AKT1
- Known as:
- AKT1
- Catalog number:
- RP17130530002
- Product Quantity:
- 2 µg
- Category:
- -
- Supplier:
- Biovend
- Gene target:
- AKT1
Related genes to: AKT1
- 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
Related articles to: AKT1
- 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 - Myocardial ischemia-reperfusion injury (MIRI) is still difficult to manage clinically, mainly due to limited effective strategies that can simultaneously address oxidative stress, mitochondrial dysfunction and myocardial cell loss. Prunasin is a cyanide glycoside derived from plants of the genus Prunus. Its biological activity has been reported, but its role in ischemia-reperfusion related cardiac injury is not yet clear. - Source: PubMed
Li JiangLi YaoshuXu ChengyangChen Yingying - Miscarriage, a prevalent adverse pregnancy outcome linked to maternal-fetal immune dysregulation, is increasingly suspected to be influenced by environmental microplastics, although specific molecular mechanisms remain elusive. This study integrated network toxicology, transcriptomics, and molecular dynamics simulations to elucidate the pathogenic role of microplastics in miscarriage. Initially, network toxicology identified 396 microplastics-related targets, yielding 38 intersection genes with miscarriage-associated targets from GeneCards. Functional enrichment revealed significant involvement in chemokine signaling and cytokine-cytokine receptor interactions. Analysis of the GSE183555 transcriptome dataset pinpointed 5 hub genes: CXCL8, EGFR, PTPRC, MYC, and AKT1. Immune infiltration analysis demonstrated that these hubs correlated significantly with altered immune cell populations, particularly CD8+ Tem cells, while gene set enrichment analysis and gene set variation analysis highlighted their enrichment in interleukin-17, nuclear factor kappa-B, and epithelial-mesenchymal transition pathways. Furthermore, regulatory networks involving specific transcription factors and miRNAs were constructed. Molecular docking confirmed stable binding affinities between hub proteins and potential ligands (e.g., Afatinib for EGFR, Eupalinin A for AKT1), which was further validated by 100-ns molecular dynamics simulations showing consistent root mean square deviation, radius of gyration, and hydrogen bond stability. In conclusion, this multi-omics approach uncovers a critical regulatory axis where microplastics may disrupt pregnancy maintenance by modulating key immune-inflammatory pathways via CXCL8, EGFR, PTPRC, MYC, and AKT1. These findings provide novel mechanistic insights into microplastics-induced reproductive toxicity and identify promising therapeutic targets for preventing environmentally triggered miscarriage, warranting further experimental validation in clinical and animal models. - Source: PubMed
Niu LijiaZhang XiaoliChen YiyiSong GuifangLi JinghuiXia Yixin - Colorectal cancer (CRC) is a malignancy with high global incidence and significant therapeutic challenges, where chemotherapy resistance is a key factor leading to treatment failure. Aberrant activation of the PI3K-Akt signaling pathway plays a central role in CRC progression and drug resistance. Fraxetin, a major active coumarin component of the traditional Chinese medicine Cortex Fraxini, possesses various biological activities, but its anti-CRC effects and underlying mechanisms remain unclear. This study aimed to systematically elucidate the mechanism of action of Fraxetin against CRC, particularly its regulation of the PI3K-Akt pathway and potential to reverse drug resistance, by integrating network pharmacology, computational simulation, and in vitro experiments. Network pharmacology screening identified 108 common targets of Fraxetin and CRC. Protein-protein interaction (PPI) analysis pinpointed 10 core targets, including TNF, AKT1, and EGFR. KEGG enrichment analysis suggested the PI3K-Akt pathway as one of the primary pathways involved. Molecular docking and dynamics simulations confirmed that Fraxetin could stably bind to core targets such as EGFR and ERBB2. In vitro experiments demonstrated that Fraxetin dose-dependently inhibited the proliferation of HCT116 and HT-29 cells, induced reactive oxygen species (ROS) generation, and significantly downregulated the phosphorylation levels of key PI3K-Akt pathway proteins, p-PI3K and p-Akt. Furthermore, Fraxetin combined with 5-fluorouracil (5-FU) or irinotecan exhibited synergistic antiproliferative effects and significantly restored the sensitivity of 5-FU-resistant cells to chemotherapeutic agents. This study systematically demonstrate that Fraxetin exerts multi-faceted effects against colorectal cancer, including anti-cancer activity, synergy with chemotherapy, and restoration of 5-FU sensitivity in 5-FU-resistant CRC cells in vitro, through multi-target inhibition of the PI3K-Akt signaling pathway. - Source: PubMed
Publication date: 2026/08/20
Guo MinfangZhu LiangdongGuo JianjinYang XunGuo TingZeng Qingling