p70S6 Kinase antibody
- Known as:
- p70S6 Kinase (anti-)
- Catalog number:
- 20r-2347
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- p70S6 Kinase antibody
Related genes to: p70S6 Kinase antibody
- Gene:
- RPS6KB2 NIH gene
- Name:
- ribosomal protein S6 kinase B2
- Previous symbol:
- -
- Synonyms:
- p70S6Kb, P70-BETA, STK14B, KLS, S6KB, S6Kbeta, S6Kβ
- Chromosome:
- 11q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-07-13
- Date modifiied:
- 2018-04-18
Related products to: p70S6 Kinase antibody
Related articles to: p70S6 Kinase antibody
- Tire and Road Wear Particles (TRWP) are pervasive environmental contaminants, yet the molecular mechanisms linking their toxic derivative, 6PPD-quinone (6PPD-Q), to bladder cancer (BLCA) progression remain obscure. This study integrates network toxicology with experimental validation to elucidate this complex pathogenicity. We screened six representative TRWP compounds and utilized a comprehensive machine learning framework involving 113 model combinations, identifying the Gradient Boosting Machine (GBM) as the optimal classifier. Crucially, SHAP interpretability analysis revealed RPS6KB2 (S6K2) as a pivotal risk driver, while molecular docking demonstrated that 6PPD-Q exhibits superior binding affinity (Binding energy = -7.405 kcal/mol) to S6K2 compared to its parent compound. In vitro assays confirmed that S6K2 is upregulated in BLCA and essential for malignancy. Exposure of BLCA cells to 6PPD-Q dose-dependently upregulated S6K2, significantly (p < 0.05) promoting proliferation, migration, and invasion as evidenced by EdU and Transwell assays. Notably, S6K2 silencing effectively reversed these 6PPD-Q-induced malignant phenotypes. These findings provide the first evidence that 6PPD-Q drives BLCA progression via the specific upregulation of S6K2, offering a novel theoretical basis for assessing the health risks of TRWP exposure. - Source: PubMed
Publication date: 2026/04/10
Wang JirongLu MengQi NienieZhang MengLi ZixiangLi HailongWang Junqi - TNIK (Traf2- and Nck-interacting kinase) is a serine/threonine kinase that plays a crucial role in cytoskeletal organization, Wnt pathway activation, and cancer progression. Recent studies have implicated the role of TNIK in oncogenic signaling pathways and neuropsychiatric regulation. However, the phosphosignaling dynamics of TNIK remain largely unknown. - Source: PubMed
Publication date: 2026/03/13
Sheela AkhilaSubair SuhailUmmar SamseeraMahin AlthafGopalakrishnan Athira PerunellyRaju RajeshSoman Sowmya - To investigate whether the novel proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitor Inclisiran exerts protective effects on the kidneys under high-glucose conditions, and to predict whether its mechanism involves the transforming growth factor-β (TGF-β) pathway using proteomic techniques, while constructing its regulatory network. - Source: PubMed
Li HongqianChen BoXiang XinQi LingZhang DongmeiTang YuhanZhang LilingOu SantaoXue LingWu Weihua - Our laboratory recently identified a novel long noncoding RNA termed CyKILR that has two splice variants with distinct cellular localizations and opposing roles in tumorigenesis. The cytoplasmic variant, CyKILRb (exon 3 exclusion), promotes tumorigenesis, whereas the nuclear variant, CyKILRa (exon 3 inclusion), functions as a tumor suppressor. In this study, the molecular mechanism of the tumorigenic role of CyKILRb was characterized. Specifically, deep RNA sequencing analysis revealed that CyKILRb regulated the PI K/AKT signaling pathway to block downstream tumor suppressors. In particular, downregulation of CyKILRb induced the loss of PIK3R2, an activator of PI K, as well as RPS6KB2 and GNB2, two implicated tumor promotors, with a concomitant increase in the tumor suppressors, CDKN1A (p21) and CDKN1B (p27). In contrast, CyKILRb ectopic expression produced the opposite effect, and suppression of either PIK3R2, PI K or AKT attenuated CyKILRb-induced cell proliferation and clonogenic survival. CyKILRb negatively regulated CyKILRa expression, which was blocked by inhibition of either PI K or AKT. PIK3R2 ectopic expression overcame the cellular effects of CyKILRb downregulation, but not PI K or AKT inhibition orienting the signaling pathway from CyKILRb→↑PIK3R2→PI3K→AKT→↓CyKILRa→enhanced oncogenicity. These findings highlight the critical role of CyKILRb in tumorigenesis and define a novel feed-forward regulatory mechanism linked to alternative RNA splicing. - Source: PubMed
Publication date: 2025/10/14
Xie XiujieMacknight H PatrickLu Amy LChalfant Charles E - B-cell non-Hodgkin lymphoma (B-NHL) is a diverse group of aggressive lymphoid malignancies characterized by its molecular complexity. This study investigated the role of the upstream stimulatory factor 1 (USF1)-ribosomal protein S6 kinase B2 (RPS6KB2) axis in B-NHL progression through the AKT/HDM2 (also known as MDM2)/p53 signaling pathway. Using data from the GEO database, RPS6KB2 was identified to be overexpressed in B-NHL, which was confirmed by RT-qPCR, immunohistochemistry, and western blotting in both B-NHL tissues and cell lines. Functional studies revealed that RPS6KB2 knockdown reduced cell proliferation, migration, and tumor growth, while promoting apoptosis, effects that could be reversed by the AKT activator SC79. Bioinformatics analysis showed that USF1 activated the transcription of RPS6KB2 by directly binding to its promoter region. USF1 downregulation inhibited B-NHL progression, which was rescued by RPS6KB2 overexpression. These findings suggest that the USF1-RPS6KB2 axis contributes to B-NHL progression by activating the AKT/HDM2/p53 pathway. - Source: PubMed
Publication date: 2025/08/31
Liu ZhaoyuSong XiangLiu ZhuangHe XiaoyuGao HongLiu Xunru