PDRG1 Over-expression Lysate Product
- Known as:
- PDRG1 Over-expression Lysate Product
- Catalog number:
- GWB-FFF430
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- GenWay
- Gene target:
- PDRG1 Over-expression Lysate Product
Related genes to: PDRG1 Over-expression Lysate Product
- Gene:
- PDRG1 NIH gene
- Name:
- p53 and DNA damage regulated 1
- Previous symbol:
- C20orf126
- Synonyms:
- dJ310O13.3
- Chromosome:
- 20q11.21
- Locus Type:
- gene with protein product
- Date approved:
- 2001-07-17
- Date modifiied:
- 2015-11-16
Related products to: PDRG1 Over-expression Lysate Product
(META) Human Metapneumovirus Type 16 (A1) Lysate(META) Human Metapneumovirus Type 18 (B2) Lysate(META) Human Metapneumovirus Type 20 (A2) Lysate(META) Human Metapneumovirus Type 27 (A2) Lysate(META) Human Metapneumovirus Type 3 (B1) Lysate(META) Human Metapneumovirus Type 4 (B2) Lysate(META) Human Metapneumovirus Type 5 (B1) Lysate(META) Human Metapneumovirus Type 8 (B2) Lysate(META) Human Metapneumovirus Type 9 (A1) Lysate0 day neonate eyeball cDNA. RIKEN full-length enriched library. clone E130107M17 product hypothetical protein. full insert seque - N_A Polyclonal0 day neonate head cDNA. RIKEN full-length enriched library. clone 4831434J02 product nuclear factor of activated T-cells. cytop - N_A Polyclonal0 day neonate head cDNA. RIKEN full-length enriched library. clone 4832421E02 product myocyte enhancer factor 2C. full insert se - N_A Polyclonal1,2,3,4-Tetrahydro-1,2-dimethyl-4,6-isoquinolinediol
(Major Product) CAS: 102830-16-0 Formula: C11H15NO21,2,3,4-tetrahydro-1,2-dimethyl-4,8-isoquinolinediol
(Minor Product) CAS: 102830-20-6 Formula: C11H15NO210 days embryo whole body cDNA. RIKEN full-length enriched library. clone 2610510L15 product poly(A)-specific ribonuclease (dead - N_A Polyclonal Related articles to: PDRG1 Over-expression Lysate Product
- The contribution of post-transcriptional regulation remains largely unexplored in thyrotropin-secreting pituitary tumors (TSHomas), a rare endocrine pathology responsible for inappropriate TSH secretion and central hyperthyroidism. We investigated the TSHoma post-transcriptional regulatory landscape by analyzing components of molecular machineries controlling RNA metabolism [spliceosome/RNA-exosome/nonsense-mediated decay (NMD)], their associations with clinical parameters, and the impact of their pharmacological inhibition in TSHoma cells. A drastic dysregulation of multiple components of spliceosome [spliceosome (/) and splicing factors (e.g., // …)], RNA-Exosome (e.g., //), and NMD [e.g., , and NMD-canonical targets (/)] was found in TSHomas vs. non-tumor pituitaries with some of these alterations associated with relevant clinical features (e.g., tumor size, TSHB/fT4-levels). Moreover, we demonstrate a clear antiproliferative action of spliceosome/RNA-Exosome/NMD inhibitors in primary patient-derived TSHoma cells. Overall, a clinically relevant spliceosome/RNA-Exosome/NMD-associated molecular dysregulation and antiproliferative actions of these machineries' inhibition are demonstrated in TSHomas, highlighting a potential source of novel diagnostic/prognostic biomarkers and therapeutic tools in TSHomas. - Source: PubMed
Publication date: 2026/08/06
G-García Miguel EFlores-Martínez ÁlvaroArroyo-Millán LauraVenegas EvaDiaz-Perdigones Cristina MMaraver SilviaCano DavidArráez CintaArráez Miguel AJapón Miguel AMartínez-Fuentes Antonio JSoto-Moreno AlfonsoFuentes-Fayos Antonio CHerrera-Martínez Aura DLuque Raúl M - The Angiopoietin-1 (Ang-1)/Tie-2 signaling axis is critical for embryonic vascular development and maintaining quiescent vasculature in adults. We recently demonstrated that Ang-1 exposure for 24 h significantly downregulates miR-1233-3p expression in endothelial cells (ECs) and that PDRG1 (P53 and DNA Damage Regulated 1) is a direct target of miR-1233-3p. However, the role of PDRG1 in Ang-1-mediated angiogenesis and the mechanisms by which PDRG1 regulates EC function remain unclear. In this study, we reveal that PDRG1 significantly enhances key angiogenic processes, including EC survival, migration, proliferation, and capillary-like tube formation, while also inhibiting Caspase-3 activity. Immunoprecipitation and mass spectrometry analyses identified multiple PDRG1-interacting proteins, including TSC2, a regulator of the mammalian target of rapamycin (mTOR) pathway. Notably, this interaction occurs not only in ECs but also in other cell types. Overexpression of PDRG1 was found to activate mTOR complex 1 (mTORC1), as evidenced by increased phosphorylation of downstream targets P70S6K and 4E-BP1. Conversely, inhibiting mTORC1 activity suppressed PDRG1-mediated effects on mTORC1 activation, EC migration, capillary-like tube formation, and proliferation. Based on these findings and our previous observation that the Ang-1/Tie-2 axis regulates miR-1233-3p expression, we propose a model in which Ang-1/Tie-2 signaling promotes angiogenesis by downregulating miR-1233-3p. This downregulation leads to increased PDRG1 expression and enhanced interaction with TSC2, ultimately alleviating the inhibitory effects of the TSC1-TSC2 complex on mTORC1 activity. - Source: PubMed
Publication date: 2026/07/08
Sanchez VeronicaMayaki DominiqueHussain Sabah Na - Hepatocellular carcinoma (HCC) remains a lethal malignancy with limited therapeutic targets. P53 and DNA damage-regulated gene 1 (PDRG1) has emerged as an oncogene in multiple cancers, yet its role and regulatory mechanism in HCC remain unclear. Here, we demonstrated that PDRG1 expression was significantly upregulated in HCC tissues compared to normal liver, correlating with advanced tumor stage, higher grade, and poor patient survival. Functionally, PDRG1 knockdown suppressed HCC cell proliferation, migration, and invasion in vitro and inhibited tumor growth and lung metastasis in vivo, whereas PDRG1 overexpression exerted opposite effects. Mechanistically, PDRG1 activated Wnt/β-catenin signaling, elevating levels of β-catenin, c-Myc, and phosphorylated GSK-3β, and the oncogenic effects of PDRG1 were reversed by the Wnt pathway inhibitor XAV939. Furthermore, transcription factor Specificity Protein 1 (SP1) bound directly to the PDRG1 promoter at the E3 site (-1927 to-1917) and activated its transcription. The pro-tumor effects of SP1 were rescued by PDRG1 silencing, indicating that SP1 acts through PDRG1. Collectively, our study identifies SP1 as an upstream transcriptional activator of PDRG1 and defines the SP1/PDRG1/Wnt/β-catenin axis as a key regulatory pathway promoting HCC progression, suggesting its potential as a prognostic biomarker and therapeutic target. - Source: PubMed
Publication date: 2026/06/05
Zhao XudongLv ShihuaWang HaikuanLu ZeyiKang PengchengLi JinglinYu LiangMa ShihuiHua ChangxingYou JunqiGe ZiqiangXu YiCui Yunfu - Hepatocellular carcinoma (HCC) remains a major global health burden with limited therapeutic options and poor prognosis. PDRG1 is upregulated in several malignancies, yet its clinical relevance and mechanistic role in HCC are not fully understood. Here, we investigated the contribution of PDRG1 to HCC progression and delineated the underlying molecular mechanism. Using public datasets, patient specimens, functional assays, and subcutaneous xenograft models, we evaluated PDRG1 expression, biological functions, and downstream pathways. Transcriptome profiling, pathway enrichment analysis, rescue experiments, co-immunoprecipitation, and ChIP-qPCR were performed to define the PDRG1-EZH2-p21 axis. PDRG1 was significantly upregulated in HCC tumor tissues compared with adjacent non-tumor liver tissues and was associated with worse patient survival. Functionally, PDRG1 enhanced HCC cell proliferation, migration, invasion, colony formation, and tumor growth . RNA-seq and enrichment analyses identified cellular senescence as a prominent downstream program regulated by PDRG1. Mechanistically, PDRG1 directly interacted with EZH2, increased H3K27me3 enrichment at the p21 promoter, and suppressed p21 transcription. Restoration of p21 expression attenuated the oncogenic effects of PDRG1, whereas EZH2 overexpression rescued the impaired malignant phenotypes caused by PDRG1 knockdown. Domain-mapping further indicated that the N-terminal residues 36-70 of PDRG1 contribute to its interaction with EZH2. Collectively, our findings identify PDRG1 as a clinically relevant oncogene in HCC and reveal an epigenetic mechanism by which PDRG1 cooperates with EZH2 to repress p21 and bypass senescence. The PDRG1-EZH2-p21 axis may represent a potential biomarker and therapeutic target for HCC. - Source: PubMed
Publication date: 2026/02/18
Yang QiangZhang LilongLi WeiZhang ZhengleTao JingRong YupingWang Weixing - Morphological hip abnormalities (MHAs) significantly influence lifelong prognosis of the hip, contributing to early-onset osteoarthritis and impaired functionality. Developmental dysplasia of the hip (DDH) and femoroacetabular impingement (FAI) represent key pathologies, resulting from insufficient or excessive femoral head coverage, respectively. These abnormalities alter hip biomechanics, leading to structural damage, pain, and accelerated joint degeneration. Advances in genetic research have illuminated the interplay between genetics and mechanical loading in shaping hip morphology. Genes associated with osteoarthritis, DDH, and FAI include , and . Genes associated with FAI and osteoarthritis include . Genes associated with DDH and osteoarthritis include , , and . The mechanisms linking morphological derangements to symptomatic osteoarthritis remain incompletely understood. Multimodal approaches integrating imaging, biomechanics, and genetics may uncover distinct disease subtypes, enabling personalized interventions. Early detection of MHAs is critical in preventing early-onset osteoarthritis. Incorporating advanced imaging techniques, such as statistical shape modelling, can enhance the understanding of complex 3D hip morphologies and their progression to osteoarthritis. Future research should explore the genetic underpinnings of other morphologic hip conditions, including Slipped Capital Femoral Epiphysis and Legg-Calvé-Perthes disease, to refine preventive and therapeutic strategies. A comprehensive approach combining genetics, imaging, and clinical insights holds promise for mitigating the lifelong impact of MHAs. - Source: PubMed
Publication date: 2025/04/18
Bukowiec Lainey GKaji Elizabeth SKoch John ASaniei SamiGirod-Hoffmann Miguel MSinnwell Jason PWyles Cody C