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Akt Mapk - Europe PMC

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Last Updated: 15 February 2022

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Phosphorylation of PI3K/Akt at Thr308, but not phosphorylation of MAPK kinase, mediates lithium-induced neuroprotection against cerebral ischemia in mice.

Therefore, we first investigated the dose-dependent effects of lithium on neurological deficits, infarct volume, brain edema, and blood-brain barrier integrity in mice exposed to focal cerebral ischemia. The discovery of 2 mmol/kg lithium significantly improved post-ischemic brain tissue survival in mice, according to our findings. Despite, 2 mmol/kg lithium had no effect on brain microcirculation, 5 and 20 mmol/kg lithium reduced brain perfusion, and there was no negative effect on brain microcirculation. In addition, a supratherapeutic dose of lithium in 20 mmol/kg cause animal death. The effect of 5 mmol/kg lithium on brain injury did not change in addition to brain perfusion with L-arginine. We showed that the neuroprotective role of lithium persists during MEK/ERK inhibition, regardless of whether neuroprotective effects of lithium are modulated by PI3K/Akt or MEK, although PI3K/Meth inhibitory was canceled, and that neuroprotective activities of lithium persists during MEK/ERK inhibition.

Source link: https://europepmc.org/article/MED/35122865


Effect of Grass Carp Scale Collagen Peptide FTGML on cAMP-PI3K/Akt and MAPK Signaling Pathways in B16F10 Melanoma Cells and Correlation between Anti-Melanin and Antioxidant Properties

Previous studies have shown that FTGML addition in vitro can effectively reduce mushroom tyrosinase production in vitro, as well as in vivo's melanogenesis inhibition, but the underlying mechanism is not fully understood. Interestingly, the therapy revealed a strong correlation between antioxidant activity and anti-melanin, which was attributed to FTGML's inhibition of reactive oxygen species in melanin synthesis. These findings showed that FTGML could reduce melanin production in mouse B16F10 melanoma cells by a variety of pathways.

Source link: https://europepmc.org/article/MED/PMC8834497


Luteolin inhibits viability, migration, angiogenesis and invasion of non-small cell lung cancer vascular endothelial cells via miR-133a-3p/purine rich element binding protein B-mediated MAPK and PI3K/Akt signaling pathways.

Although Luteolin reduces tumor formation in non-small cell lung cancer, non-small cell lung cancer, the exact mechanism of the disease needs to be clarified, We hereby investigated the effects of luteolin in NSCLC vascular endothelial cells. Cells were treated with luteolin and transfected after extraction and determination of NSCLC-VECs. MiR-133a-3p and PURB were found to have a mutual connection. However, miR-133a-3p inhibitor counteracted the repressive effect of luteolin on the viability, migration, angiogenesis, and invasion of NSCLC-VECs, up-regulated migration, angiogenesis, and invasion of NSCLC-VECs in NSCLC-VECs. Luteolin restricted the expressions of migration-and invasion-associated proteins, PI3K/Akt, and MAPK signaling pathways-related factors, while miR-133a-3p inhibitor reversed the inhibitory effect of Luteolin on NSCLC-VECs. In NSCLC-VECs, ShPURB introduced miR-133a-3p in miR-133a-3p, while reversing the promoting effects of miR-133a-3p inhibitor on migration, invasion, and levels of migration- and invasion-associated proteins, PI3K/Akt, and MAPK pathways-associated factors, NSCLC-VECs.

Source link: https://europepmc.org/article/MED/35101688


Capturing the signalling dynamics of the MAPK-AKT-mTOR pathway in a single targeted phosphoproteomics assay

This novel approach leads to the most comprehensive review of mTOR signaling to date, which can be applied to both in vitro and in vivo systems, and has the ability to be used in small sample sizes. We demonstrate the ability of this assay to track MAPK-AKT-mTOR phosphorylation dynamics in reaction to cellular stimuli with high temporal sensitivity and amino acid residue specificity. In addition, starvation of glucose and amino acids demonstrated upregulation of AKT-targets PRAS40 T246 and FOXO3 T32, underscoring the role of AKT in cell response to starvation. Highlights Robust hoped to study the MAPK-MTOR network's phosphorylation dynamics, amino acids, and glucose metabolism thanks to a series of important biological processes, such as cell growth and metabolism, assay to determine cellular fate, and evolution are highly flexible and adaptable assay for in vivo and in vitro networks. PET-AKT-mTOR network The MAPK-AKT-mTOR network's growth factors, amino acids, and glucose network are highly cellular receptor network cellular Phosphore mTOR network evolution and mTOR network's, mTOR network's, mTOR network's, assay's, cytogenomics, assay. We present a targeted phosphoproteomics assay in this report to track the phosphorylation events of the MAPK-AKT-mTOR pathway with amino acid residue specificity and in a high throughput manner. This novel approach yields the most comprehensive review of MAPK-AKT-mTOR signalling to date, which can be applied to in vitro and in vivo human samples and has the ability to be used with small amounts of starting material.

Source link: https://europepmc.org/article/PPR/PPR443712


Glytabastan B, a coumestan isolated from Glycine tabacina, alleviated synovial inflammation, osteoclastogenesis and collagen-induced arthritis through inhibiting MAPK and PI3K/AKT pathways.

In folk medicine, the Glycine tabacina plant's roots are used to treat rheumatoid arthritis and joint infection. GlyB also stopped RANKL-induced osteoclastogenesis, decreased the expression of osteoclastogenic markers, and osteoclast-mediated bone resorption, which has led to decreased bone resorption. The integration of network pharmacology, quantitative phosphoproteomic, and experimental pharmacology findings showed that these helpful steps were closely linked to GlyB's blockade of MAPK, PI3K/AKT and their downstream indicators, including NF-B and GSK3/NFATc1, as a result of GlyB's blockade of NP3K/AKT and their downstream signals, including NF-A and GSK3/5.

Source link: https://europepmc.org/article/MED/35032460


LncRNA MIR205HG accelerates cell proliferation, migration and invasion in hepatoblastoma through the activation of MAPK signaling pathway and PI3K/AKT signaling pathway.

Histoblastoma has been dubbed the most common liver disease among children. Multiple cancers have been studied, but the role in HB remains to be clear. In HB cells, system assays were carried out to investigate the underlying mechanism of MIR205HG in HB cells. MIR205HG has also been attached to microRNA-514a-5p and a specific mitogen-activated protein kinase 9 to promote mitogen activated protein kinase signaling pathway in MIR205HG. MIR205HG promotes the progression of HB, which may be a good marker and a new therapeutic goal for HB.

Source link: https://europepmc.org/article/MED/34996511


S100A8/A9 Induced by Interaction with Macrophages in Esophageal Squamous Cell Carcinoma Promotes the Migration and Invasion of Cancer Cells via Akt and p38 MAPK Pathways.

More malignant phenotypes of esophageal squamous cell carcinoma cells are found in Tumor-associated macrophages. The authors established several contributing factors to ESCC cell proliferation, first using an indirect co-culture assay of ESCC cells and macrophages. Compared to monocultured ESCC cells, direct co-cultured ESCC cells had significantly raised migration and invasion capabilities, as well as phosphorylation levels of Akt and p38 mitogen-activated protein kinase. Both the production and release of S100 calcium binding protein A8 and A9, which commonly occur and function as a heterodimer, were greatly enhanced in co-cultured ESCC cells, according to a cDNA microarray analysis of monocultured and co-cultured ESCC cells. In addition, ESCC patients with high S100A8/A9 expression had significantly shorter disease-free survival and cause-specific survival. These results reveal that S100A8/A9 expression and release in ESCC cells can be enhanced by direct co-culture with macrophages, and that S100A8/A9 enhances ESCC proliferation by Akt and p38 MAPK signaling pathways.

Source link: https://europepmc.org/article/MED/34954212


AZD5153 reverses palbociclib resistance in ovarian cancer by inhibiting cell cycle-related proteins and the MAPK/PI3K-AKT pathway.

The CDK4/6 inhibitor, palbociclib, and the palbociclib have recently joined the clinic for breast cancer therapy. In multiple ovarian cancer models, we discovered that the effect of palbociclib as a single agent was limited due to primary and acquired resistance. Patients with OC are two of the most common models of drug sensitivity in patients with OC. This research also showed that AZD5153 and palbociclib had a synergistic lethal effect on cell cycle arrest and rising apoptosis in RB-deficient cell lines.

Source link: https://europepmc.org/article/MED/34942306


VF-4 and DR-8 Derived from Salted Egg White Inhibit Inflammatory Activity via NF-κB/PI3K-Akt/MAPK Signal Transduction Pathways in HT-29 Cells Induced by TNF-α.

Scope Inflammation is the pathological source of several chronic illnesses, and chronic intestinal inflammation is a key factor in colon cancer's progression. Egg white treated with salt contains a lot of rich protein, but it is uncertain whether its peptides have anti-inflammatory action and how their mechanism of action is still unclear. VF-4 and DR-8 significantly inhibit TNF-induced IL-8 secretion in HT-29 cells in a concentration-dependent manner, with a more prominent anti-inflammatory effect than DR-8.

Source link: https://europepmc.org/article/MED/34821458


Cepharanthine Suppresses Herpes Simplex Virus Type 1 Replication Through the Downregulation of the PI3K/Akt and p38 MAPK Signaling Pathways.

Cepharanthine, a naturally occurring isoquinoline alkaloid obtained from Stephania cepharantha Hayata, is a naturally occurring isoquinoline alkaloid extracted from Stephania cepharantha Hayata. Whereas HSV-1 infection increases the expressions of phosphoinositide 3-kinase, protein kinase B, and p38 mitochondrial protein kinase in host cells, CEP was also useful in reducing the targets' phosphorylation levels in PI3K/Akt and p38 MAPK signaling pathways. In addition, CEP markedly reduced G 0/G 1 phase and increased G 2 /M phase cells, as well as reduced the expression of cyclin-dependent kinase1 and cyclinB1 in a dose-dependent manner. Alongside, CEP increased apoptosis in infected cells, reduced B cell lymphoma-2 protein levels, and raised the Bcl-associated X protein's, cleaved-caspase3 and nuclear IrB kinase kinase, increasing the protein levels of Bcl-associated X protein, cleaved-caspase3 and nuclear IB kinase. CEP could suspend the cell cycle in the G2/M phase and promote apoptosis in infected cells by limiting the PI3K/Akt and p38 MAPK signaling pathways, thereby decreasing HSV-1 infection and subsequent reproduction.

Source link: https://europepmc.org/article/MED/34956164

* 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