AKT2 Antibody (S474)
- Known as:
- AKT2 Antibody (S474)
- Catalog number:
- AP7029d
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- AKT2 Antibody (S474)
Related genes to: AKT2 Antibody (S474)
- Gene:
- AKT2 NIH gene
- Name:
- AKT serine/threonine kinase 2
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 19q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1992-11-05
- Date modifiied:
- 2016-10-05
- Gene:
- RNA5SP474 NIH gene
- Name:
- RNA, 5S ribosomal pseudogene 474
- Previous symbol:
- RN5S474
- Synonyms:
- -
- Chromosome:
- 20p13
- Locus Type:
- pseudogene
- Date approved:
- 2012-01-30
- Date modifiied:
- 2014-11-19
Related products to: AKT2 Antibody (S474)
Related articles to: AKT2 Antibody (S474)
- Pyrola incarnata, a medicinal herb and functional food with diverse bioactive compounds, was systematically screened for in vitro anti-RSV activities of its constituents, combined with antiviral assays and computational analyses. Among ten compounds, pyrolin, gallic acid, and quercetin as main phytochemicals showed the most potent efficacy, with IC values of 0.56 ± 0.08 μM, 10.60 ± 1.08 μM, and 12.63 ± 1.00 μM, respectively, outperforming positive control ribavirin. Indirect immunofluorescence and high-content analysis indicated these three compounds target the early RSV replication cycle. Gallic acid showed inhibited RSV infection during virus pretreatment and adsorption, with inhibition rates of 72.79% and 48.25% (P < 0.01), respectively. Furthermore, gallic acid suppressed early post-infection replication, and mechanistically it disrupted RSV-F protein mediated membrane fusion, reducing cell-cell fusion to 22.52%, consistent with docking results. Moreover, exploratory network pharmacology suggests that gallic acid might exert anti-RSV effects by modulating targets such as MAPK, AKT1, and AKT2. In additional, it was discovered for the first time that pyrolin as the one of the component indicators from P. incarnata, markedly inhibited RSV infection during virus pretreatment and adsorption, with inhibition rates of 94.50% and 43.50% (P < 0.01) respectively. While quercetin also exhibited direct virucidal activity. In conclusion, P. incarnata acts as promising natural inhibitors targeting the early stages of RSV replication. These findings establish a scientific basis for future in vivo validation and the development of new drugs against respiratory syncytial virus. - Source: PubMed
Publication date: 2026/06/26
Yang XiliangWu LiWan GuoqingChen RuiLiu ChenxuZhang HaiweiZhang ZheZhou YiDuan LixinGong Rui - This study aimed to investigate the effects and mechanism of polysaccharides (SLPs) on hepatic glucose metabolism disorders induced by a high-fat diet combined with streptozotocin (STZ) in mice. A mouse model of hepatic glucose metabolism disorder was established and treated with different doses of SLPs (100, 200, and 400 mg/kg) via gavage for 8 weeks, alongside control, model, and positive control groups (metformin hydrochloride). The effects of SLPs were systematically evaluated through pyruvate tolerance tests (PTT), hepatic glycogen content measurement, liver histomorphological analysis (HE and oil red O staining), transcriptomics, and validation of key signaling pathways using RT-qPCR and Western blot. The results showed that, compared to the model group, medium and high doses of SLPs significantly reduced area under the curve (AUC) of PTT, increased hepatic glycogen content, and ameliorated liver histopathological damage and lipid accumulation in the liver. Transcriptomic analysis revealed that SLPs intervention significantly modulated differentially expressed genes related to glucose and lipid metabolism, which were enriched in signaling pathways such as phosphatidylinositol-3-kinase (PI3K)/protein kinase B (AKT)/forkhead box O1 (FOXO1) signaling pathway. Further validation demonstrated that SLPs up-regulated mRNA expression levels of insulin-like growth factor 1 receptor (), protein kinase B2 (), and phosphatidylinositol-3-kinase regulatory subunit 1 () in the liver of mice with glucose metabolism disorders, and down-regulated the mRNA expression levels of and fructose-1,6-bisphosphatase 1 (). Additionally, SLPs up-regulated p-FOXO1 protein expression level and down-regulated phosphoenolpyruvate carboxykinase (PEPCK) protein expression level. These results suggest that SLPs can effectively improve hepatic glucose metabolism disorders in mice induced by a high-fat diet combined with STZ by activating the PI3K/AKT/FOXO1 signaling pathway, involving the inhibition of key gluconeogenic enzymes and promotion of glucose utilization. - Source: PubMed
Yang Er-ChenJia Feng-YingZhang Li-MinJin Li-YangRen Dao-QinJiang YueYun Shao-JunFeng Cui-Ping - A fraction of the insulin-stimulated uptake of long-chain fatty acids (FAs) is mediated by the FA translocase cluster of differentiation 36 (CD36) in white adipocytes. Intracellular vesicle-localized CD36 is redistributed to the plasma membrane following insulin stimulation, enhancing the uptake of long-chain FAs across the plasma membrane. We previously developed an epitope-tagged CD36 reporter, which enabled the visualization and quantification of the plasma membrane translocation of CD36. Herein, we demonstrate that the insulin-stimulated CD36 translocation is regulated by the phosphoinositide 3-kinase (PI3K)/Akt2/Rac1/RalA axis in adipocytes of subcutaneous white adipose tissue (WAT) in living mice. The uptake of long-chain FAs by insulin was completely abrogated in white adipocytes isolated from adipocyte-specific -knockout (adipo--KO) mice. Correspondingly, the translocation of CD36 to the plasma membrane by insulin was also totally inhibited in Rac1-deficient white adipocytes. PI3K and Akt2 acted upstream of Rac1, and the guanin nucleotide exchange factor FLJ00068 served as a regulator for Rac1. Furthermore, the involvement of another small GTPase RalA was suggested by inhibitory effects of a dominant-negative mutant. Taken together, these results support the notion that insulin regulates the plasma membrane translocation of CD36 by mechanisms similar to those for the translocation of the glucose transporter GLUT4 in white adipocytes. - Source: PubMed
Publication date: 2026/06/20
Takenaka NobuyukiSakata MizukiAbe YukiIha KokoaSatoh Takaya - In this study, polysaccharides from L. fruits (FCPs) were extracted using a deep eutectic solvent (DES)-based ultrasound-assisted extraction (UAE) method. The physicochemical properties of the FCPs were then characterized, and the anti-aging effects of FCPs were evaluated in (). It was demonstrated that FCPs significantly extended the lifespan of the nematodes, while improving locomotor activity without affecting the body size or reproductive capacity. Meanwhile, FCPs reduced lipofuscin accumulation, decreased intracellular reactive oxygen species (ROS) levels, and increased the survival of under oxidative stress. Moreover, FCPs upregulated the expression of antioxidant genes , , , and . The expression of (), a homologue gene of mammalian () in , was also elevated upon FCPs treatment. Knockdown of expression by RNA interference abolished the lifespan extension and ROS reduction in FCPs-treated , indicating that the SKN-1-mediated signaling was essential for the anti-aging effects of FCPs. Additionally, FCPs caused downregulation of the key components of the insulin/IGF-1 signaling (IIS) pathway, , , and . Overall, these results suggested that FCPs promoted longevity in via modulation of SKN-1 and IIS pathway. - Source: PubMed
Publication date: 2026/05/30
Li LianyuDing FengSheng YongZhao Yan - Optineurin (OPTN) is widely recognized as a multifunctional selective autophagy receptor involved in cargo turnover. However, our recent findings uncover an unexpected function of OPTN that challenges the conventional view of autophagy adaptors. In dendritic cells (DCs), OPTN binds to and stabilizes Rictor, a key component of the mTORC2 complex. Loss of OPTN leads to depletion of Rictor, reduced Akt2 activity, and activation of the mTORC1/p70S6K1 pathway, culminating in enhanced phosphorylation of STAT3 at Ser727. Activated STAT3 transcriptionally induces the E3 ubiquitin ligase MARCH1, which promotes MHC II internalization, resulting in a striking inverse relationship between MARCH1 and MHC II expression in Optn-deficient cells. Together, these findings identify an unexpected signaling function of OPTN, independent of its canonical autophagy activities. By stabilizing Rictor and maintaining mTORC2-Akt2 signaling, OPTN links a classical autophagy adaptor to the regulation of antigen presentation and adaptive immunity. More broadly, our findings raise the possibility that selective autophagy receptors preserve cellular homeostasis not only through cargo clearance but also through context-dependent, non-degradative regulation of protein stability and signaling networks.: OPTN: Optineurin; mTORC1: mammalian target of rapamycin complex 1; mTORC2: mammalian target of rapamycin complex 1; Rictor: Rapamycin-Insensitive Companion of mTOR. - Source: PubMed
Publication date: 2026/06/18
Kadam RashmiShukla Deepak