RICTOR & AKT1 Protein Protein Interaction Antibody Pair
- Known as:
- RICTOR & AKT1 Protein Protein Interaction Antibody Pair
- Catalog number:
- DI0520
- Product Quantity:
- 1 Set
- Category:
- -
- Supplier:
- Abno
- Gene target:
- RICTOR & AKT1 Protein Interaction Antibody Pair
Related genes to: RICTOR & AKT1 Protein Protein Interaction Antibody Pair
- 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
- 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 & AKT1 Protein Protein Interaction Antibody Pair
Related articles to: RICTOR & AKT1 Protein Protein Interaction Antibody Pair
- 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 - Benzo[a]pyrene (B[a]P) is a typical environmental persistent organic pollutant and a known nephrotoxicant. However, its toxicological profile under short-term, high-dose exposure conditions remains incompletely characterized. To address this, we established a C57BL/6J mouse model in which a single oral dose of 50 mg/kg B[a]P was administered. The results showed that time-dependent renal injury following Bla]P exposure. Within 3 days serum creatinine (Scr) and blood urea nitrogen (BUN) levels increased significantly (P < 0.05), coinciding with elevated renal malondialdehyde (MDA) content. Concurrently, superoxide dismutase (SOD) and catalase (CAT) activities, as well as total antioxidant capacity (T-AOC) were markedly reduced (P < 0.05). By days 7-14 days, the pathological changes shifted to inflammation and apoptosis, evidenced by upregulated TNF-α, IL-6, and caspase-3 at both gene and protein levels, alongside elevated nitric oxide synthase (NOS) and lactate dehydrogenase (LDH) activities (P < 0.05). While the Rictor/mTORC2 pathway regulates renal pathology, its role in B[a]P-induced injury remains unelucidated. Our study found that B[a]P exposure (7-14 days) significantly upregulated key components of and its downstream effectors (AKT1 and PKC-ζ) at both transcriptional levels (P < 0.05). Mechanistic studies in macrophage-specific Rictor knockout mice (Mac Rictor-/-) showed that, inhibiting Rictor/mTORC2 suppressed B[a]P-induced renal oxidative stress, inflammatory factor release, and apoptosis. This study first revealed that the Rictor/mTORC2 pathway serves as a potential molecular therapeutic target for B[a]P-induced kidney injury. - Source: PubMed
Publication date: 2025/12/24
Han Jian-QiuQu YingZhu Yuan-RongQi Ya-LeiLiu Teng-FeiLi Yong-MeiZhang Yan-JiaTan JuanHan Hong-HuiMa Xue-Yun - Colorectal cancer (CRC) progression is driven by aberrant activation of oncogenic pathways, including AKT1, which requires mTORC2-mediated phosphorylation at Ser473. This study identifies PHLDB3 and Liprin-α1 as key regulators of RICTOR-dependent, mTORC2-mediated AKT1 signaling, independently of p53. PHLDB3 interacts with RICTOR to enhance AKT1 phosphorylation and promote tumor progression. In p53-null CRC cells, PHLDB3 knockdown reduces AKT1 activation, whereas PHLDB3 overexpression increases it. Liprin-α1 stabilizes PHLDB3 by limiting its proteasomal degradation, thereby maintaining mTORC2 activity. Liprin-α1 depletion lowers PHLDB3 levels and impairs AKT1 signaling, whereas Liprin-α1 overexpression boosts PHLDB3-mediated AKT1 activation and CRC cell proliferation. Importantly, the Liprin-α1-PHLDB3 axis depends on RICTOR, underscoring a hierarchical regulation essential for AKT1 activation. PHLDB3 is significantly overexpressed in CRC and is associated with poor prognosis. These findings reveal a Liprin-α1-PHLDB3-mTORC2-AKT1 signaling pathway important for CRC growth and present this pathway as a promising therapeutic target in CRC. - Source: PubMed
Publication date: 2025/12/16
Ko Hyun MinCao BoLi LiPark Hee-WonZeng Shelya XLu Hua - High-grade serous ovarian cancer (HGSOC) diagnosed at stage IVB typically carries a poor prognosis. Here, we describe a rare case of with an exceptional and sustained response to therapy. To explore potential drivers of this favorable outcome, we combined clinical evaluation with molecular profiling of liquid biopsy samples. - Source: PubMed
Publication date: 2025/11/24
Wolańska MartynaSieczczyński MichałPastuszak KrzysztofSamelak-Czajka AnnaJackowiak PaulinaBednarz-Knoll NataliaŁapińska-Szumczyk SylwiaKlasa-Mazurkiewicz DagmaraŻaczek Anna JSupernat Anna - : The mTOR serine/threonine kinase coordinates protein translation, cell growth, and metabolism, and its dysregulation promotes tumorigenesis. We present a reproducible, pan-cancer, network-aware framework that integrates curated resources with genomics to move beyond pathway curation, yielding falsifiable hypotheses and prioritized candidates for mTOR axis biomarker validation. : We assembled -related genes and interactions from GeneCards, KEGG, STRING, UniProt, and PathCards and harmonized identifiers. We formulated a concise working model linking genotype → pathway architecture (mTORC1/2) → expression-level rewiring → phenotype. Three analyses operationalized this model: (i) pan-cancer alteration mapping to separate widely shared drivers from tumor-specific nodes; (ii) expression-based activity scoring to quantify translational/nutrient-sensing modules; and (iii) topology-aware network propagation (personalized PageRank/Random Walk with Restart on a high-confidence STRING graph) to nominate functionally proximal neighbors. Reproducibility was supported by degree-normalized diffusion, predefined statistical thresholds, and sensitivity analyses. : Gene ontology analysis demonstrated significant enrichment for mTOR-related processes (TOR/TORC1 signaling and cellular responses to amino acids). Database synthesis corroborated disease associations involving MTOR and its partners (e.g., , , , , across selected carcinomas). Across cohorts, our framework distinguishes broadly shared upstream drivers (, ) from lineage-enriched nodes (e.g., RICTOR-linked components) and prioritizes non-mutated, network-proximal candidates that align with mTOR activity signatures. : This study delivers a transparent, pan-cancer framework that unifies curated biology, genomics, and network topology to produce testable predictions about the mTOR axis. By distinguishing shared drivers from tumor-specific nodes and elevating non-mutated, topology-inferred candidates, the approach refines biomarker discovery and suggests architecture-aware therapeutic strategies. The analysis is reproducible and extensible, supporting prospective validation of prioritized candidates and the design of correlative studies that align pathway activity with clinical response. - Source: PubMed
Publication date: 2025/10/24
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