AKT1
- Known as:
- AKT1
- Catalog number:
- 000039A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- 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
- This study combined network pharmacology with in vivo and in vitro experiments to investigate the molecular mechanisms of quercetin against vocal fold fibrosis (VFI). - Source: PubMed
Publication date: 2026/08/26
Feng YujieYang QiurongHu YuanjiaWu ShengtaoZhuang Peiyun - Tangzukang Ointment (T-Ointment) is formulated by adding ingredients such as Astragalus, Angelica sinensis, Cinnamomi Cortex, and Coix seed to the traditional formula ErMiao Pill. This ointment has the effects of clearing heat and removing dampness, warming the yang energy, strengthening the qi, promoting blood circulation and tissue regeneration. Clinically, it is used by traditional Chinese medicine to treat diabetic foot ulcers (DFU). This study established an experimental rat model of ischemic DFU to investigate its therapeutic effect and potential mechanism in DFU. The results showed that T-Ointment significantly promoted wound healing in diabetic rats by inhibiting excessive inflammation, promoting epithelial regeneration, angiogenesis and collagen deposition. Network pharmacology analysis indicated that the core compounds (quercetin, phellochin, fumarine, poriferast-5-en-3beta-ol, and jaranol) in T-Ointment targeted multiple key genes (AKT1, TGF-β, HIF-1, TNF, IL-6, EGFR, TP53 and MAPK) and were closely associated with multiple important signaling pathways (PI3K/AKT, EGFR, TGF-β/Smad, and MAPK/ERK etc.). Analysis of combined results from KEGG pathway enrichment analysis and molecular docking, the key pathways potentially promoted by T-Ointment for diabetic foot ulcer healing were identified: the PI3K/AKT and EGFR pathways. Further research has confirmed that T-Ointment indeed reversed the downregulation of the PI3K/AKT and EGFR pathways in the diabetic foot ulcer group. This indicates that its role in accelerating ulcer healing is closely related to the activation of these two pathways. In conclusion, this study clarified the multi-component, multi-target and multi-pathway mechanism of T-Ointment in treating diabetic foot ulcers, providing a scientific basis for its clinical application. - Source: PubMed
Publication date: 2026/08/18
Tang ShuoZhu LiusuyuWu XiaoqinZhu JieLiu JiahaoGao DengsiyuanXue JiahuiShi RongfengPan YujieChen XiaGuo AisongGu Yunjuan - Diabetic nephropathy (DN) is a leading cause of chronic kidney failure. We hypothesized that mitochondrial Akt1 dysfunction in renal proximal tubules plays a pathogenic role in DN development and that its activation may reverse DN progression. - Source: PubMed
Publication date: 2026/08/25
Salem Esam S BTa AlbertBloom-Saldana ElizabethFueger Patrick TWang Ping H - Alterations in the PI3K signaling pathway are common in hormone receptor-positive (HR+)/HER2-negative metastatic breast cancer (MBC) and are associated with response to PI3K and AKT inhibitor-targeted therapies. When metastasis biopsy is unavailable for genetic testing, circulating tumor DNA (ctDNA) analysis is an alternative strategy for tumor genotyping, but it is less sensitive for gain and loss analysis. Here, we assess molecular alterations of the genes of this axis-PIK3CA, AKT1, and PTEN-in circulating tumor cells (CTCs) from patients with HR+/HER2- MBC. CTCs from blood were isolated as single cells with DEPArrayNxT. Libraries were prepared for copy number analysis (CNA) and investigation of PIK3CA, AKT1, and PTEN mutational status. A subset of viable CTCs underwent 3' RNA sequencing for transcriptomic profiling. CTCs of 4/5 MBC patients (80%) exhibited single nucleotide variants (SNVs), and heterogeneity was observed at inter- and intra-patient levels. CNA profiling of CTCs from 8 patients revealed amplifications and gains of chromosomal regions hosting PIK3CA, AKT1, and PTEN. Notably, one patient presented both 10q32.31 loss and a nonsense mutation of the remaining PTEN allele, suggesting PTEN loss of function, an event potentially missed by ctDNA analysis. Integrated transcriptomic analysis highlighted patient-specific enrichment of pathways related to metabolism and RNA processing. Conclusively, single-CTC analysis enables comprehensive characterization of the PI3K/AKT/PTEN pathway, revealing molecular heterogeneity and capturing events not detectable by tumor tissue or ctDNA. This approach may enhance molecular stratification and guide the use of targeted therapies in MBC, supporting its integration into future precision oncology frameworks. - Source: PubMed
Publication date: 2026/08/25
Rossi TaniaPalleschi MichelaGianni CaterinaMerloni FilippoVirga AlessandraBandini SaraAngeli DavideTebaldi MichelaMaltoni RobertaUlivi PaolaMusolino Antonino - Aflatoxin B1 (AFB1) is a pervasive feed contaminant that poses a silent threat to male reproductive health under chronic low‑dose exposure. In this study, a male quail model was established with graded doses of AFB1 (25, 50, and 75 μg/kg). Integrated database prediction, multi‑omics profiling, and molecular docking revealed that AFB1 potentially targets AKT1, BCL2, TP53, and BID, disrupts testicular sphingolipid and steroid metabolism, and triggers the intrinsic mitochondrial apoptotic pathway. In vivo experiments confirmed that AFB1 exposure reduced body weight, sperm viability, and serum reproductive hormone levels, while inducing oxidative stress, inflammatory responses, and activation of the BAX‑Cyt‑c‑Caspase‑9/3 cascade. To move beyond correlative evidence, primary avian testicular Sertoli cells were employed for in vitro functional validation. Pharmacological interventions with GW4869 and all‑trans retinoic acid demonstrated that ceramide accumulation functions as an upstream driver of AFB1‑induced mitochondrial impairment and apoptosis. Collectively, these findings establish that AFB1 activates the sphingomyelin/ceramide‑dependent sphingolipid‑mitochondrial apoptotic axis, culminating in testicular cell death. This study provides novel mechanistic insights into AFB1‑induced male reproductive toxicity and offers a theoretical foundation for aflatoxin risk management in livestock production. - Source: PubMed
Publication date: 2026/08/21
Ping ZhenleiWang YuFu LinlinCui XiaoyingZheng SongtaoJiang XiaowenYu Wenhui