Ask about this productRelated genes to: LRRC25 antibody
- Gene:
- LRRC25 NIH gene
- Name:
- leucine rich repeat containing 25
- Previous symbol:
- -
- Synonyms:
- MAPA, FLJ38116
- Chromosome:
- 19p13.11
- Locus Type:
- gene with protein product
- Date approved:
- 2004-02-18
- Date modifiied:
- 2014-11-19
Related products to: LRRC25 antibody
Related articles to: LRRC25 antibody
- The immune system has been linked to periodontitis risk in oral inflammation and systemic consequences. Specifically, this study investigated whether hub genes were associated with immune cells via integrating single-cell RNA sequencing (scRNA-seq) and Mendelian randomization (MR). We analyzed scRNA-seq data to identify differentially expressed genes (DEGs) and immune cell subtypes in periodontitis. First, MR analysis was conducted using eQTL data to determine causal relationships between immune cell gene expression and periodontitis risk. Then, Gene ontology (GO) and pathway enrichment analyses were performed to understand functional implications. In addition, CellChat trajectory analysis explored intercellular communication. Finally, reverse transcription quantitative polymerase chain reaction (RT-qPCR) and immunohistochemistry (IHC) were used to validate hub genes. Comprehensive bioinformatics analysis delineated 23 immunologically distinct cell populations and identified 7 pivotal regulatory genes (ANXA1, ARL4C, CD79B, LRRC25, NKG7, SLC11A1, and VIM) demonstrating significant causal associations with periodontitis pathogenesis. Functional pathway analysis demonstrated these molecular markers participate in critical immunomodulatory pathways. RT-qPCR validation confirmed concordance between mRNA expression patterns of these DEGs and MR findings. Immunohistochemical analysis substantiated the causal relationships predicted by MR analysis, showing positive correlations for ANXA1 and SLC11A1 expression, while CD79B exhibited an inverse association. Advanced computational modeling of immune cell receptor-ligand interactions and cellular communication networks uncovered distinct functional roles during periodontitis development, providing novel insights into disease progression mechanisms. This study highlights the crucial role of immune cells and hub genes in periodontitis. These findings provide valuable insights into immune-related mechanisms and potential interventions for periodontitis. - Source: PubMed
Publication date: 2025/10/13
Qiu XuediYang FanLi ChenxiWang JianYuan YawenGuo Chao - In light of the challenges posed by global climate change, the environmental adaptability of organisms is becoming increasingly important. The Wuzhishan (WZS) pig, tolerant to high heat and humidity, is an ideal model for genomic study. By characterizing its genome and assessing its genetic diversity and runs of homozygosity (ROH), we can gain insights into its current conservation status and genomic architecture. To this end, we analyzed whole-genome resequencing data from WZS pigs, identifying a comprehensive set of genetic variations: 12,844,858 single nucleotide polymorphisms (SNPs), 4,723,303 insertions and deletions (InDels), 39,311 copy number variations (CNVs), and 70,392 structural variations (SVs). ROH analysis revealed mostly short segments, indicating limited recent admixture and relatively low inbreeding, reflecting high genetic diversity. Linkage disequilibrium decay and effective population size analyses supported these findings, consistent with previous studies. Population genetic analyses of pig populations from Asia, Europe, and the Americas were conducted using SNPs, InDels, and SVs. The results obtained from different variant types were largely concordant, suggesting that the constructed genomic variation database is robust. Notably, the WZS pig displayed relatively unique genetic characteristics compared to other breeds. By intersecting the top 5 % of genes under selection signatures, we identified key pathways and candidate genes associated with important traits in WZS pigs, including reproduction (ABCC9, APC2, CABS1, CSNK1G1), immunity (ARPIN, CMAS, ITPR1, SLC25A13), meat quality (GANC, OBSCN, SLC5A4), environmental adaptability (MAGI1, PHF3), and heat tolerance (GABPB1, LRRC25). Further integrative analyses based on transcriptomic, single-cell transcriptomic, and epigenomic data were conducted to explore the regulatory mechanisms of key genes such as LRRC25 and ITPR1. We identified relevant expression quantitative trait loci (eQTLs), associated tissues, and distal regulatory elements that potentially influence gene expression. These findings suggest that epigenetic modifications may contribute to the enhanced heat tolerance and immune function observed in WZS pigs. In conclusion, WZS pigs represent a valuable genetic resource. Further research on this breed will deepen our understanding of mechanisms underlying environmental adaptability, and provide important insights into evolutionary biology and breeding strategies for improved resilience in livestock. - Source: PubMed
Publication date: 2025/09/04
Zhong ZiqiWang FengXie XinfengWang ZiyiPan DeyouWang ZhenXiao Qian - Leucine-rich repeat containing 25 (LRRC25), a type I membrane protein, is specifically expressed in myeloid cells including neutrophils and macrophages. The anti-inflammatory role of LRRC25 was suggested in a few pathogenic models. However, its role in cancer immunity has not been interrogated. Here, we demonstrate that LRRC25 is robustly expressed in tumor-associated macrophages (TAMs). Lrrc25 deficiency in the tumor microenvironment (TME) suppresses growth of multiple murine tumor models by reprogramming TAMs toward an anti-tumor phenotype and thereby enhancing infiltration and activation of CD8 T cells. The Nox2-ROS-Nlrp3-Il1β pathway is elevated in Lrrc25-deficient TAMs. Furthermore, a human myeloid cell line or mice with loss of Lrrc25 appear normal, indicating that LRRC25 is a safe immune target. Our results suggest that as an unappreciated immune checkpoint for tumor immunotherapy, the myeloid-specific membrane protein LRRC25 orchestrates the activity of TAMs via the canonical Nlrp3-IL1β inflammatory pathway and influences CD8 T cell chemotaxis to the TME. - Source: PubMed
Publication date: 2025/04/24
Zhang GuorongYu HanzhiLiu JingjingDong GeCai Zhigang - The genetic component of early-onset Alzheimer disease (EOAD), accounting for ~10% of all Alzheimer's disease (AD) cases, is largely unexplained. Recent studies suggest that EOAD may be enriched for variants acting in the lipid pathway. The current study examines the shared genetic heritability between EOAD and the lipid pathway using genome-wide multi-trait genetic covariance analyses. Summary statistics were obtained from the GWAS meta-analyses of EOAD by the Alzheimer's Disease Genetics Consortium (n=19,668) and five blood lipid traits by the Global Lipids Genetics Consortium (n=1,320,016). The significant results were compared between the EOAD and lipids GWAS and genetic covariance analyses were performed via SUPERGNOVA. Genes in linkage disequilibrium (LD) with top EOAD hits in identified regions of covariance with lipid traits were scored and ranked for causality by combining evidence from gene-based analysis, AD-risk scores incorporating transcriptomic and proteomic evidence, eQTL data, eQTL colocalization analyses, DNA methylation data, and single-cell RNA sequencing analyses. Direct comparison of GWAS results showed 5 loci overlapping between EOAD and at least one lipid trait harboring APOE, TREM2, MS4A4E, LILRA5, and LRRC25. Local genetic covariance analyses identified 3 regions of covariance between EOAD and at least one lipid trait. Gene prioritization nominated 3 likely causative genes at these loci: ANKDD1B, CUZD1, and MS4A64.The current study identified genetic covariance between EOAD and lipids, providing further evidence of shared genetic architecture and mechanistic pathways between the two traits. - Source: PubMed
Publication date: 2025/03/17
Ray Nicholas RBradley JosephYilmaz ElanurKizil CaghanKurup Jiji TMartin Eden RKlein Hans-UlrichKunkle Brian WBennett David ADe Jager Philip L Beecham Gary WCruchaga CarlosReitz Christiane - The purpose of this study was to identify molecular subtypes and hub genes in fibromyalgia [FM] based on immune-related genes [IRGs]. - Source: PubMed
Zhao WeiWang Pengcheng