Ask about this productRelated genes to: Rictor antibody
- Gene:
- RICTOR NIH gene
- Name:
- RPTOR independent companion of MTOR complex 2
- Previous symbol:
- -
- Synonyms:
- MGC39830, AVO3, PIA, KIAA1999
- Chromosome:
- 5p13.1
- Locus Type:
- gene with protein product
- Date approved:
- 2009-05-29
- Date modifiied:
- 2019-03-19
Related products to: Rictor antibody
Related articles to: Rictor antibody
- Miscarriage and abnormal embryonic development in women of advanced maternal age (AMA) are often associated with impaired decidualization. mTORC2 is an evolutionarily conserved protein kinase. As a core component of mTORC2, RICTOR has been implicated in nutrient sensing and is closely linked to implantation disorders; however, its role in regulating age-related decidualization disorders remains unreported. In this study, we identified pronounced decidualization defects in AMA foster mice, accompanied by a significant reduction in RICTOR in the decidual tissues of AMA women. Uterine-specific genetic deletion of Rictor in mice resulted in pregnancy loss and impaired decidualization. Notably, Rictor knockdown led to attenuated Akt3-FoxO1 signaling and impaired nuclear export of FoxO1. Molecular and histological analyses demonstrated that the specific RICTOR activator MHY1485 effectively rescued decidualization defects in vivo and in vitro. These findings indicate that RICTOR plays an essential role in the aging decidual microenvironment and may serve as a potential biomarker for uterine stromal cell decidualization. Furthermore, therapeutic activation of RICTOR represents a promising strategy to counteract senescent decidual impairment in AMA women and improve pregnancy outcomes. - Source: PubMed
Lin YifengSun JiweiYing YueLi DanYing YuewenShen XilinSun XiaoZhang DanWu YiqingZhang Runju - By integrating transcriptomics and network pharmacology, we systematically investigated the potential hemostatic mechanism of (BS). - Source: PubMed
Yang TaoXiong YanYang LingWang Xing-GangHuang YongFu Zhi-Li - Neuroendocrine prostate cancer (NEPC) is characterized by strong immune evasion and profound metabolic reprogramming. A high regulatory T cell (Treg)/CD8 T cell ratio and an increased proportion of M2/M1 tumor-associated macrophages (TAMs) in the NEPC tumor microenvironment (TME) are associated with poorer progression-free survival, a phenomenon linked to lipid accumulation within the TME. Understanding the regulatory mechanisms governing both the metabolic and immune landscapes of NEPC is critical. - Source: PubMed
Publication date: 2026/07/29
Sun YiJing JunRen ShangqingLuo XuWen WeiJin XinZeng GuohuaJiang XuewenZhang MoGuo Ju - Progression-free survival (PFS) is an important clinical endpoint in Luminal A breast cancer (BC), yet the molecular determinants of recurrence remain incompletely understood. This study aimed to identify recurrence-associated transcriptomic alterations across age-defined patient subgroups and evaluate their predictive utility using machine learning (ML). Gene expression profiles and clinical data from the METABRIC cohort were analyzed in premenopausal, postmenopausal non-geriatric, and geriatric patients with Luminal A BC. Differential expression analysis identified 32 significantly dysregulated genes, of which 15 genes with |logFC| ≥ 2 were selected for detailed characterization. Among these, , , , and exhibited consistent recurrence-associated expression patterns across patient subgroups, whereas , , and displayed subgroup-dependent expression profiles. Feature selection analysis identified as the most influential molecular predictor, while age, NPI, and tumor size were the most important clinical variables. The integrated clinicopathological-transcriptomic XGBoost model achieved the best predictive performance (AUC = 0.71; accuracy = 0.78) and outperformed baseline models based only on clinicopathological variables. Sensitivity analysis and independent external validation supported the robustness of the principal candidate biomarkers. These findings provide preliminary evidence supporting the investigation of transcriptomic biomarkers in combination with clinical variables for recurrence classification in Luminal A BC. However, further validation in independent cohorts is needed before their potential utility can be fully assessed. - Source: PubMed
Publication date: 2026/07/15
Kivrak MehmetNalkiran IhsanSevim Nalkiran Hatice - Phenethyl isothiocyanate (PEITC), isolated from cruciferous vegetables, exhibits anticancer activity against various human cancer cells. Our previous studies demonstrated that PEITC suppresses the growth of glioblastoma multiforme (GBM) 8401 cells in vitro and in vivo. In this study, we investigated the effects of PEITC on autophagy and its underlying molecular mechanisms in GBM 8401 cells. PEITC altered the morphology of GBM 8401 cells and triggered acidic vesicular organelle and autophagosome formation, as confirmed by acridine orange (AO) and monodansylcadaverine (MDC) staining, respectively. PEITC-treated cells transfected with green fluorescent protein (GFP)-microtubule-associated protein 1A/1B-light chain 3 (LC3) exhibited punctate autophagosomes, and autophagosome formation was further confirmed via transmission electron microscopy (TEM). Treatment with chloroquine (CQ) inhibited autophagy, resulting in a decrease in the number of autophagosome puncta. CQ also enhanced PEITC-induced cytotoxicity in GBM 8401 cells. Furthermore, the expression of autophagy-associated proteins including GβL, mTOR, mTOR, Raptor, Rictor, and, Beclin 1 was decreased, whereas the expression of AMPKα, AMPKα1/AMPKα2, PI3K class III, VPS34, autophagy protein 5 (Atg5), Atg7, Atg12-Atg5, Atg16L1, Atg3, sequestosome 1 (SQSTM1/p62), and LC3 II was increased. Confocal laser scanning microscopy further revealed decreased Beclin 1 and increased LC3 levels following PEITC treatment. After CQ pre-treatment, the expression levels of SQSTM1/p62 and LC3 II were elevated. PEITC induces protective autophagy via the adenosine monophosphate-activated protein kinase/mammalian target of rapamycin (AMPK/mTOR) signaling pathway in GBM 8401 cells. Elucidation of the molecular mechanism of PEITC in GBM 8401 cells in vitro may provide a potential therapeutic approach for glioblastoma in the future. - Source: PubMed
Publication date: 2026/07/26
Peng Shu-FenLiu Hsin-ChungChueh Fu-ShinLee Hsu-TungHsu Sheng-YaoChen Jaw-ChyunChung Jing-GungChou Yu-Cheng