Ask about this productRelated genes to: PDRG1 antibody
- 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 antibody
Related articles to: PDRG1 antibody
- 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 - p53 AND DNA DAMAGE-REGULATED GENE1 (PDRG1) is part of the prefoldin-like complex (PFDLc) in plants and animals. Whether PDRG1 acts primarily as a subunit of PFDLc or as an independent subunit is not known in any eukaryote. Here, we show that impairment of PDRG1 activity in Arabidopsis thaliana leads to embryonic lethality, as is the case for the other prefoldin-like proteins UXT and AtURI. The subunits of PFDLc are the main interactors of PDRG1 in vivo, and the interactomes of PDRG1, UXT, and AtURI show strong overlaps, including subunits of nuclear RNA polymerases and various complexes of the spliceosome. Our results show that PDRG1 plays an essential role in Arabidopsis mainly as a subunit of PFDLc. - Source: PubMed
Publication date: 2025/03/03
Hernández-Villa LauraPalacios-Abella AlbertoGómez-Mínguez YaizaCostigliolo-Rojas CeciliaMinguet Eugenio GAlabadí David - Angiopoietin-1 (Ang-1) and its receptor Tie-2 promote vascular integrity and angiogenesis. MicroRNAs (miRNAs) are involved in the regulation of many cellular functions, including endothelial cell (EC) survival, proliferation, and differentiation. Several reports indicate that these effects of miRNAs on EC functions are mediated through the modulation of angiogenesis factor signaling including that of vascular endothelial growth factor (VEGF). To date, very little is known about the roles played by miRNAs in the signaling and angiogenesis promoted by the Ang-1-Tie-2 receptor axis. Our high-throughput screening of miRNAs regulated by Ang-1 exposure in human umbilical vein endothelial cells (HUVECs) has identified miR-1233-3p as a mature miRNA whose cellular levels are significantly downregulated in response to Ang-1 exposure. The expression of miR-1233-3p in these cells is also downregulated by other angiogenesis factors including VEGF, fibroblast growth factor 2 (FGF-2), transforming growth factor β (TGFβ), and angiopoietin-2 (Ang-2). The overexpression of miR-1233-3p in HUVECs using specific mimics significantly attenuated cell survival, migration, and capillary-like tube formation, and promoted apoptosis. Moreover, miR-1233-3p overexpression resulted in reversal of the anti-apoptotic, pro-migration, and pro-differentiation effects of Ang-1. Biotinylated miRNA pull-down assays showed that p53 and DNA damage-regulated 1 (PDRG1) is a direct target of miR-1233-3p in HUVECs. The exposure of HUVECs to Ang-1, angiopoietin-2 (Ang-2), fibroblast growth factor 2 (FGF2), vascular endothelial growth factor (VEGF), or transforming growth factor β (TGFβ) triggers the regulation of PDRG1 expression. This study highlights that miR-1233-3p exerts inhibitory effects on Ang-1-induced survival, migration, and the differentiation of cultured ECs. - Source: PubMed
Publication date: 2025/01/08
Sanchez VeronicaHarel SharonSa'ub Anas KhalidMayaki DominiqueHussain Sabah N A - To reveal the prognostic role of unfolded protein response (UPR) -related genes in hepatocellular carcinoma (HCC). - Source: PubMed
Zhang ShuqiaoLi XinyuZheng YiluHu HaoLiu JiahuiZhang ShijunTang ChunzhiMo ZhuomaoKuang Weihong