Ask about this productRelated genes to: PTGDR Blocking Peptide
- Gene:
- PTGDR NIH gene
- Name:
- prostaglandin D2 receptor
- Previous symbol:
- -
- Synonyms:
- DP, DP1, PTGDR1
- Chromosome:
- 14q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1995-11-09
- Date modifiied:
- 2016-07-01
Related products to: PTGDR Blocking Peptide
Related articles to: PTGDR Blocking Peptide
- This study aimed to identify prognostic biomarkers for gastric cancer (GC) by analyzing the methylation status of multiple tumor suppressor genes. - Source: PubMed
Publication date: 2026/02/03
Nam Soo KyungPark JuhyeongKwak YoonjinBatochir ChinbayarKim Eun-BiKong Seong-HoPark Do JoongLee Hyuk-JoonYang Han-KwangLee Hye Seung - Autoinflammatory diseases involve recurrent systemic inflammation caused by dysregulated innate immunity, arising from genetic or multifactorial mechanisms, as seen in periodic fever, aphthous stomatitis, pharyngitis, and adenitis (PFAPA) syndrome. About 10% of PFAPA patients show autosomal dominant inheritance. We describe a three-generation family with a PFAPA-like recurrent fever syndrome displaying clear autosomal dominant transmission. All affected individuals tested negative on a diagnostic panel of 13 known autoinflammatory genes. Whole-exome sequencing was performed in two distantly related affected members, followed by variant filtering, segregation analysis, and phenotype-based prioritization. A single heterozygous missense variant in , c.154G>A p.(Asp52Asn), co-segregated with disease in all affected relatives. This variant is extremely rare in population databases, absent from ClinVar, present in COSMIC, and predicted as damaging by REVEL and CADD. RXFP1, not previously implicated in autoinflammatory or innate immune disorders, encodes the relaxin family peptide receptor 1, a G protein-coupled receptor involved in extracellular matrix regulation, anti-fibrotic pathways, and modulation of inflammatory cytokine production. Protein network analysis showed interactions with RLXN1-3, inflammatory mediators, PTGDR, ADORA2B, and C1QTNF8, supporting an immunomodulatory function. This is the first report linking variation to a hereditary recurrent fever syndrome, identifying relaxin signalling as a potential immune regulatory pathway. - Source: PubMed
Publication date: 2026/01/08
Buttarelli MariannaRapari GiuliaRiccio MelaniaManna RaffaeleRigante DonatoSangiorgi Eugenio - The risk of developing melanoma increases with age. Although immune checkpoint blockade (ICB) therapy has shown considerable success, a significant portion of melanoma patients either fail to respond to ICB or eventually develop resistance. This leads to the urgent need for exploring novel treatments. Phospholipase A2 group IID (PLA2G2D) is an inducible enzyme found in myeloid cells, especially in aging dendritic cells (DCs), that exert an immunosuppressive effect by producing anti- or proinflammatory small lipid molecules, including prostaglandin D2 (PGD2). An aging-related increase of PLA2G2D-PGD2 expression makes this signaling a promising target for treating aging-associated diseases. The overexpression of hematopoietic PGD2 synthase identified in both human and mouse melanoma tissue further highlights the potential of PLA2G2D-PGD2-targeting therapy. In this study, we show that the absence of PLA2G2D or the PGD2 receptor, PTGDR, restricts primary tumor growth and lung metastasis of subcutaneously implanted melanoma, as demonstrated using middle-aged Pla2g2d-/- and Ptgdr-/- mice. These therapeutic benefits are linked to increased tumor infiltration of activated γδ T cells, which can be amplified in B16F10-bearing wild-type mice through the adoptive transfer of Ptgdr-/- DCs. These tumor-restraining effects were also confirmed in DC-specific PTGDR-deficient (zDCcrePtgdrfloxp) mice. Mechanistically, the enhanced production of IL-1β by Ptgdr-/- DCs contributes to the activation and accumulation of γδ T cells in tumor tissue. In summary, our findings highlight the effectiveness of targeting the PLA2G2D-PGD2/PTGDR axis to reprogram aging dendritic cells, thereby inhibiting melanoma progression and presenting a promising therapeutic target, particularly for elderly patients. - Source: PubMed
Liu MingDhakal HimaLi HongMurakami MakotoNarumiya ShuhYan JunYaddanapudi KavithaPerlman StanleyZheng Jian - Necroptosis plays a critical role in the onset and progression of numerous malignancies, with colorectal cancer (CRC) ranking among the leading causes of cancer-related mortality worldwide. However, the relationship between necroptosis-related genes (NRGs) and CRC remains contentious. Hence, this study aims to develop a novel NRG-based signature to predict the prognosis of CRC patients and explore its potential role. - Source: PubMed
Publication date: 2025/09/01
Tan LuluWang ShuaifengChang WeilongZhang XiaoyingDeng RuiYan HuifangZhu WeiweiWang HuifenCai YudieLiu ZhiboTan YuyanCui Jinyuan - To investigate the transcriptomic signature of refractory nasal polyps (NP) after endoscopic sinus surgery. Tissue samples were collected from 36 patients with NP who underwent endoscopic sinus surgery at the Seventh Affiliated Hospital of Sun Yat-sen University and the First Affiliated Hospital of Sun Yat-sen University from January 2020 to December 2021. Raw sequencing data of normal nasal mucosa samples were downloaded from publicly available GEO database (Accession Number: GSE136825). Differential expression genes (DEGs) and Gene Ontology (GO) enrichment analysis were conducted to analyze the differences between refractory NP and normal controls, as well as among refractory, controlled, and partially controlled NP. Hierarchical clustering method was employed to analyze the inflammatory endotypes of NP. Weighted Gene Co-expression Network Analysis (WGCNA) and STRING database were used in combination with Cytoscape software to identify the characteristic transcriptional expression profiles of refractory NP. R software (version 4.3.1) was used for statistical analysis. Refractory NP patients had significantly higher asthma comorbidity rates than controlled/partially controlled groups (<0.05). The numbers and percentages of peripheral blood and tissue eosinophilic granulocytes were significantly higher in the refractory subgroup than in the other two subgroups (<0.05). Compared to normal mucosa, controlled and partially controlled NP groups, 27 genes were consistently upregulated in refractory NP. Hierarchical cluster analysis showed that the refractory NP exhibited a mixed endotype dominated by type 2 inflammation with co-existing type 1 features. Differential genes were enriched in extracellular matrix organization, leukocyte activation, cytokine receptor activation, cystatin-mediated protease inhibition, granule exocytosis, and olfactory nerve development regulation. Further WGCNA analysis and protein-protein interaction network identified 33 hub genes represented by and This study reveals the distinctive transcriptional signature of refractory NP through transcriptomic methods, providing novel research avenues and therapeutic targets for the treatment of refractory NP after surgery. - Source: PubMed
Wang K HXu LFan Y PShi J BSun Y Q