Ask about this productRelated genes to: TCIRG1 antibody
- Gene:
- TCIRG1 NIH gene
- Name:
- T cell immune regulator 1, ATPase H+ transporting V0 subunit a3
- Previous symbol:
- -
- Synonyms:
- TIRC7, OC-116, OC116, ATP6N1C, Atp6i, a3, ATP6V0A3
- Chromosome:
- 11q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1999-02-15
- Date modifiied:
- 2019-04-23
Related products to: TCIRG1 antibody
Related articles to: TCIRG1 antibody
- Osteopetrosis is a heterogeneous group of bone diseases with increased bone density as a result of defective osteoclast function or differentiation. The clinical presentations range from the early, often lethal, infantile malignant forms to the mild autosomal dominant forms. This review provides recent updates in preclinical findings regarding molecular genetics, diagnosis, and novel therapeutic approaches in osteopetrosis. - Source: PubMed
Publication date: 2026/05/07
Donati SimoneAurilia CinziaPalmini GaiaFalsetti IreneMarini FrancescaGiusti FrancescaZonefrati RobertoRanaldi FrancescoIantomasi TeresaBrandi Maria Luisa - Clear cell renal cell carcinoma (ccRCC) represents the most prevalent form of kidney cancer, yet age-related molecular heterogeneity remains poorly characterized in clinical specimens. We performed comprehensive transcriptomic profiling of 73 formalin-fixed paraffin-embedded (FFPE) ccRCC samples using RNA sequencing to investigate age-dependent molecular signatures and their clinical implications. Principal component analysis (PCA) revealed that PC1 significantly separated younger versus older patients (p = 0.04), while PC2 distinguished tumors by gender (p = 0.00012), size (p = 8 × 10 ⁻ ⁴), and histological class (p = 0.043), suggesting an orthogonal aging molecular axis alongside with disease progression. Differential gene expression analysis identified 330 age-associated genes, with elderly patients showing upregulation of immune checkpoint regulators (CD70), apoptosis modulators (DEDD, HTATIP2), and proton pump components (TCIRG1), alongside downregulation of metabolic enzymes (DIO2) and cytoskeletal regulators (MICALL2). Pathway enrichment analysis revealed dysregulation of aldosterone-regulated sodium reabsorption, B cell receptor signaling, and Th17 cell differentiation pathways, reflecting age-related immunometabolic reprogramming. Integrative analysis of DEGs across clinical variables identified 1,536 shared genes between tumor size and stage comparisons, with CK7-positive tumors exhibiting distinct transcriptional profiles potentially representing a novel molecular subtype. These findings demonstrate that aging fundamentally alters the ccRCC transcriptome through coordinated changes in immune surveillance, metabolic homeostasis, and tumor microenvironment composition, providing a molecular framework for age-stratified therapeutic approaches and precision oncology strategies in renal cell carcinoma. - Source: PubMed
Publication date: 2026/03/10
Niu YunSu YunchaoWang XiaoxiYang XiaoyuanZhong Dingrong - Differentiated embryo chondrocyte 1 (Dec1, protein DEC1) plays a critical role in bone metabolism, but its interaction with the Runt-related transcription factor 2 (RUNX2) signaling pathway remains poorly understood. To investigate how DEC1 regulates osteoblast and osteoclast differentiation through the RUNX2 signaling pathway. To model estrogen deficiency-induced osteoporosis, ovariectomy (OVX) was performed in DEC1 knockout (DEC1) and wild-type (DEC1) mice, and bone parameters were assessed by micro-computed tomography (micro-CT). Primary bone marrow mesenchymal stem cells (BMSCs) were isolated for osteoblast induction, and RAW 264.7 macrophage-like cells were used for osteoclast differentiation. Flow cytometry was applied to assess lineage markers. RUNX2 expression and transcriptional activity were analyzed by qRT-PCR, Western blotting, GFP-tagging, and chromatin immunoprecipitation sequencing (ChIP-seq). DEC1 mice showed significant reductions in bone mineral density (BMD), bone volume fraction (BV/TV), trabecular number (Tb.N), and trabecular thickness (Tb.Th) under OVX. , DEC1 knockdown increased RUNX2 expression but impaired osteoblast differentiation, with reduced ALP, Osterix, and Osteocalcin expression. ChIP-seq confirmed RUNX2 enrichment near transcription start sites (TSS). Osteoclast markers (CD254, TCIRG1, ACP5) were also reduced in DEC1 mice. DEC1 regulates bone metabolism by modulating RUNX2 signaling, highlighting its dual role in osteoblast and osteoclast differentiation. - Source: PubMed
Publication date: 2026/02/24
Qian WenjieMei KaiZhu LeiLv JinpengYun Changjun - Tongue squamous cell carcinoma (TSCC) is associated with an unfavorable prognosis, and the involvement of systemic inflammation and tumor-associated neutrophils (TANs) remains inadequately elucidated. This study was designed to assess the prognostic significance of inflammatory biomarkers and to delineate functionally distinct TAN subsets in TSCC. - Source: PubMed
Publication date: 2026/02/24
Huang GuoxinLi ChenchangWu YupengHuo JingbinHan JingjingCheng ZhengMai LianxiRao GuangxinMa YingnanSun WenhaoWang XiaojuanLi QunxingLin ZhaoyuLi Bowen - Ischemic stroke is one of the leading causes of disability and mortality worldwide. Its pathogenesis extends beyond focal cerebral ischemia-induced neuronal injury, encompassing profound immune dysregulation and secondary inflammatory responses. Recent studies have highlighted T cell dysfunction, particularly T cell exhaustion, as a critical driver of post-stroke immunosuppression and increased susceptibility to infection. However, the molecular mechanisms underlying this process remain unclear. This study focuses on a novel immunoregulatory axis involving cuproptosis, metabolic reprogramming, and T cell exhaustion, and systematically investigates the role of the key regulatory molecule TCIRG1 in post-ischemic immune homeostasis disruption. Through integrative analysis of human peripheral blood transcriptomic data (GSE58294) and single-cell transcriptomic datasets from mouse brain and bone marrow following middle cerebral artery occlusion (MCAO) (GSE174574 and GSE293098), we found that the cuproptosis pathway was markedly activated after ischemic stroke. Notably, TCIRG1 was highly expressed in T cells and co-upregulated with the cuproptosis regulator Fdx1 and T cell exhaustion markers. Metabolic flux analysis revealed that high TCIRG1 expression was associated with enhanced pyruvate metabolism and was accompanied by downregulation of MYC signaling and upregulation of Zfp644, suggesting a role for TCIRG1 in driving T cell exhaustion through metabolic reprogramming. Furthermore, CellChat analysis indicated that TCIRG1 altered intercellular communication between T cells and microglia, thereby reshaping the local immune communication network. Collectively, these findings suggest that TCIRG1 may promote T cell dysfunction via cuproptosis and metabolic pathways, contributing to immune microenvironmental imbalance after ischemic stroke. This study proposes a novel multi-axis regulatory model and provides a potential molecular target for post-stroke immunotherapy. - Source: PubMed
Publication date: 2026/02/12
Zhou JiajunChen LingLi JunhengLuo LianShao Sen