Ask about this productRelated genes to: AKT1 Blocking Peptide
- 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 Blocking Peptide
Related articles to: AKT1 Blocking Peptide
- Psoriasis is a chronic immune-mediated skin disease driven by cytokine dysregulation, particularly through the TNF-α/IL-23/IL-17 axis. Current treatments targeting these cytokines are effective yet limited by cost, relapse risk, and safety concerns. This study investigates the therapeutic potential of Clitoria ternatea extract (CTE) using a multi-approach strategy combining phytochemical profiling, in silico analysis, molecular docking, and in vitro antioxidant assays. UPLC-QToF-MS/MS identified 14 major compounds in CTE, predominantly flavonoids. SAR-based prediction and ADMET profiling suggested that compounds C1, C4, C5, C7, and C8 exhibit anti-inflammatory potential with favorable safety profiles. Protein-protein interaction analysis and gene ontology revealed that these compounds target pathways associated with cytokine regulation. Molecular docking demonstrated strong affinities of C5 and C4 against IL-23 and TNF-α, exceeding that of clobetasol. In vitro antioxidant assays showed CTE had moderate scavenging activity against DPPH and ABTS radicals (IC ~ 90 μg/mL). In vitro studies using the RAW 264.7 macrophage cell line stimulated with lipopolysaccharide (LPS) revealed that treatment with CTE significantly suppressed the expression of pro-inflammatory proteins AKT1, IL-23, and TNF-α. These findings indicate that CTE, particularly its flavonoid components, may modulate key inflammatory pathways associated with the TNF-α/IL-23/IL-17 axis. Given its phytochemical composition and predicted safety profile, CTE may be better positioned as a functional food or nutraceutical candidate, rather than as a direct pharmacological agent, for supporting inflammatory balance. However, as this study is limited to in vitro and in silico analyses without in vivo validation, further mechanistic and clinical studies are required to determine its translational applicability. - Source: PubMed
Publication date: 2026/06/06
Mustika ArifaPurba Abdul Khairul RizkiKhaerunnisa SitiAzzahra Zumara Ma'rifahHerisulistyo AldilatamaMayangsari EllyAwaludin RizkyBalan Santhra SegaranYang UnhoPark Moon NyeoKo Seong-GyuNurkolis FahrulKim Bonglee - Lipopolysaccharide (LPS)-induced sepsis is one of the leading causes of acute kidney injury (AKI). Gallic acid (GAL), a natural polyphenolic compound, exhibits potent antioxidant, anti-inflammatory, and cytoprotective properties. This study aimed to investigate the renoprotective effects of GAL. - Source: PubMed
Publication date: 2026/06/05
Altuntas AtilaAsci HalilTepebasi Muhammet YusufIlhan IlterTaner RumeysaAkpinar ZeynepDonmez NihanOzturk Sefa AlperenOzmen Ozlem - The global burden of respiratory disorders is significant and affecting humans socially, physically and economically, therefore, effective multi-target therapeutic strategies have been required. Indian medicinal plants have long been employed for control of respiratory diseases. However, their molecular mechanisms are not fully characterized. This study employed a network pharmacology strategy for testing the multi-target therapeutic activity of a series of medicinal plants, including , , , and . Phytoconstituents were selected from the literature and compared to those with established respiratory disease-associated targets from the GeneCards database. Compound-protein interaction networks, protein-protein interaction (PPI) analysis, GO enrichment, and disease association studies were conducted by Cytoscape, STRING, Metascape and DisGeNET. The major bioactive compounds detected by the results included quercetin, kaempferol, glycyrrhizin and emodin that interacted with critical targets like NOS1 or NOS3 and AKT1 and CASP3 and were included in the target list. Functional enrichment characterization showed considerable engagement as an integral part of these pathways in the control of inflammation, vasodilation, immune response and metabolic pathways. Patterns of PPI network analysis indicated prominent connection and clustering with target proteins to highlight synergistic effects in therapy. The combined conclusions have reinforced the multifactorial and synergistic actions of Indian medicinal plants in the treatment of respiratory diseases. This study offers a systems-level perspective on their pharmacological actions, and also validates their ability to act in a system as a complementary therapy agent. These results should be confirmed by further experimental validation. - Source: PubMed
Publication date: 2026/06/02
Kumar SantoshYadav Dinesh KumarSingh MhaveerSalar SapnaSingh AnjaliSingh Manju - spp. are widespread intracellular animal pathogens that cause brucellosis, a significant zoonosis. Despite the global impact of brucellosis on animal and human health, the host genes that support infection remain incompletely defined. To address this knowledge gap, we developed a flow cytometry-based infection assay with fluorescent and performed a genome-wide CRISPR-Cas9 loss-of-function screen in human macrophage-like cells. Disruption of >150 host genes significantly reduced intracellular burden at 3 h post-infection. In addition to recovering known host factors, the screen revealed previously unappreciated genes linked to endosomal trafficking, cytoskeletal remodeling, and lipid homeostasis. The screen was robust, as validation within these functional categories confirmed that the small GTPase RAB14, the Src-family kinase regulator CSK, and the phospholipid flippase subunit TMEM30A support early infection by and without impairing general phagocytosis. Gene set enrichment analysis further revealed positive regulators of mTORC1 signaling as key host factors; this result was validated through targeted disruption of LAMTOR2 and AKT1, and pharmacologic inhibition of AKT1. Thus, the AKT-Ragulator-mTORC1 signaling axis contributes to the establishment of a permissive intracellular niche during early infection. Finally, to assess whether these host requirements extend beyond , we examined infection by the unrelated intracellular pathogen . CSK, AKT1, and LAMTOR2 were required for efficient infection, whereas RAB14 was dispensable. Together, these results define host genes that support early infection and distinguish shared versus pathogen-specific host dependencies exploited by intracellular bacteria. - Source: PubMed
Publication date: 2026/05/19
Kim ThomasScheeres Eleanor CFiebig ArethaOlive Andrew JCrosson Sean - Non-phthalate plasticizers (NPPs) are replacing phthalate esters in food packaging, but their comparative hepatotoxicity profiles remain poorly characterized. Here we established an integrated computational framework to evaluate five common food-packaging NPPs, identifying bis(2-ethylhexyl) adipate (DEHA) as the compound with the highest hepatotoxicity risk through multi-model validation. Network toxicology analysis of 127 DEHA-associated hepatotoxicity targets revealed significant enrichment in the PI3K-Akt signaling pathway, EGFR tyrosine kinase inhibitor resistance, TNF signaling, and key pathological processes of liver diseases. Topology centrality analyses further identified ALB, AKT1, and EGFR as hub targets. Two-sample Mendelian randomization confirmed causal associations between genetic predispositions to ALB, AKT1, and EGFR expression levels and liver disease susceptibility, while molecular docking demonstrated stable DEHA-target binding conformations (binding energy below -5.0 kcal/mol). Disease progression analyses showed significantly decreased ALB and EGFR expression in advanced liver disease stages, whereas AKT1 exhibited elevated expression. Single-cell transcriptomic profiling revealed predominant ALB expression in hepatocytes and pan-cellular distribution of AKT1/EGFR across liver cell types. Virtual knockout simulations indicated acute-phase response disruption following hepatocyte-specific deletions of ALB, AKT1, or EGFR. Finally, in vitro and in vivo exposure models validated DEHA-induced hepatotoxicity, demonstrating dysregulation of hepatic Alb, Akt1, and Egfr post-exposure. We propose a mechanistic hypothesis that DEHA compromises hepatic functions by disrupting the ALB-AKT1-EGFR regulatory axis. Collectively, this work provides a computational framework for NPP toxicity risk assessment and nominates ALB, AKT1, and EGFR as potential therapeutic targets for mitigating DEHA-induced hepatotoxicity. - Source: PubMed
Publication date: 2026/06/02
Zhu YihaoFu GuixiangWang ZhijieDing JinGuo Jianrong