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AKT ERK Signaling - Crossref

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Last Updated: 15 February 2022

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Programmed death-ligand 1 signaling and expression are reversible by lycopene via PI3K/AKT and Raf/MEK/ERK pathways in tongue squamous cell carcinoma

Tongue Squamous Cell Carcinoma therapy is hopeful because of a trial based on programmed death receptor-1 or programmed death-ligand 1. Methods We obtained TSCC tissues and normal tissues for the purpose of determining PD-L1 expression by immunohistochemical method and western blotting. We measured the expression of PD-L1 in three TSCC cell lines and cell lines with knockdown and overexpression of PD-L1 in three TSCC cell lines and constructed cell lines. We also systematically reviewed the PD-L1 constitutive signaling pathways and their effect on EMT pathways. Our research showed that PD-L1 upregulation stimulated IGF-1R to launch the PI3K/AKT pathway in cell line CAL27, but not activated Raf/MEK/ERK pathway, increasing/increase p-GIXOs and boosting/increase p-GSK-3, resulting in more changes in EMT, proliferation, migration, invasion, and apoptosis. Lycopene reversed PD-L1 signaling and expression by devices related to PD-L1 upregulation but not similar to the PD-L1 knockdown.

Source link: https://doi.org/10.1186/s12263-022-00705-y


The Protective Role of Celastrol in Renal Ischemia-Reperfusion Injury by Activating Nrf2/HO-1, PI3K/AKT Signaling Pathways, Modulating NF-κb Signaling Pathways, and Inhibiting ERK Phosphorylation

We investigated celastrol's antioxidant capacity by investigating calcium phosphate 3-kinase B pathways, nuclear factor-kappa B pathways, and extracellular signal-regulated kinase activation in kidney ischemia-reperfusion injury rats. Rats were given celastrol 2 mg/kg orally for 1 week before subjection to renal ischemia-reperfusion surgery. Pretreatment for Celastrol attenuated oxidative stress, elevated Nrf2 gene expression, and HO-1 level. Celastrol showed a reno-protective role against renal IRI by enhancing the Nrf2/HO-1 pathway, increasing cell survival PI3K/AKT signaling pathways, and reducing inflammation by inhibiting NF-B activation.

Source link: https://doi.org/10.1007/s12013-022-01064-6


Non-Structural Protein 3 of Duck Tembusu Virus Induces Autophagy via the ERK and PI3K–AKT–mTOR Signaling Pathways

Despite autophagy's pivotal role in the replication of viruses such as duck Tembusu virus, which has caused significant economic losses to the poultry industry around the world, the precise links between DTMUV and cellular autophagy remain largely unknown. In response, we investigated autophagy and DTMUV, the effects of the DTMUV's structural and non-structural proteins on autophagy, as well as the autophagy-related signaling pathways induced by DTMUV. DTMUV upped the autophagy flux in duck embryo fibroblasts and BHK-21 cells, according to the study, while autophagy promoted viral replication. The findings revealed that non-structural protein 3 caused significant autophagy in DEF cells, primarily because DTMUV protein triggered autophagy. All three structural proteins and seven non-structural proteins of DTMUV were transfected into cells, and the remaining DTMUV proteins were shown to cells, and the results revealed that non-structural protein 3 triggered autophagy in DTMUV cells.

Source link: https://doi.org/10.3389/fimmu.2022.746890


Down-Regulation of C1GALT1 Enhances the Progression of Cholangiocarcinoma through Activation of AKT/ERK Signaling Pathways

Multiple cancers have been reported as dysregulation of C1GALT1 in multiple cancers, as well as aberrant core 1 Oglycosylation and cancer inflamation, and aggressiveness; however, the role of C1GALT1 in CCA progression is unclear. Increased in the activation/phosphorylation of AKT and ERK cells in silencing C1GALT1 cells demonstrated by an increase in the transcription and phosphorylation of C1GALT1 cells by siRNA; induction of CCA cell proliferation and 5-fluorouracil resistance in a dose-dependent manner; up-regulation of growth-related genes, ABC transporter genes, and anti-apoptotic proteins; and an increase in the transcription of C1GALT1 cells In C1GALT1's knockdown, we reported that silencing C1GALT1 in CCA cell lines was associated with immature core 1 O-glycosylation, as shown by the proliferation of VVL-binding glycans and down-regulation of other key O-linked glycosyltransferases 1,3-N-acetyl glycosylation, illustrated by the expression of immature core 1 O-glyl gly glyl-GALT1'sas asasasasasasasa cell lines was associated with immature oglycosylgly ogly cytogenoogly glyzanyl-tyl-gly glyn-linked glycosyl-linked glycosyl-syl-glycosyl-glyzacyl-glyzetylglycosyl-genyl-glycosyl-glyguy.

Source link: https://doi.org/10.3390/life12020174


Effect of dexmedetomidine on AKT/ERK signaling pathway and EMT-related proteins in high glucose-induced apoptosis in human renal tubular epithelial cells

In apoptosis in human kidney tubular epithelial cells, the aim of this study was to investigate the effect of dexmedetomidine on the AKTERK signaling pathway and EMT-related proteins. Flow cytometry was used to determine cell apoptosis and cell cycle in cell apoptosis and cell cycle in the western blot, but Western blot was used to determine PI3K, Akt, p-Akt, ERK, and p-ERK at assay rates. P13K protein levels in high glucose and Dex groups were significantly lower in Dex group relative to the high glucose group, relative to the high glucose group, although similar control values were much lower in high glucose and Dex groups than their corresponding control groups. AKT protein expression was downregulated, relative to the control group, and p-AKT expression was markedly reduced in the Dex group, according to the above table. In a high glucose group, protein expressions of ERK and p-ERK were lower than control values, but they were significantly elevated in the Dex group, relative to the high glucose group.

Source link: https://doi.org/10.4314/tjpr.v20i3.14


An ApoA-I Mimic Peptide of 4F Promotes SDF-1α Expression in Endothelial Cells Through PI3K/Akt/ERK/HIF-1α Signaling Pathway

The purpose of this research is to determine whether 4F, an apolipoprotein A-I mimic peptide, can upregulate SDF-1 in mice and human umbilical vein endothelial cells and the underlying mechanism. The results reveal that L-4F significantly raises protein levels of HIF-1, Akt, and ERK, which can be blocked by the PI3K inhibitor, LY294002 or ERK inhibitor, PD98059, respectively. In the abdominal aorta and inferior vena cava from mice, the levels of HIF, Akt, and p-ERK can be upregulated. Through the PI3K/Akt/ERK/HIF-1 signaling pathway, 4F promotes SDF-1 expression in ECs, according to these results.

Source link: https://doi.org/10.3389/fphar.2021.760908

* 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