Ask about this productRelated genes to: KLRC3 antibody
- Gene:
- KLRC3 NIH gene
- Name:
- killer cell lectin like receptor C3
- Previous symbol:
- -
- Synonyms:
- NKG2-E
- Chromosome:
- 12p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1998-01-16
- Date modifiied:
- 2016-10-05
Related products to: KLRC3 antibody
Related articles to: KLRC3 antibody
- Macrophage activation syndrome (MAS) represents a subtype of hemophagocytic lymphohistiocytosis (HLH) associated with autoimmune diseases. Systemic lupus erythematosus (SLE) is one of the most common autoimmune diseases that induce MAS. The overlapping systemic symptoms of SLE and clinical manifestations of HLH pose challenges in clinical diagnosis, contributing to significant rates of underdiagnosis and misdiagnosis, warranting further investigation. Identifying early diagnostic biomarkers with high sensitivity and specificity for MAS in SLE holds significant clinical importance. - Source: PubMed
Publication date: 2026/02/13
Pei YuanyuanZhou YiranYang FengtaoCao LingjieYao RanranLiang RengeHan XiaoWang XiLiu ZhenmingZhu JihongSu Yin - This study aimed to explore the molecular mechanisms associated with mitophagy in BO and identified mitophagy-associated BO diagnostic genes. Using Gene Expression Omnibus database data, differentially expressed genes in BO patients vs controls were analyzed via Gene Ontology enrichment. Algorithms like Boruta, least absolute shrinkage and selection operator, and Random Forest screened BO-specific genes. Mitophagy genes were sourced from PathCards and correlated with BO-specific genes via single-sample gene set enrichment analysis (ssGSEA). Receiver operating characteristic curves evaluated the diagnostic performance of these genes. Two hundred and six differentially expressed genes were identified, in which immune-related pathways such as the B-cell receptor signaling pathway and lymphocyte differentiation were significantly enriched. Machine learning screening yielded 30 BO signature genes, among which KLRC3 and CD36 were significantly correlated with ssGSEA enrichment score of the mitophagy gene sets. Receiver operating characteristic analysis confirmed their diagnostic value with AUCs of 0.648 and 0.640, respectively. This finding indicated that KLRC3 and CD36 are not only significantly correlated with ssGSEA enrichment score of the mitophagy gene sets but also have diagnostic value for BO. - Source: PubMed
Wang YingPeng Wenbin - Understanding the activation mechanisms of γδ T cells in colorectal cancer (CRC) is critical for harnessing their therapeutic potential. Here, using an atlas of human CRC-infiltrating γδ T cells that we built by integrating multiple single-cell RNA-seq datasets, we developed a γδ T cell-refined ligand inference pipeline by combining differential gene expression, gene regulatory network prediction, ligand inference, and in silico perturbation analysis. This approach identified ligands, including IL-15 and TNFSF9 (4-1BBL), as candidates promoting γδ T cell effector function and highlighted NCR2 and KLRC3 (NKG2E), whose in silico overexpression was associated with γδ T cell activation. Ligand enrichment analyses further indicated that monocytes and dendritic cells are key contributors to γδ T cell activation in the tumor microenvironment. Our results also highlighted transcription factors IKZF1, FOSL2, and FOXO1 in the less activated γδ T cells and IRF1, KLF2, and BHLHE40 in the effector γδ T cells that plausibly regulated the differential activation state. Together, our results offer a systems-level view of the signaling and transcriptional programs governing γδ T cell phenotypes in CRC and provide a foundation for γδ T cell-based immunotherapies with enhanced antitumor functions. - Source: PubMed
Publication date: 2026/01/13
Ran RanBrubaker Douglas K - Obesity is a well-known risk factor for developing obstructive sleep apnea (OSA) in children. Both OSA and obesity are independently associated with cardiovascular and metabolic comorbidities. These comorbidities are driven by shared pathophysiological pathways, making it difficult to distinguish the individual contributions of obesity and OSA. This study aimed to investigate the molecular mechanisms of OSA in children with obesity through whole blood mRNA sequencing. - Source: PubMed
Publication date: 2025/09/14
Affaticati FabioVermeiren ElineMeysman PieterBartholomeus EstherVan Hoorenbeeck KimOgunjimi BensonVerhulst StijnVan Eyck Annelies - The objective of this study was to investigate the immunomodulatory effects of whey protein isolate (WPI)-galacto-oligosaccharide conjugates following dynamic high-pressure microfluidics pretreatment (DHPM) in cyclophosphamide-induced immunosuppressed mice. DHPM facilitated the conjugation of WPI and galacto-oligosaccharide, and inhibited the generation of fluorescent advanced glycation end products (AGEs) and pentosidine. The conjugates demonstrated a significant immune recovery effect on CTX-induced immunosuppressed mice, as evidenced by the enhancement of IgG antibody levels (from 3.5 to 4.1) and the reduction of the levels of immunosuppressive effector factors TGF-β (from 148.1 to 111.2) and IFN-γ (from 34.4 to 17.9). Furthermore, the conjugates exhibited a notable ability to repair histological lesion in the spleen of CTX-induced immunosuppressed mice. Spleen transcriptomics revealed that the Marco, Klrc3 and Cd209b genes were associated with the immune enhancement activity of the conjugates. Metabolomic analysis identified arginine biosynthesis, sphingolipid metabolism, alanine, aspartate and glutamate metabolism, and phenylalanine, tyrosine and tryptophan biosynthesis as key pathways in the immune enhancement activity of the conjugates. Metabolomics combined with transcriptomics indicated the importance of macrophage activation in the restoration of immunosuppressed mice's immunity by the conjugates. Therefore, the improvement in immunity observed with WPI-galacto-oligosaccharide conjugates may be related to the activation of macrophages. - Source: PubMed
Publication date: 2024/09/21
Mao Ji-HuaChen Wen-MeiWang YangWang Xu-MeiShao Yan-HongLiu JunTu Zong-Cai