PDPK1 antibody - middle region (ARP30313_P050)
- Known as:
- PDPK1 (anti-) - middle region (ARP30313_P050)
- Catalog number:
- arp30313_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- PDPK1 antibody - middle region (ARP30313_P050)
Related genes to: PDPK1 antibody - middle region (ARP30313_P050)
- 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 antibody - middle region (ARP30313_P050)
Related articles to: PDPK1 antibody - middle region (ARP30313_P050)
- Prostate cancer (PCa) is the second most common cancer in men and shows high inter- and intra-patient heterogeneity. Consequently, treatment options are limited and there is a lack of representative preclinical models. Here, we establish a comprehensive biobank of murine organoids and tumoroids that reflect common patient mutations. We demonstrate that the deletion of Pten alone, or in combination with Stat3, or Tp53, drives the activation of cancer-related pathways in both prostate organoids and tumor-derived tumoroids. A medium-throughput drug screen identified two potent compounds, the PDPK1/AKT/FLT dual pathway inhibitor and the sirtuin inhibitor tenovin-6, which effectively suppressed tumoroid proliferation. Notably, these compounds also inhibited the growth of several human PCa cell lines and displayed synergistic effects when combined with the standard-of-care antiandrogen enzalutamide. Together, our findings provide evidence that murine tumoroids are versatile preclinical models for studying PCa tumorigenesis and drug sensitivities to develop therapeutic options for PCa patients. - Source: PubMed
Publication date: 2026/03/30
Kalla JessicaDillinger ThomasPavlovicova ZlataJacob ReemaAtas EmineMišura KatarinaBaskan AnilDraganić KristinaTiefenbacher AndreasLimberger TanjaMair TheresiaWasinger GabrielVillanti LudovicaKubicek StefanKenner LukasEgger Gerda - - Source: PubMed
Publication date: 2026/03/20
Shao HuapingXu KanLiu Yi - PTEN hamartoma tumor syndrome (PHTS), caused by germline PTEN variants, exhibits marked phenotypic heterogeneity, most notably cancer, neurodevelopmental disorders (NDD), or both. The basis for this divergence, even among carriers of identical PTEN variants, remains poorly defined. We performed whole-genome sequencing of 599 individuals with PHTS and family members, complemented by analyses of PTEN variant carriers from the All of Us Research Program. Analyses included both targeted evaluation of genes previously implicated in cancer and NDD and agnostic genome-wide single-variant and rare-variant burden testing. The analytic cohort comprised 543 PHTS probands, including individuals with NDD (n = 171), cancer (n = 221), both phenotypes (n = 21), or neither (n = 130) at the time of enrollment. Pathogenic or likely pathogenic variants in cancer-associated genes were identified in 37 (6.8%), most frequently in MITF, DICER1, and BRCA2, while 43 (7.9%) harbored variants in NDD-related genes, including DHCR7, POLG, and ARSA. Such secondary variants were less common in PTEN variant carriers in All of Us. Genome-wide analyses identified candidate modifier loci functionally linked to PTEN, including in ZNF713, TPTE2P1, and PDPK1. These findings demonstrate that PHTS phenotypes are shaped by complex gene-gene interactions beyond PTEN alone, informing mechanisms underlying the cancer-NDD dichotomy and advancing precision risk stratification. - Source: PubMed
Publication date: 2026/03/17
Yehia LamisLi LinIdumah GideonFrazier Thomas WMakarov VladimirBose AritraParida LaxmiHardan AntonioMartinez-Agosto Julian ARitter David MSahin MustafaEng CharisNi Ying - MicroRNAs (miRNAs) have been verified to be involved in various biological processes through regulating their target genes, and some previous studies have revealed the antitumour role of microRNA-374b-5p (miR-374b-5p) in several tumours. Therefore, the purpose of this study was to explore the functions and potential mechanisms of miR-374b-5p in osteosarcoma (OS) progression. - Source: PubMed
Publication date: 2026/01/26
Xi YongSun ZhengyiWu JingbinRen YongxinZhou Dong - The phosphatidylinositol 3-kinase (PI3K) gene family plays a crucial role in key biological processes such as cell signal transduction, inflammatory response, metabolism and cell movement. Although its function in mammals, especially the mutation association in cancer, has been widely studied, the immune function of this family in teleosts, particularly the important economic fish species large yellow croaker, remains unclear. This study systematically identified 18 pi3k genes in the genome of large yellow croaker. Phylogenetic analysis indicated that this family had a high degree of evolutionary conservation among teleosts. Expression analyses revealed that multiple pi3k genes exhibited significant changes in expression levels under conditions of infection with Pseudomonas plecoglossicida and hypoxic stress, indicating that these genes might play pivotal roles in immune function and stress regulation. Protein-protein interaction network analysis further elucidated that PI3K members extensively interacted with key immune signaling molecules such as PDPK1, MTOR, and PTEN, and were enriched in various innate immune-related pathways. Notably, Lcpik3r3b was significantly up-regulated following both acute hypoxia exposure and P. plecoglossicida infection, and was predicted to occupy a central hub in the signaling network. Based on these observations, we further conducted functional verification on Lcpik3r3b and discovered that its recombinant protein could significantly inhibit the proliferation of E. coli. These results would provide valuable insights into the roles of the PI3K family in mediating immune and stress responses in large yellow croaker, and laid a foundation for future investigations into their molecular mechanisms as well as potential applications in aquaculture disease management. - Source: PubMed
Publication date: 2026/02/07
Lu ChenpengHan PingXue YadongLiu XiumeiChen JianmingWang Xubo