Akt1 (Phospho-Thr72) Polyclonal Antibody
- Known as:
- Akt1 (Phospho-Thr72) Polyclonal Antibody
- Catalog number:
- 12312
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- Akt1 (Phospho-Thr72) Polyclonal Antibody
Related genes to: Akt1 (Phospho-Thr72) Polyclonal Antibody
- 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 (Phospho-Thr72) Polyclonal Antibody
Related articles to: Akt1 (Phospho-Thr72) Polyclonal Antibody
- Gastrointestinal (GI) cancer remains a leading cause of cancer-related mortality worldwide, with epigenetic alterations progressively recognized as key drivers of tumorigenesis and therapeutic resistance. Through its role in facilitating cell proliferation, inhibiting apoptosis, driving epithelial-mesenchymal transition (EMT) and metastasis, reinforcing angiogenesis, inducing metabolic reprogramming, mediating chemoradiotherapy resistance and maintaining cancer stem cell (CSC) properties, protein arginine methyltransferase 5 (PRMT5) has emerged as a key oncogenic regulator among these epigenetic modifiers implicated in GI cancer progression. Elevated PRMT5 expression has been observed in multiple GI cancer subtypes, comprising gastric cancer (GC), colorectal cancer (CRC), hepatocellular carcinoma (HCC) and pancreatic cancer, where PRMT5 markedly contributes to tumorigenesis via symmetric dimethylation of histone (e.g., dimethylation of histone H4 at arginine 3) and non-histone substrates [e.g., AKT1 and sterol regulatory element-binding protein 1a (SREBP1a)]. In GC, PRMT5 activates the PI3K/AKT pathway [e.g., by methylating AKT1 at arginine (R)391 and upregulating c-Myc], facilitating tumor cell proliferation and survival. In CRC, PRMT5-mediated methylation of SMAD4 (e.g., at R361) reinforces TGF-β signaling, facilitating EMT and metastasis, while its interaction with EGFR further amplifies proliferative signals. PRMT5 also upregulates VEGF expression (e.g., via chromatin remodeling at its promoter), stimulating angiogenesis and inhibits ferroptosis (e.g., by suppressing the solute carrier family 7 member 11/glutathione peroxidase 4 axis in HCC), supporting tumor survival. Furthermore, PRMT5 markedly contributes to metabolic reprogramming (e.g., accelerating lipogenesis via SREBP1a methylation and glycolysis via epigenetic silencing of F-box and WD repeat domain-containing protein 7), while strengthening DNA repair (e.g., homologous recombination) and CSC self-renewal (e.g., via the β-catenin/IL-8 axis in CRC) to confer therapy resistance. However, PRMT5 inhibitors (e.g., GSK3326595 and JNJ-64619178) demonstrate antitumor effects in preclinical models and methylthioadenosine phosphorylase (MTAP) deletion may serve as a potential biomarker for patient selection. The clinical translation of PRMT5 inhibitors is limited by hematological toxicity, lack of robust predictive biomarkers beyond MTAP and potential resistance from compensatory PRMT family members. It is key to clarify GI cancer-specific PRMT5 mechanisms and potentially develop optimized combination therapies in the future. - Source: PubMed
Publication date: 2026/04/23
Zhang RuiLu YiwenFang XiaohuaZhang FengquanWu WeidongSong JieLiang Zhenzhen - The present study aimed to explore the therapeutic effects and underlying mechanisms of the active constituents of . in gastric cancer (GC) and to identify potential targets for its prevention and treatment. Active compounds and their corresponding targets were screened using the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform. In comparison, GC-related targets were retrieved from GeneCards and Online Mendelian Inheritance in Man databases. Common targets were identified using Venny 2.1.0. Cytoscape 3.10.2 was then employed to construct a traditional Chinese medicine component-target-disease network and a protein-protein interaction network. Core compounds and targets were further assessed through molecular docking, and the potential mechanisms were investigated using Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses. The biological activity of luteolin, the principal active component of ., was experimentally validated in AGS cells using Cell Counting Kit-8 assays, wound-healing (scratch) assays, Transwell migration assays, flow cytometry and western blotting. A total of 10 active ingredients and 166 shared targets were identified. Among them, quercetin, luteolin and acacetin were identified as key bioactive constituents, whereas AKT serine/threonine kinase 1 (AKT1), TNF and hypoxia-inducible factor-1 (HIF-1A) were recognized as central targets. Molecular docking analysis revealed strong binding affinities between the core compounds and these targets. Enrichment analyses further indicated that the therapeutic effects of . may involve pathways related to oxidative stress, the phosphatidylinositol 3-kinase-protein kinase B signaling pathway, and the HIF-1 signaling pathway. Among the identified compounds, luteolin showed the most pronounced inhibitory effects on GC cells and was therefore selected for further mechanistic investigation. experiments demonstrated that luteolin significantly suppressed GC cell proliferation and migration, reduced AKT phosphorylation and HIF-1A expression, and did not induce apoptosis. These findings suggest that luteolin may exert its anti-GC effects primarily by modulating the AKT1/HIF-1A signaling axis. The present study provides experimental support for the therapeutic potential of -derived compounds and offers insights into novel molecular targets for GC treatment. - Source: PubMed
Publication date: 2026/04/27
Yu WeizhouNi XiaohuiWang JingXia WeiShen XinyaQiu FanChen Yuping - A combination of bioinformatics methods including network pharmacology, molecular docking and molecular dynamics simulation was utilized to investigate the potential mechanism of Roxb. (SG) in the treatment of ulcerative colitis (UC). - Source: PubMed
Publication date: 2026/04/30
Cui YuanHu JingyiLi YananTong YihengShen Hong - Traditional phthalate esters （PAEs） and their novel alternatives are widely used as plasticizers. Owing to their non-covalent bonding with polymer matrices， these compounds readily migrate from materials and accumulate in indoor dust， posing potential risks to human health. Although their carcinogenic and reproductive toxicities have been extensively studied， their neurotoxicity， particularly that of novel alternatives， remains poorly understood. To address this knowledge gap， this study adopted an integrated approach combining pollution profiling， health risk assessment， and mechanistic investigation to systematically evaluate the neurotoxicity risks and potential mechanisms of PAEs and their alternatives in typical campus microenvironments （classrooms， laboratories， offices， cafeterias， and dormitories）. The contamination profile of target compounds in indoor dust was determined using comprehensive two-dimensional gas chromatography coupled with time-of-flight mass spectrometry （GC×GC-TOF MS）. By integrating three exposure pathways （ingestion， inhalation， and dermal contact of dust） with absorption， distribution， metabolism， excretion， and toxicity （ADMET） models， the estimated daily intakes （EDIs） and neurotoxic health risks for different populations were assessed. Furthermore， network toxicology and molecular docking techniques were employed to elucidate the potential toxic mechanisms. Results indicated that dormitories exhibited the highest contents of target compounds， with major components including di-2-ethylhexyl phthalate （DEHP）， di（2-ethylhexyl） tetrahydrophthalate （DEHTH）， acetyl tri-n-butyl citrate （ATBC）， and trioctyl trimellitate （TOTM）. Exposure assessment identified ingestion as the predominant exposure route. Using the ADMET model， toxicity equivalency factor （TEF） and toxic equivalent quantity （TEQ） were quantified for five neurotoxicity-related health endpoints， including phenotypic neurotoxicity， estrogen receptor activity， oxidative stress， mitochondrial dysfunction， and DNA damage. Risk assessment based on TEQ revealed that females aged 18-60 years faced higher neurotoxicity risks than males， although no statistically significant gender differences in EDI were observed across all age groups. Mechanistically， network toxicology identified 59 core targets associated with neurotoxicity， including oncogene， non-receptor tyrosine kinase （SRC）， serine/threonine kinase 1 （AKT1）， estrogen receptor 1 （ESR1）， mitogen-activated protein kinase （MAPK1， MAPK3）， heat shock protein 90 alpha family class a member 1 （HSP90AA1）， and Kirsten rat sarcoma viral oncogene homolog （KRAS）. Functional enrichment analysis showed that these core targets were predominantly enriched in pathways related to endocrine resistance and cancer， suggesting that these compounds may induce neurotoxicity by disrupting cellular homeostasis and signal transduction. Molecular docking supported specific binding interactions between representative compounds and core proteins， validating the predicted associations. Notably， diphenyl phthalate （DPhP） and dicyclohexyl phthalate （DCHP） were identified as the key risk drivers. In contrast， novel alternatives with fewer aromatic rings and ester groups， such as diheptyl， -nonyl adipate （DHeNoA）， diisobutyl adipate （DiBA）， and diisodecyl adipate （DiDeA）， exhibited lower neurotoxic potential. Structure-activity relationship analysis suggested that the synergistic effect of aromatic rings and ester groups is a critical mechanism inducing neurotoxicity. By integrating environmental exposure profiling， TEQ-based risk assessment， and molecular mechanism analysis， this study not only delineates the neurotoxicity risk profile for specific campus populations but also elucidates the influence of molecular structure on neurotoxicity， providing a scientific basis for the targeted screening of low-neurotoxicity alternatives and informed risk management of indoor environmental health. - Source: PubMed
Li WeiGao KeHua KaiWang LinxiaoWei WeiLu Liping - 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