AKT1 (phospho-Thr308) Antibody
- Known as:
- AKT1 (phosphorilated-Thr308) Antibody
- Catalog number:
- abx000352
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- AKT1 (phospho-Thr308) Antibody
Related genes to: AKT1 (phospho-Thr308) 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-Thr308) Antibody
Related articles to: AKT1 (phospho-Thr308) Antibody
- Triple-negative breast cancer (TNBC) is an aggressive subtype of breast cancer with limited treatment options due to the absence of estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2) receptors. This study investigates the anticancer potential and underlying molecular mechanisms of the traditional ayurvedic formulation Kanchanara guggulu in TNBC cells. The cytotoxic, anti-migratory, and membrane integrity-modulating effects of Kanchanara guggulu on MDA-MB-231 cells were assessed using MTT, wound-healing, and Live/Dead assays. Untargeted LC-MS/MS metabolomics identified over 1,019 metabolites, of which 237 met drug-likeness and Absorption, Distribution, Metabolism, Excretion and Toxicity (ADMET) criteria. Network pharmacology revealed 50 shared targets with TNBC-associated proteins, highlighting enrichment in PI3K/AKT/mTOR, HIF-1, AGE-RAGE, calcium signaling, and microRNA-related pathways. Molecular docking (LibDock and CDOCKER) identified top bioactive candidates with strong binding affinity towards AKT1, supported by density functional theory (DFT) showing favorable electronic stability. Experimental validation demonstrated significant dose-dependent cytotoxicity (IC₅₀ = 45 µg/mL), inhibition of migration, and increased cell death. Western blot analysis confirmed downregulation of phospho-AKT and mTOR, indicating suppression of PI3K/AKT/mTOR signaling. Overall, TNBC cells showed reduced proliferative and migratory potential upon treatment, suggesting that Kanchanara guggulu extract exerts anticancer effects and provides promising lead compounds for TNBC therapy development. - Source: PubMed
Publication date: 2026/07/03
Hemavathi Kadabagere NarayanaswamyPervaje RavishankarPrasad Thottethodi Subramanya KeshavaDagamajalu Shobha - Exertional heat stroke (EHS) is a life‑threatening condition characterized by hyperthermia, systemic inflammation and central nervous system injury, particularly in desert dry‑heat environments. Excessive activation of inflammatory signaling pathways, notably the Toll‑like receptor (TLR)4/myeloid differentiation factor 88 (MyD88)/NF‑κB axis, critically contributes to brain damage and neuroendocrine dysfunction in EHS. Curcumin exhibits anti‑inflammatory and neuroprotective effects; however, poor bioavailability limits its clinical application. Notably, nanocrystal formulations may improve the therapeutic efficacy of curcumin. In the present study, network pharmacology and molecular docking were employed to identify the potential therapeutic targets of curcumin in EHS. A rat model of desert dry‑heat‑induced EHS was established and nanocurcumin was administered intravenously following heat exposure. Histopathological examination, ELISA analyses of neuroendocrine hormones and inflammatory cytokines, serum biochemical assays and western blotting were subsequently performed. These evaluations assessed brain injury, hypothalamic‑pituitary‑adrenal and hypothalamic‑pituitary‑thyroid axes functions, systemic inflammation, peripheral organ injury indicators and activation of the TLR4/MyD88/NF‑κB signaling pathway. Network analysis revealed 138 overlapping target genes between curcumin and EHS, identifying AKT1, TNF, EGFR, BCL2, STAT3, SRC and NFKB1 as key hub genes. Kyoto Encyclopedia of Genes and Genomes pathway analysis highlighted enrichment of the 'Toll‑like receptor signaling pathway' and 'NF‑κB signaling pathway'. Molecular docking indicated favorable binding affinities of curcumin to essential inflammatory proteins, including TLR4, MyD88 and NFKB1. In vivo experiments demonstrated that nanocurcumin reduced neuronal injury in the cerebral cortex and hypothalamus of rats. Furthermore, nanocurcumin significantly decreased serum concentrations of corticotropin‑releasing hormone, corticosterone, thyrotropin‑releasing hormone and thyroid‑stimulating hormone, and restored adrenocorticotropic hormone, total triiodothyronine and free triiodothyronine levels. Nanocurcumin also lowered serum TNF‑α, IL‑6 and IL‑1β levels, and improved biochemical markers of liver, kidney and tissue injury (alanine aminotransferase, aspartate aminotransferase, blood urea nitrogen, creatine kinase and lactate dehydrogenase). Within the 4‑h observation period, medium and high doses of nanocurcumin did not worsen biochemical markers compared with those in the EHS or saline groups. Additionally, nanocurcumin administration dose‑dependently inhibited TLR4, MyD88 and NF‑κB protein expression in brain tissues. In conclusion, nanocurcumin may alleviate brain injury, neuroendocrine dysfunction and systemic inflammation associated with desert dry‑heat‑induced EHS, and may improve biochemical indicators of peripheral organ damage; these effects likely involve suppression of the TLR4/MyD88/NF‑κB signaling pathway. These findings support the use of nanocurcumin as a promising adjunctive therapy for managing EHS. - Source: PubMed
Publication date: 2026/07/03
Su LisongQu JinquanLi JiajiaShi WenhuiSong LaiyangLiang FeixingLiu Jiangwei - In preclinical models, PCSK9 mediates cancer immunotherapy resistance and may serve as a novel immuno-inhibitory target. Herein, we report the results from a multi-center, single arm, phase II study evaluating the clinical activity and safety of the PCSK9 inhibitor alirocumab, in combination with the anti-PD1 antibody cemiplimab, in non-small cell lung cancer (NSCLC) patients with disease progression after previous immune checkpoint blockade. The primary endpoint was objective response rate (ORR). Secondary endpoints were progression-free survival (PFS), overall survival (OS), duration of response (DOR), disease control rate (DCR) and safety, and an exploratory objective was to analyze potential biomarkers of response. Sixty patients were enrolled, and 58 were evaluable for ORR. The ORR was 14.78% (90% CI, 5.30, 25.43), the median PFS was 2.5 months (95% CI, 1.5-3), and the median OS was 7.3 months (95% CI, 5.4 - 12.3). The most common treatment related adverse events (all grades) were anemia and fatigue. Grade 3 adverse events occurred in seven (12%) patients and were anemia, Guillain-Barre Syndrome and elevated amino transferase. There were no treated related adverse events of grade 4 or greater in the study population. Biomarker analysis identified superior outcomes in NSCLC harboring PIK3CA, PTEN, or AKT1 alterations. The ORR in patients with PIK3CA, PTEN, or AKT1 alterations (n=17) was 29.4% (95% CI, 10.3% - 56.0%). No objective responses were observed in the absence of PIK3CA, PTEN or AKT1 alterations (n=39). The presence of PIK3CA, PTEN or AKT1 alterations was significantly associated with response, p 0.0032 (two-sided, Fisher's exact test). Further translational studies revealed the impact of PIK3CA, PTEN or AKT1 alterations on intratumoral PCSK9, providing a biological rationale for the pattern of response and clinical benefit. These findings provide clinical proof-of-principle that PCSK9 inhibition can overcome immunotherapy resistance in a subset of patients and suggest that PIK3CA/PTEN/AKT1 pathway plays a significant role in PCSK9 mediated immune evasion and could be a biomarker of response. These findings warrant further investigation in larger confirmatory studies. - Source: PubMed
Publication date: 2026/06/24
Oduah EziafaGray JhanelleStinchcombe ThomasWolf StevenQin XiaodiIreland AbbieRivera-Concepcion JoelClarke JeffreyCrawford JeffreyAlder LauraOswalt CameronChen AlanLyniv LilianaAbbasi AamnaSaltos AndreasJung Sin-HoOwzar KourosReady NealOliver TrudyAntonia Scott - : Gout, an inflammatory arthritis driven by urate crystal deposition, still lacks therapies that are effective and well-tolerated. (iguratimod), an immunomodulatory drug approved for rheumatoid arthritis, has shown promise in Gout, but its molecular and immunogenetic mechanisms remain unclear. : We assessed the druggability and pharmacokinetic properties of using SwissADME and ADMET Lab 2.0. Network pharmacology identified overlapping targets between and Gout and constructed a STRING-based protein-protein interaction network with GO/KEGG enrichment. A two-sample Mendelian randomization (MR) analysis of 731 immune-cell traits and Gout (FinnGen R9) identified causal immunophenotypes. Molecular docking, 100 ns molecular dynamics (MD) simulations, and MM/GBSA calculations were carried out for (with docking support for and ). Public single-cell RNA sequencing (scRNA-seq) data of peripheral blood mononuclear cells were analyzed to profile cell-type-specific expression of core targets. : displayed favorable oral drug-likeness (QED = 0.641), high predicted plasma protein binding (PPB ≈ 94.22%), and limited blood-brain barrier penetration. , , and were prioritized as putative hub targets by network-based analyses in PI3K/AKT, MAPK, and TNF signaling. Docking and representative MD/MM-GBSA analyses supported a thermodynamically favorable and dynamically stable binding mode complex. MR identified 29 immune-cell traits genetically associated with Gout susceptibility, providing population-level causal inference and highlighting proinflammatory CD16 monocytes and dysfunctional CD25 Tregs, and scRNA-seq confirmed expression of , and in these Gout-relevant immune subsets. : This integrative in silico framework suggests that could structurally engage multiple immunomodulator targets relevant to Gout and generates genetically and cell-type-informed hypotheses that require biochemical, cellular, and validation. - Source: PubMed
Publication date: 2026/06/16
Zeng HuiqiongLin SongqingLiu ZebinLai JundaLiu WeiZhang Ye - [This retracts the article DOI: 10.1002/humu.22100.]. - Source: PubMed
Publication date: 2026/03/17
Mutation Human