pathway. MK-2206 effectively blocks gastric cancer cell formation by attenuation of Akt phosphorylation and synergistically raises the antitumor activity of doxorubicin and 5-FU via caspase-dependent apoptosis.

Source link: https://doaj.org/article/910123ee7ab0447d8f87460a9de37277


Da-Bu-Yin-Wan Improves the Ameliorative Effect of DJ-1 on Mitochondrial Dysfunction Through Augmenting the Akt Phosphorylation in a Cellular Model of Parkinson’s Disease

In addition, DJ-1 could also shield the cells by regulating gene expression and modulating the Akt signal pathways. In this study, we also sought to investigate the ameliorative effect of DBYW on mitochondria in the era of the DJ-1 and Akt signaling. PC-12, Rat's adrenal pheochromocytoma cell line, was transfected with the plasmid pcDNA3-Flag-DJ-1. The DJ-1 overexpression not only increased the mitochondrial mass, but also increased the total ATP content. These results suggest that DBYW promotes mitochondrial dysfunction at least by raising the Akt phosphorylation in 1-methyl-4-pyridinium-treated PC-12 cells, according to conscientily.

Source link: https://doi.org/10.3389/fphar.2018.01206

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions