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
- Identifying novel therapeutic targets for pancreatic cancer (PC) is crucial for improving patient outcomes. This study identified the functions, expression, and associated mechanisms of adhesion G protein-coupled receptor G6 (ADGRG6/ GPR126) in PC. Bioinformatics analyses revealed substantial upregulation of ADGRG6 in human PC, correlating with poor survival rates and advanced tumor stages. Elevated ADGRG6 expression has been observed in human PC tissues and cell lines. Targeted depletion of ADGRG6 via the CRISPR/Cas9 knockout (KO) or lentiviral shRNA technology in established and primary PC cells (priPC-1) resulted in a substantial decrease in cell cycle progression, cell proliferation, viability, as well as reduced migratory and invasive capabilities. Conversely, ADGRG6 overexpression further enhanced the malignant behavior of PC cells. Mechanistically, ADGRG6 is crucial for Akt-mTOR cascade activation. ADGRG6 depletion markedly decreased Akt, S6, and 4E-BP1 phosphorylation. Constitutively active mutant Akt1 (S473D, caAkt1) reversed the anti-proliferative and anti-migratory effects of ADGRG65 shRNA and restored Akt-mTOR phosphorylation. Further analysis revealed that ADGRG6-driven Akt-mTOR activation is mediated by G protein inhibitory subunit 3 (Gαi3). ADGRG6 shRNA significantly inhibited subcutaneous PC xenograft growth in mice, accompanied by reduced Akt-mTOR signaling activation. In contrast, ADGRG6 overexpression promotes xenograft growth. Together, these findings establish ADGRG6 as a critical mediator of PC progression via Gαi3-dependent activation of the Akt-mTOR axis. Targeting ADGRG6 is a promising therapeutic strategy for combating PC. - Source: PubMed
Publication date: 2026/05/06
Gu Qian-HuiZhu Xiao-RenJiang Jian-ZhuoLiu NaJin An-QiZhang YanLu Jing-JingLi PingYe Zhen-YuLiu Yuan-YuanChen Min-Bin - This study combined serum pharmacochemistry, metabolomics, and network pharmacology to uncover potential active components and mechanisms of Shenling Baizhu Powder (SLBZP) in treating ulcerative colitis with spleen deficiency and dampness stagnation (UC-SDDS), providing scientific evidence for its efficacy. Pharmacodynamic investigations demonstrated that SLBZP exhibits substantial anti-inflammatory properties and confers protection to the intestinal barrier in UC-SDDS rat models. Further, 16 active components and six core targets (BCL2, NFKB1, TNF, IL6, AKT1, CASP3) were obtained using serum pharmacochemistry and network pharmacology. Twenty-six differential metabolites in serum and 25 differential metabolites in urine were identified using untargeted metabolomics analyses. Subsequently, nine active components (butein, calycosin-7-o-β-d-glucoside, glabridin, isochlorogenic acid B, naringenin chalcone, naringenin, neoliquiritin, oroxyloside, and vanillic acid) were identified from SLBZP for treating UC-SDDS by integrating network pharmacology and chinmedomics. Molecular docking and dynamics simulation revealed that these compounds exhibit superior binding affinities to six core targets. Finally, the expression levels of AKT1, p-AKT1, mTOR, Caspase 3, TLR2, TLR4, ERK1/2, STAT1, MyD88, NFκB, and BCL2 in colon tissues were detected in UC-SDDS rats treated with SLBZP. The study showed that SLBZP effectively treats UC-SDDS rats by modulating multiple components, targets, and pathways using serum pharmacochemistry, network pharmacology, and metabolomics. - Source: PubMed
Shen BixinYang ZhenyuPan YixiaoYang WeijinChen Jing - Hepatocellular carcinoma (HCC) is one of the most prevalent malignant tumors worldwide. Both experimental and clinical studies confirm the anti-HCC effects of Yiguanjian (YGJ), though its material basis and pharmacological mechanisms remain unclear. This study integrated UHPLC-Q-TOF-MS with network pharmacology, molecular docking, and MDS to explore YGJ's potential anti-HCC mechanisms and active ingredients. In vitro analysis identified 96 chemical constituents in the YGJ extract, while network pharmacology revealed 57 potential targets and 51 bioactive compounds related to HCC treatment. The top nine key targets were AKT1, CTNNB1, EGFR, IL6, STAT3, BCL2, CASP3, MMP9, and TNF-α; the top seven active compounds included kaempferol, quercetin, luteolin, senkyunolide O, jasmolone, azaron, and dihydroartemisinin. These components may regulate HCC cell processes like gene expression, signal transduction, proliferation, apoptosis, and angiogenesis through pathways such as PI3K-Akt, TNF signaling pathway, and HIF-1 signaling pathway. Molecular docking and MDS showed that kaempferol, quercetin, luteolin, and dihydroartemisinin bind favorably to TNF-α, MMP9, BCL2, and IL6 proteins. Therefore, these proteins may serve as YGJ's therapeutic targets, while the compounds contribute to its pharmacological effects. - Source: PubMed
Wen XiaoliZhang XinyuanFang WenLiu HongningCai Fangyan - Gastrointestinal symptoms in Parkinson's disease (PD), in particular chronic constipation, are common and are treated in China using the traditional Chinese medicine (Jia-Wei-Ji-Chuan-Jian decoction) (JWJCJ)). However, information on therapeutic targets and the underlying mechanism is limited. - Source: PubMed
Publication date: 2026/05/05
Loong Shi KayWu FeifeiLiu YizhouVoratunyakit NapattharinWei ShangyuLi WeiLi RuiPan Weidong - Coronary heart disease (CHD) is a leading cause of morbidity and mortality worldwide, yet therapeutic options remain limited. Guanxinning tablet (GXNT), a component-based Chinese medicine containing Danshen and Chuanxiong, has demonstrated clinical efficacy and safety for CHD patients with heart-blood stagnation syndrome. However, its bioactive constituents and underlying pharmacological mechanisms remain undefined. This study aimed to identify the bioactive components of GXNT and elucidate its anti-CHD mechanisms. - Source: PubMed
Publication date: 2026/04/27
Li JunWang YingchaoLi MiaofuWang MulanShen PeiqiangTao YiWang Yule