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
- Diabetic retinopathy (DR) is a leading cause of vision loss in working-age adults, and current treatments (anti-VEGF drugs, steroids, laser photocoagulation) mainly target late-stage microvascular complications while offering little for the neurodegeneration and neurovascular unit dysfunction that characterize early DR. Multi-component, multi-target traditional Chinese medicine compound decoctions are attractive candidates for early intervention. Here we investigated the protective effect and molecular mechanism of Alpinia Oxyphylla-Shenqi Siwu Decoction (AOSWSD) in a high glucose-induced ARPE-19 injury model of early DR. - Source: PubMed
Publication date: 2026/09/10
Zhang WeilingJing Chunying - Aging, as an inevitable biological process, is an inevitable process of multisystem functional decline, with cellular senescence being one of its hallmarks. Although total saponins from (TSG) offer health benefits, its precise anti-aging mechanisms have not been fully elucidated. - Source: PubMed
Publication date: 2026/07/06
Tan Yu-JingJin Wen-QiWang JingWang HuiLou Ting-TingSun Li-WeiLiu Fang-BingZhang Shuai - Ochratoxin A (OTA) is a persistent foodborne environmental contaminant with recognized systemic toxicity, but the molecular basis of its reproductive effects remains incompletely defined. We integrated network toxicology, molecular docking, molecular dynamics simulation and public single-cell RNA sequencing to generate candidate mechanisms, and then evaluated selected predictions using cell-viability and transcript-level assays. Intersections between OTA-related and reproductive-injury targets yielded 318 testicular and 426 ovarian candidate targets. AKT1, MAPK1, PIK3CA, SRC and TP53 were shared network hubs, while enrichment analysis prioritized PI3K-Akt signaling, apoptosis, p53, FoxO and MAPK pathways. Docking predicted favorable OTA poses for the five hub proteins, and 100-ns simulations of the selected AKT1-OTA and PIK3CA-OTA complexes showed persistence of the predicted poses within the modeled systems; these computational findings do not establish biological binding or direct target engagement. Public single-cell data localized the candidate genes to germ, somatic and steroidogenic cell populations. In vitro, OTA reduced 24-h viability with IC50 values of 9.25 micromolar in GC-1 cells and 27.94 micromolar in KGN cells and altered hub-gene transcripts. Taken together, the results suggest that OTA-associated reproductive cell stress may involve PI3K-Akt-related survival signaling and apoptosis-linked responses, but protein-level and functional validation is required. - Source: PubMed
Publication date: 2026/09/09
Xu YingkunHua RuiZhang PeizhiYu HanpuQiu Jiechuan - Kaixuan Jiedu Decoction (KXJD) is a compound herbal formula rooted in the classical "Xuanfu theory" of Traditional Chinese Medicine and has long been clinically used for psoriasis management, yet the cellular and molecular mechanisms remain incompletely understood. The study aims to explore the effects of KXJD on psoriasis-like inflammation, with a focus on oxidative stress, mitochondrial homeostasis, and the potential involvement of PI3K/AKT/mTOR signaling. - Source: PubMed
Publication date: 2026/09/09
Jiaqi LiNingxin ZhangHaoruo YangMengyao JiangWenqi CaoMeiqi SunJiarong WuRongjia ZhuHuiyan ChiBin YangPing Song - Medullary thyroid carcinoma (MTC) is a neuroendocrine tumor originating from calcitonin producing C-cells and accounts for 1-5% of thyroid cancers. Total thyroidectomy is curative in localized disease (N0), whereas lymph node metastases (N1) are associated with poorer prognosis. However, the molecular mechanisms driving the metastatic shift remain poorly understood. This study aimed to identify miRNA features linked to metastatic spread in MTC, focusing on the transition from N0 to N1. Co-expression networks were constructed for N0 and N1 tumors, and differential connectivity analysis was used to identify key miRNAs acting as regulatory hubs. Functional annotation of their target genes was performed using the Kyoto Encyclopedia of Genes and Genomes (KEGG), Gene Ontology (GO), and Reactome pathway analyses. Validation experiments were carried out in MTC cells to evaluate the effects of selected miRNAs on cell proliferation, survival, and MAPK pathway activation. Network analysis revealed distinct miRNA co-expression patterns between N0 and N1 tumors. Differential network analysis highlighted miR-145-3p as a central regulatory hub, exhibiting 29 altered co-expression changes and a marked loss of connectivity in N1. Target enrichment identified 59 validated genes, including key oncogenic drivers such as MYC, PTEN, BCL2, PIK3CA, AKT1, and MAPK7. In MTC cells, simultaneous inhibition of miR-145-3p together with its top co-expressed miRNAs increased proliferation and survival, and enhanced ERK phosphorylation, indicating MAPK pathway activation and a shift toward a more aggressive phenotype. In conclusion, this study identifies a miRNA regulatory hub centered on miR-145-3p that is associated with metastatic progression and highlights the value of network-based approaches in uncovering mechanisms of cancer dissemination. © 2026 The Author(s). The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland. - Source: PubMed
Publication date: 2026/09/09
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