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
- Tumour-associated macrophages (TAMs) exert a pivotal function in tumour progression, and M2-type TAMs are closely linked to tumour-promoting functions. Mechanistic target of rapamycin complex 2 (mTORC2) may mediate TAM polarization and subsequent tumour development, yet their roles in liposarcoma (LPS) remain unclear. Macrophage polarization was assessed via flow cytometry for CD206. Western blot for Arg-1, Rictor, PPAR-γ, CD36, ACSL1 and CPT2, qPCR for IL-10, Arg-1 and Ym1, and ELISA for IL-10 secretion. Fatty acid metabolism was evaluated using free fatty acid (FFA) uptake assays and Oil Red O staining for intracellular lipid droplets. A Transwell assay was established to assess the effect of treated macrophages on LPS cell biology, and EdU assays were used for proliferation assessment. Transwell migration and invasion assays were utilized for assessing cellular motility. IL-4 induced RAW264.7 macrophages to undergo M2 polarization, characterized by upregulated CD206, Arg-1, and IL-10. During this process, mTORC2 was activated, promoting FFA uptake, lipid droplet accumulation, and fatty acid oxidation via the PPAR-γ/CD36 axis. Co-culture experiments showed that IL-4-polarized M2 macrophages enhanced LPS cell proliferation, migration, and invasion; these effects were inhibited by JR-AB2-011 and restored by LPA, confirming mTORC2-PPAR-γ/CD36-mediated TAMs drive LPS progression. mTORC2 regulates M2 TAM polarization and metabolic reprogramming via the PPAR-γ/CD36 pathway, thereby promoting LPS cell proliferation, migration, and invasion. - Source: PubMed
Publication date: 2026/04/29
Xiao WeihuaSheng JingdanLiu ChunjiaoLi JunqiangShu PengJiang MaofenWang MinHe JiMa HaifenDing Yaxin - Metformin, a widely used biguanide for the treatment of type 2 diabetes, has been extensively studied for its potential anti-cancer properties, primarily attributed to its inhibitory effects on mTORC1 signaling. However, accumulating evidence suggests that its impact on tumor progression is highly context-dependent, varying with cellular and metabolic conditions. In this study, we investigated the mechanistic effects of metformin on RUNX2 and mTORC2 signaling pathways in breast cancer. - Source: PubMed
Publication date: 2026/04/10
Gayatri Meher BolisettiBehera AbhayanandaChava SureshVyakaranam PreetiVenkatraman GaneshRayala Suresh KumarReddy Aramati Bindu Madhava - Acute myeloid leukemia (AML) is a highly lethal hematologic malignancy, and reliable prognostic biomarkers remain urgently needed. We investigated the expression and clinical relevance of the actin cytoskeleton regulator N-WASP in AML. Analysis of TCGA data revealed significantly reduced N-WASP expression in AML compared with normal tissues, and low expression was associated with adverse clinical features, including FAB-M1/M4 subtypes, DNMT3A mutations, and cytogenetic abnormalities such as t(8;21)/RUNX1::RUNX1T1 and del(7q). Patients with low N-WASP expression exhibited shorter overall survival, and multivariate Cox regression identified N-WASP reduction as an independent risk factor, alongside advanced age and FLT3, DNMT3A and TP53 mutations. Co-expression and enrichment analysis highlighted FNIP1, CLIP1, RICTOR and BRAF as N-WASP-associated regulators converging on mTOR signaling. Experimental validation via RT-qPCR and western blotting in AML bone marrow samples and cell lines confirmed the downregulation of N-WASP and key co-expressed genes. Collectively, these results demonstrate that N-WASP is suppressed in AML and is closely associated with disease risk and clinical outcome. N-WASP may serve as a novel prognostic biomarker and potential therapeutic target warranting further investigation. - Source: PubMed
Publication date: 2026/04/22
Liu CuiSun JianLuo YanHuang PeiChen Yan - Herpes simplex virus 1 (HSV-1) infection contributes to immunopathogenic diseases and lacks an effective vaccine. Improving antigen presentation is key to better vaccine strategies and more robust immune responses. Here, we show that optineurin (OPTN), an autophagy receptor traditionally involved in protein recycling, unexpectedly stabilizes RICTOR (mechanistic target of rapamycin complex 2 [mTORC2]), a crucial step in enhancing MHC class II surface expression in dendritic cells. OPTN regulates the AKT/mTOR/signal transducer and activator of transcription 3 (STAT3) pathway, with the AKT2 isoform playing a central role. Using single-cell RNA sequencing (scRNA-seq) and transgenic mouse models, we identify the mechanistic details of this pathway. Dysregulation impairs antigen presentation, weakening immunity and vaccine efficacy. Our findings uncover a previously unknown function of OPTN and highlight its role in coordinating innate and adaptive immune defenses, with implications for vaccine development and immune response modulation in HSV-1 and other viral and bacterial diseases. - Source: PubMed
Publication date: 2026/04/16
Kadam RashmiPatil ChandrashekharFeferman LeonidMaienschein-Cline MarkChlipala GeorgeBorole PiyushBhattacharya IlinaOrameh ChimaNyugen TaraTseng HenryShukla Deepak - Loss-of-function mutations in KCNJ10, encoding Kir4.1, cause EAST/SeSAME syndrome, with renal salt-wasting tubulopathy and hypokalemia. We hypothesized that Kir4.1 deletion specifically in the distal convoluted tubule (DCT) stimulates ENaC activity via the mammalian target of rapamycin (mTOR)-dependent mechanisms, contributing to hypokalemia. - Source: PubMed
Gao Zhong-XiuziYang Yuan-YuanZhang Rui-JuanLi Fei-HongMu Ya-FanShu Ting-TingMao Zi-HuiZhang QingPan Shao-KangLiu Dong-WeiLiu Zhang-SuoWu Peng