Ask about this productRelated genes to: Akt1 protein
- Gene:
- AKT1 NIH gene
- Name:
- AKT serine/threonine kinase 1
- Previous symbol:
- -
- Synonyms:
- RAC, PKB, PRKBA, AKT
- Chromosome:
- 14q32.33
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2019-04-23
Related products to: Akt1 protein
Related articles to: Akt1 protein
- Danggui Shaoyao Powder (DSP), a classical prescription in Traditional Chinese Medicine (TCM), has garnered growing evidence for its promising therapeutic effects on ulcerative colitis (UC). Nevertheless, the specific molecular mechanisms responsible for its anti-UC activity remain poorly understood. Herein, we integrated network pharmacology with experimental validation to systematically explore and clarify the underlying mechanisms of DSP in the treatment of UC. - Source: PubMed
Publication date: 2026/08/05
Huang YanxiaLin QiaoHongZhu MinChen KeCai XuehuaPan AizhenZhang Bin - This research aimed to elucidate the potential therapeutic efficacy of evodiamine (Evo) in alleviating IR associated with T2DM, and to further explain its underlying mechanism. The candidate bioactive components and targets of EVO were identified by using biomedical databases. Targets associated with IR were acquired from various databases. Intersectional analysis of Evo-related and IR-specific targets facilitated the construction of a PPI network. Cytoscape software was employed for the visualization of the "compound-target-disease" interactions, enabling the identification of key proteins. GO and KEGG analyses were then carried out to clarify the biological roles of the core Evo targets. MD analysis further confirmed the interactions between Evo and these key proteins. Additionally, the CCK-8 assay evaluated the influence of Evo on cell viability. The effects of Evo on glucose uptake and release were quantified, while Western blotting (WB) was employed to identify changes in protein expression driving the IRS-1/PI3K/AKT/GLUT4 signaling pathway. Furthermore, immunofluorescence techniques were implemented to visualize and quantify the expression levels of IRS-1, phosphorylated IRS-1 (p-IRS-1), and GLUT4 in insulin-resistant HepG2 cells. A total of 122 Evo-associated targets were obtained, among which 37 intersected with IR-related targets. Notably, AKT1, STAT3, SRC, and PTGS2 were identified as crucial proteins within this network. KEGG pathway analysis revealed enrichment of 126 significant pathways, among which the PI3K/AKT signaling pathway was particularly critical in mediating the therapeutic effects of Evo on IR. HepG2 cells in the model group showed lower glucose consumption and higher glucose production than controls, whereas Evo administration enhanced glucose consumption and reduced glucose production. Using metformin as a positive control, statistically significant differences in glucose consumption and production were found between HepG2 cells treated with Evo and metformin. Additionally, the model group exhibited significantly lower p-AKT and p-PI3K expression versus controls. In IR-HepG2 cells, Evo treatment dose-dependently restored diminished p-AKT and p-PI3K levels, mirroring metformin's action. Relative to controls, the model group exhibited elevated p-IRS-1, which was downregulated by Evo in IR-HepG2 cells; metformin, however, failed to reduce p-IRS-1 significantly. The results of our study indicate that Evo's ability to function as a therapy for IR might be linked to its role in modulating the IRS-1/PI3K/AKT signaling pathway and increasing the GLUT4 expression. - Source: PubMed
Publication date: 2026/08/24
Wang XinZhang NaWang MingshanLiu JiayiTong LeLiang XurongLi AilinGu YumingSong BailinXie XinxingChen Jiamei - Phthalate esters (PAEs) are environmental pollutants with potential neuroendocrine effects, yet systematic comparisons across congeners remain scarce. We employed electrostatic potential analysis (ESP), network toxicology, molecular docking, and molecular dynamics with MM-PBSA (Molecular Mechanics Poisson-Boltzmann Surface Area) binding free energy calculations to evaluate six PAEs. Target prediction from public databases and neuroendocrine-related gene compilation yielded 176 common genes, identifying five hubs AKT1, ESR1, MAPK3, PPARG, and TNF-α. MM-PBSA binding energies ranged from -40.23 to -8.25kcal/mol, with DINP binding strongest to ESR1 and DEHP exhibiting the highest affinities to PPARG and TNF-α. ESP revealed congener-specific surface properties, with DEP and DIBP exhibiting strong negative potentials on carbonyl oxygens, whereas DEHP and DINP were predominantly hydrophobic. We propose a tentative in silico hierarchy with DEHP > BBP ≈ DBP > DINP > DIBP > DEP. This work provides a theoretical basis for congener specific risk assessment of PAEs. - Source: PubMed
Publication date: 2026/08/23
Guan YilinWang YueBao GengxinOuyang JieWei FangXu Liheng - AD is a neurodegenerative disorder marked by progressive cognitive decline, particularly memory impairment, largely driven by cholinergic dysfunction. This study aimed to investigate the pharmacological basis and modes of action of the identified TT-TeMac™ compounds againsts cholinergic dysfunction associated with memory loss. TT-TeMac™ compounds targets which were identified by LC-MS were extracted from SwissTarget Prediction and PharmMapper, while cholinergic dysfunction-related targets were obtained from DisGeNET and GeneCards. Fifteen common targets were identified, with nine key targets highlighted by STRING, Cytoscape, and Venny analyses and confirmed by molecular docking using MOE. The validation used a rat model with scopolamine-induced cholinergic dysfunction (1 mg/kg bw/day, ip) for 7 days. Subsequently, behavioral (NOR and MWM), biochemical (AchE and BuhE) and histological (H&E and CV) analyses were performed. Seven compounds were identified in TT-TeMac™ (terminolic acid, sericic acid, arjunolic acid, gallic acid, ellagic acid, 3-O-methyl ellagic acid and 3,3'-di-O-methyl ellagic acid). Network pharmacological analysis showed that TT-TeMac™ acted on 15 common targets of which ACHE, IL6, TNF, SNCA, AKT1, SERPINE1, STAT3, ACE, and ALB were the pivotal genes. Also, docking studies confirmed the involvement of the target within the network with meaningful binding energies. Furthermore, TT-TeMac™ prevented cholinergic dysfunction associated with memory loss in rats by significantly reducing cholinesterase activity and protecting against morphological alterations and neuronal loss in the hippocampus. Our study shows that the ingredient TT-TeMac™ has a multi-targeted mode of action on protein targets involved in cholinergic dysfunction and counteracts this dysfunction in scopolamine-treated rats. - Source: PubMed
Publication date: 2026/08/10
Ambamba Bruno Dupon AkambaJonathan Messanga Me Ngo'oMarc Akono Fama YvesSandrine Nyabissick MondjiepReine Njayou Mbouangouore IngridEmmanuel NgarchindiLaurent Nkodo AbegaBlonde Njanjo Ejanmoua Merveille LaAlexandra Ebogo Enyegue FrançoiseElla Fils ArmandMandob Damaris EnyegueNgondi Judith Laure - Perimenopausal depressive-like symptoms are closely related to estrogen fluctuations, neuroinflammation and impaired neuroplasticity. Icariin has phytoestrogen-like and neuroprotective activities, but its multi-target mechanism in intervening in this pathological state remains unclear. - Source: PubMed
Chen Xiaoyu