Active Akt2
- Known as:
- Active Akt2
- Catalog number:
- ASAPPK-411Z
- Product Quantity:
- 5 µg
- Category:
- -
- Supplier:
- Other suppliers
- Gene target:
- Active Akt2
Related genes to: Active Akt2
- 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
Related products to: Active Akt2
Related articles to: Active Akt2
- Triple-negative breast cancer (TNBC) remains lethal due to its aggressive molecular heterogeneity and drug resistance. We report a biomimetic nanoplatform (PLL/TNA@CM NPs) integrating biostable threose nucleic acid (TNA) with a donor-derived cell membranes (CMs) "cloak" for subtype-specific therapy. By complexing TNA antisense oligonucleotides with poly-L-lysine (PLL) and coating them with TNBS-subtype membranes (MDA-MB-468 or MDA-MB-231), we achieve potent homotypic affinity. PLL/TNA@468CM NPs exhibited significant enhanced uptake in donor-matched basal-like 1 cells compared to heterotypic TNBC, non-TNBC and normal epithelial cells. Mechanistically, these nanoparticles internalize via a rapid membrane-fusion, bypassing endosomal entrapment for direct cytosolic delivery. This facilitates robust silencing of the AKT2 oncogene, achieving a ∼70% protein knockdown and outperforming conventional transfection reagents. In a drug-resistant MDA-MB-468 xenografts, systemic administration led to superior tumor accumulation, effective AKT2 knockdown, and significant tumor regression via the p21/Caspase-3 apoptotic axis, without systemic toxicity. This versatile "plug-and-play" strategy addresses tumor heterogeneity and endosomal sequestration, providing a transformative paradigm for targeted nucleic acid delivery in refractory cancers. - Source: PubMed
Publication date: 2026/06/12
Zheng WeiChang Tristan Juin HanLi XinchaoZhou ZhongqiTin ChungVong KenwardKaram PierreLo Pik Kwan - Metabolic disorders, particularly insulin resistance, are increasingly recognized as accelerators of female reproductive decline. However, the molecular mechanisms by which peripheral metabolic stress translates into impaired ovarian reserve remain incompletely understood. Here, we propose that protein tyrosine phosphatase 1B (PTP1B), a negative regulator of insulin signaling, serves as a molecular bridge linking systemic insulin resistance to aging-relevant ovarian dysfunction and can be pharmacologically targeted. By integrating transcriptomic profiling of granulosa cells from women with diminished ovarian reserve (DOR) with network-based pharmacology and IR-DOR-associated gene annotations, we identified PTP1B as a candidate mediator of a metabolic stress-associated ovarian dysfunction axis. In a high-fat diet (HFD)-induced mouse model of systemic insulin resistance and metabolic stress-associated ovarian dysfunction, treatment with the traditional multi-herbal formula Gengnianchun (GNC) improved systemic glucose homeostasis, restored estrous cyclicity, and preserved primordial and growing follicles. These effects were accompanied by reduced ovarian PTP1B expression, reactivation of IRS1-AKT2 signaling, and enhanced GLUT4-mediated glucose handling in granulosa cells. In human granulosa-like KGN cells, GNC selectively restored insulin signaling and cell migration under insulin-resistant conditions; these effects were phenocopied by PTP1B knockdown and attenuated by PTP1B overexpression or pharmacological inhibition of AKT2. Collectively, these findings identify ovarian PTP1B as a key mediator of metabolic stress-associated, aging-relevant ovarian dysfunction and highlight PTP1B-directed interventions, including GNC, as potential strategies to preserve ovarian function in metabolically vulnerable states. - Source: PubMed
Rao YanqiuXu TingDing YanLi JunGao LingyunWang YunWang Wenjun - Zingerone (Zin) exhibits multiple pharmacological properties, including anti-inflammatory, immunomodulatory, anxiolytic, anti-thrombotic, radioprotective, and antimicrobial activities. However, the therapeutic potential of Zin in coronary artery atherosclerotic heart disease (CHD) remains unexplored. This study aims to elucidate the role and underlying molecular mechanisms of Zin in CHD treatment. Putative Zin targets associated with CHD were identified through online database screening followed by functional enrichment analysis. Core target genes were screened using Protein-protein interaction (PPI) Network analysis, machine learning algorithms, molecular docking, and molecular dynamics simulations. Protein expression was examined using western blot. The levels of interleukin (IL)-6 and tumor necrosis factor-α (TNF-α) were detected using detection kits. The senescence of cells was analyzed using senescence-associated β-galactosidase (SA-β-gal) staining kits. Zin was predicted to target several core genes, including v-akt murine thymoma viral oncogene homolog 2 (AKT2), heat shock protein 90α family class B member 1 (HSP90AB1), nuclear receptor subfamily 3 group C member 1 (NR3C1), forkhead box O1 (FOXO1), and toll-like receptor 4 (TLR4), potentially contributing to the alleviation of CHD. Furthermore, molecular docking and molecular dynamics simulation predicted a stable binding interaction between Zin and HSP90AB1. Zin ameliorated ox-LDL-stimulated inflammation, an effect that was associated with downregulation of HSP90AB1. Furthermore, Zin alleviated ox-LDL-induced senescence and apoptosis in a manner correlated with reduced HSP90AB1 levels in vitro. Zin suppresses inflammation, senescence, and apoptosis of oxidized low-density lipoprotein-induced primary human coronary artery endothelial cells in a manner associated with HSP90AB1 silencing. These findings provide a foundation for the further development of Zin-based treatment strategies for CHD. - Source: PubMed
Ma ShucanLi RuLiu ZhifenXiao HongYing Junqi - Proteus syndrome is a rare genetic disorder characterized by progressive, abnormal overgrowth that can affect any organ or tissue in the body. This abnormality is caused by a mosaic activating variant in AKT1 that encodes a key serine/threonine kinase of the phosphoinositide-3-kinase (P13K)/AKT signaling pathway and is involved in cell growth, survival, and metabolism. Miransertib (MK-7075, formerly ARQ 092) is a novel, orally bioavailable allosteric pan-AKT inhibitor that selectively targets AKT1, AKT2, and AKT3, demonstrating potent suppression of AKT signaling and tumor growth in murine xenograft models with dysregulated signaling pathways. It has also been evaluated as a potential therapeutic option for individuals with Proteus syndrome, both in pre-clinical studies and in clinical trials. In this study, we have developed and validated a sensitive, robust, and specific LC-MS/MS method for quantifying miransertib in human plasma. The calibration curve ranged from 0.5 to 500 ng/mL in human plasma with a linearity of r = 0.9945 ± 0.0019 across multiple days. Accuracy of assay ranged from -3.38 to 3.53% and precision was between 2.90 and 8.42%. Miransertib also showed excellent stability following multiple freeze-thaw cycles, during bench-top storage, and while on the autosampler overnight. This method enabled us to assess the pharmacokinetic parameters of participants enrolled in a phase II clinical trial (NCT04316546). - Source: PubMed
Publication date: 2026/05/29
Khan R M NaseerArisa Oluwatobi TZeng YiRostagni OliviaRedick CarolineParis Kathryn MBiesecker Leslie GOurs Christopher AFigg William D - Periodontitis is a chronic inflammatory disease characterised by progressive destruction of periodontal tissues and alveolar bone resorption. Triphala (TRP), a traditional Ayurvedic formulation comprising equal proportions of Terminalia chebula, Terminalia bellirica, and Phyllanthus emblica, has demonstrated anti-inflammatory and antioxidant properties. This study aimed to investigate the molecular mechanisms underlying TRP's therapeutic effects on periodontitis through an integrated approach combining network pharmacology with experimental validation, focusing on the PI3K/AKT signalling pathway. - Source: PubMed
Publication date: 2026/05/28
Zhao YiweiLi SiminKreher DeborahHaak RainerFichter AndreasSchmalz Gerhard