PDPK1 pTyr9 antibody Ab
- Known as:
- PDPK1 pTyr9 (anti-) Antibody
- Catalog number:
- 1488109
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Acris antibodies
- Gene target:
- PDPK1 pTyr9 antibody
Related genes to: PDPK1 pTyr9 antibody Ab
- Gene:
- PDPK1 NIH gene
- Name:
- 3-phosphoinositide dependent protein kinase 1
- Previous symbol:
- -
- Synonyms:
- PDK1
- Chromosome:
- 16p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-03-23
- Date modifiied:
- 2015-08-25
Related products to: PDPK1 pTyr9 antibody Ab
Related articles to: PDPK1 pTyr9 antibody Ab
- Non-small cell lung cancer (NSCLC) is the predominant subtype of lung malignancy. Accumulating epidemiological evidence demonstrates that environmental lead (Pb) exposure as a critical driver of its initiation and progression. - Source: PubMed
Publication date: 2026/07/30
Xu YinlanDong JieLiu HejunZheng JinmeiGuo HaonanChen YueWang JialinWu Weidong - B-cell lymphomas (BCLs) are the most prevalent group of hematologic cancers, encompassing various subtypes, each with a distinct clinical course shaped by cell of origin, genetics, and etiology. Recent advances in subtype-specific immunochemotherapy, targeted therapies, and cellular immunotherapy have improved outcomes for BCLs; nonetheless, some cases remain resistant to existing treatments. To address these resistant disease states, especially across multiple subtypes, the development of new universal targeted therapies could be transformative. - Source: PubMed
Publication date: 2026/07/25
Kuroda JunyaTsukamoto TakuShimura Yuji - Excessive or inappropriate radiation can seriously harm organisms. Radiation-induced thymus injury (RITI) is a severe complication driven by dysregulated RNA networks. However, current studies have mostly focused on single non-coding RNAs or late pathological stages, and a complete competing endogenous RNA (ceRNA) regulatory network had not been constructed. The thymus tissues of C57BL/6 mice exposed to 6 Gy X-ray radiation for 24 h were analyzed by RNA-sequencing (RNA-seq) with library construction. We functionally annotated target messenger RNAs (mRNAs) and predicted long non-coding RNA (lncRNA) -targeted microRNAs (miRNAs) and miRNA-targeted mRNAs post-irradiation, to construct the lncRNA-miRNA-mRNA ceRNA regulatory axis. Furthermore, multiple experimental approaches including quantitative real-time PCR (qRT-PCR), western blotting, flow cytometry and CCK-8 cell viability assays were utilized to validate the involvement of the phosphatidylinositol 3-kinase (PI3K)-Protein Kinase B (PKB or AKT) pathway. The results revealed that after irradiation, 6214 mRNAs, 160 miRNAs, and 1999 lncRNAs were significantly upregulated while 2676 mRNAs, 165 miRNAs, and 941 lncRNAs were considerably downregulated. The most significantly altered Gene Ontology (GO) terms were angiogenesis and ameboid cell migration (Biological Process, BP), actin cytoskeleton and cell-cell junctions (Cellular Component, CC), as well as actin binding and phospholipid binding (Molecular Function, MF). A total of 333 cellular functions mediated by phosphatase and tensin homologue deleted on chromosome ten (PTEN) exhibited significant alterations, whereas 175 cellular functions regulated by 3-phosphoinositide-dependent protein kinase 1 (PDPK1) showed substantial changes. Key biological pathways, including cancer-associated pathways, the PI3K-AKT signaling pathway, the human papillomavirus infection pathway, the focal adhesion pathway, the Rap1 signaling pathway, and the cardiomyocyte calcium signaling pathway, were uncovered through Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis. Based on the results of both GO enrichment analysis and KEGG pathway analysis, a consistent conclusion was drawn that RITI was closely associated with the PI3K-AKT signaling pathway. So the PI3K-AKT pathway was selected for experimental validation, which confirmed that it was a key regulatory pathway for thymic degeneration in RITI. A lncRNA-miRNA-mRNA ceRNA axis of RITI was successfully developed in a mouse model after irradiation. The PI3K-AKT pathway contributes to preventing radiation-induced cell death in RITI, and the differentially expressed RNAs in the initial stage of this injury may result in serious consequences. - Source: PubMed
Publication date: 2026/07/16
Wang FeiYu Qing-HuaFan Xin-MingGuo Cun-YangXu Si-GuangZhang Wen-BoXu Ping - Multiple myeloma (MM) is an incurable malignancy of bone marrow plasma cells. Tumor-associated macrophages (TAMs) are the predominant immune cells in the bone marrow microenvironment of MM and play important roles in MM. The effect of RBMS1 on MM has not yet been reported. This study aimed to investigate the function of RBMS1 in MM. Through the analysis of GSE datasets, we identified RBMS1 as a potential pathogenic factor in MM. We further investigated the effects of RBMS1 on the proliferation of MM cells (RPMI8226, MM1S, and KMS11) and its regulation of TAM polarization. An animal model was established by intravenous injection of MM cells into 6-week-old male NOG mice. Bioinformatics analyses, including RRA, WGCNA, and GO enrichment, screened for potential pathogenic genes in MM. Kaplan - Meier survival identified RBMS1 as a prognostic marker associated with poor outcomes in MM. Functionally, RBMS1 enhanced MM cell proliferation, colony formation, and cell cycle. Moreover, RBMS1 promoted M2 polarization of macrophages, as evidenced by elevated levels of M2 macrophage markers, as well as increased CCL2 secretion. Consistently, in a male NOD/Shi-scid IL-2 Rγ mouse xenograft model, RBMS1 accelerated tumor growth and enhanced M2 macrophage polarization. Mechanistically, RBMS1 bound to the 3'UTR of PDPK1 mRNA, enhancing its stability and activating the pro-tumorigenic β-catenin signaling pathway, thereby promoting tumor growth. Collectively, this study is the first to report the functional role of RBMS1 in MM and highlights the importance of the RBMS1/PDPK1/β-catenin signaling axis in MM, providing new insights for basic research on MM. - Source: PubMed
Publication date: 2026/06/11
Liu YanGeng Yue-QiJiang LiLiu Ai-Chun - Colorectal cancer (CRC) is a major cause of cancer mortality worldwide. Here, we identified the antipsychotic drug penfluridol as a potent anticancer agent that induces cuproptosis in CRC through a newly defined signaling mechanism. Using real-world clinical datasets, we demonstrated that PDPK1 is significantly upregulated in CRC and further increases in its expression level are correlated with a worse outcome, whereas CTR1 is downregulated in CRC and further decreases in its expression level are correlated with favourable outcomes, directly establishing the clinical relevance of these two proteins to CRC. Mechanistically, drug affinity responsive target stability assays revealed PDPK1 as a direct binding target of penfluridol. Penfluridol inhibited PDPK1 kinase activity and reduced AKT1 phosphorylation, which in turn decreased CTR1 ubiquitination and stabilized CTR1 on the plasma membrane. Enhanced CTR1 expression promoted intracellular copper influx, leading to copper overload and cuproptosis. Functionally, penfluridol suppressed CRC growth in cell lines, patient-derived organoids, and PDX models and was well-tolerated with limited systemic toxicity. Genetic and pharmacologic modulation confirmed that the PDPK1-p-AKT1-CTR1 axis governs copper homeostasis and mediates penfluridol-induced cell death. Collectively, our findings revealed a previously unrecognized link between oncogenic kinase signaling and copper metabolism, established PDPK1 and CTR1 as clinically relevant biomarkers, and provided a strong rationale for repurposing penfluridol as a dual-function therapeutic that induces cuproptosis and enhances chemosensitivity in colorectal cancer. - Source: PubMed
Publication date: 2026/05/25
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