Ask about this productRelated genes to: PRRG1 Blocking Peptide
- Gene:
- PRRG1 NIH gene
- Name:
- proline rich and Gla domain 1
- Previous symbol:
- -
- Synonyms:
- PRGP1
- Chromosome:
- Xp21.1
- Locus Type:
- gene with protein product
- Date approved:
- 1997-10-16
- Date modifiied:
- 2016-04-27
Related products to: PRRG1 Blocking Peptide
Related articles to: PRRG1 Blocking Peptide
- Transfusion management of Kx- individuals with McLeod phenotype (MLP) is highly challenging, particularly as cryopreservation affects red blood cell (RBC) concentrate quality. We developed a concept to provide non-cryopreserved Kx- RBCs over the complete period of hematopoietic stem cell transplantation (HSCT) for treatment of X-linked chronic granulomatous disease (X-CGD) with MLP. An infant with a large deletion affecting 12 protein-coding genes, including , , , , , and , leading to CGD, Duchenne muscular dystrophy, and MLP, was scheduled for HSCT with the need of Kx- blood supply. No Kx- and RhD compatible donors were identified by rare donor programs, and autologous blood collection was not possible. In an interdisciplinary multicenter effort pre- and post-HSCT blood management, including procurement of non-cryopreserved allogeneic Kx- RBCs from an individual with MLP, was orchestrated, balancing donations, storage, pediatric RBC preparation, and irradiation with the clinical schedule. Our concept ensured compatible blood supply from 100 days prior HSCT to the peritransplant phase. The patient received 5 non-cryopreserved Kx- pediatric RBCs and was discharged with complete chimerism at day +68. The screen was repeatedly negative for antibodies to high frequency RBC antigens. After 2.8 years, the patient remained independent of transfusions and was without signs of graft-versus-host disease. Close coordination between institutions and disciplines and process optimization allow readily available provision of non-cryopreserved Kx- RBCs to support HSCT to a patient with unique contiguous gene deletion syndrome of X chromosome. - Source: PubMed
Publication date: 2025/08/11
Thalhammer JulianEngström CharlotteStrahm BrigitteSpeckmann CarstenYoshimi AyamiScharberg AndreasWeinig ElkePauly Marie-ChristinUmhau MarkusMeyer StefanEhl StephanFrey Beat MSchäfer Richard - In this study, we investigated the expression patterns, biological functions, and molecular mechanisms of Proline-rich γ-carboxylated Gla protein 1 (PRRG1) in pancreatic cancer pathogenesis. Our bioinformatics analysis revealed that PRRG1 expression is markedly upregulated in human PC tissues compared to normal pancreatic tissues, with elevated levels significantly correlating with poor prognosis and advanced histological grade. We verified the high expression of PRRG1 in pancreatic cancer tissue specimens and pancreatic cancer cell lines. Using established PC cell lines (CFPAC-1 and PATU-8988T), we demonstrated that shRNA-mediated PRRG1 silencing effectively suppressed malignant phenotypes, including cell viability, proliferation, migration, and invasion in vitro. Conversely, lentivirus-induced PRRG1 overexpression enhanced these oncogenic behaviors. RNA-sequencing analysis identified the PI3K-Akt signaling pathway as a key downstream effector of PRRG1, with pathway activation status directly correlating with PRRG1 expression levels. Mechanistically, we identified KLF4 as a critical transcription factor binding to the PRRG1 promoter region. In vivo, PRRG1 knockdown inhibited tumor growth and PI3K-Akt activation in subcutaneous xenograft models, while PRRG1 overexpression accelerated tumor progression. Low-dose warfarin (2uM) decreased the levels of PRRG1 and GAS6/AXL axis, markedly suppressed the pro-tumorigenic effects driven by PRRG1 overexpression in vitro and in vivo. Notably, single-cell sequencing analysis revealing high PRRG1 expression specifically in PC epithelial cells. These PRRG1-positive epithelial cells not only exhibited enriched PI3K-Akt signaling activity but also showed significant interactions with macrophages and endothelial cells, which were further validated in immunocompetent models in vivo. However, warfarin effectively reversed the PRRG1 overexpression-driven changes in TME. In conclusion, our findings establish PRRG1 as a key driver of pancreatic cancer progression through PI3K/Akt pathway activation and KLF4-mediated transcriptional regulation. PRRG1 facilitates the establishment of a pro-tumorigenic and immunosuppressive TME in PC. Low-dose warfarin significantly suppressed the pro-tumorigenic effects and the PRRG1 overexpression-driven alterations in the tumor immune microenvironment. - Source: PubMed
Publication date: 2026/05/10
Chen Jia-JieZhu Xiao-RenGu Qian-HuiLiu Yuan-YuanChen Min-Bin - Gestational diabetes mellitus (GDM) is a common pregnancy complication linked to adverse outcomes, highlighting the need for new diagnostic markers. This study aimed to identify oxidative stress-related genes as potential biomarkers for GDM using integrated bioinformatics and experimental validation. - Source: PubMed
Publication date: 2026/03/06
He HaiyuWu Wen - Vitamin K-dependent γ-glutamic acid carboxylation (Gla) proteins are calcium-binding and membrane-associated, participating in coagulation, bone turnover, and cancer biology. The molecular function of transmembrane proline-rich Gla proteins (PRRGs) remains unexplored. - Source: PubMed
Wu ZhengYe QingZhang ShanHu Li-PengWang Xiao-QiYao Lin-LiZhu LeiXiao Shu-YuDuan Zong-HaoZhang Xue-LiJiang Shu-HengZhang Zhi-GangLiu De-JunLi Dong-XueYang Xiao-Mei - Many years and billions spent for research did not yet produce an effective answer to prostate cancer (PCa). Not only each human, but even each cancer nodule in the same tumor, has unique transcriptome topology. The differences go beyond the expression level to the expression control and networking of individual genes. The unrepeatable heterogeneous transcriptomic organization among men makes the quest for universal biomarkers and "fit-for-all" treatments unrealistic. We present a bioinformatics procedure to identify each patient's unique triplet of PCa Gene Master Regulators (GMRs) and predict consequences of their experimental manipulation. The procedure is based on the Genomic Fabric Paradigm (GFP), which characterizes each individual gene by the independent expression level, expression variability and expression coordination with each other gene. GFP can identify the GMRs whose controlled alteration would selectively kill the cancer cells with little consequence on the normal tissue. The method was applied to microarray data on surgically removed prostates from two men with metastatic PCas (each with three distinct cancer nodules), and DU145 and LNCaP PCa cell lines. The applications verified that each PCa case is unique and predicted the consequences of the GMRs' manipulation. The predictions are theoretical and need further experimental validation. - Source: PubMed
Publication date: 2022/01/15
Iacobas SandaIacobas Dumitru Andrei