Ask about this productRelated genes to: TMEM173 antibody
- Gene:
- TMEM173 NIH gene
- Name:
- transmembrane protein 173
- Previous symbol:
- -
- Synonyms:
- FLJ38577, NET23, ERIS, MPYS, STING, MITA
- Chromosome:
- 5q31.2
- Locus Type:
- gene with protein product
- Date approved:
- 2006-08-24
- Date modifiied:
- 2019-04-23
Related products to: TMEM173 antibody
Related articles to: TMEM173 antibody
- Neurodegenerative diseases share features of neuronal loss, neuroinflammation, and protein aggregation. The cGAS-STING pathway, a key DNA sensor, mediates neuroinflammation via TBK1-IRF3 and IKK-NF-κB axes, inducing type I interferons and pro-inflammatory cytokines. This pathway upregulates ZBP1, promotes PANoptosome assembly, and triggers PANoptosis, releasing DAMPs and creating a self-amplifying "inflammation-death" cycle. In Alzheimer's, Parkinson's, and amyotrophic lateral sclerosis, pathological proteins (Aβ, Tau, α-synuclein, TDP-43) or genetic defects (e.g., C9orf72 repeats) cause mitochondrial DNA leakage or genomic instability, activating this axis. This review highlights the cGAS-STING-PANoptotic cascade as a shared pathogenic mechanism and discusses the current evidence and remaining challenges in confirming this hypothesis. - Source: PubMed
Publication date: 2026/09/09
Hou XinyiYu Wei - SLE features aberrant type I interferon production, with the stimulator of interferon genes (STING) pathway acting as a key upstream driver. However, its expression patterns in patients with SLE and contributions to clinical phenotypes and tissue injury remain insufficiently defined. - Source: PubMed
Publication date: 2026/09/23
Kong WeiZhou KangxingZhang XinSun YueYao GenhongWang FanLi WenchaoSun Lingyun - Bladder cancer (BLCA) is an aggressive malignancy characterized by metastasis and drug resistance, creating an urgent demand for novel therapeutic targets. The lysosomal protein LAMP2 acts as a key oncogenic driver in BLCA and modulates the degradation of STING. As reported in prior studies, mechanistically, p62-mediated macroautophagy and HSC70-dependent chaperone-mediated autophagy (CMA) facilitate STING degradation. LAMP2 increases STING ubiquitination, leading to its lysosomal degradation in BLCA. Moreover, LAMP2 knockdown suppresses BLCA cell proliferation and migration. In our experimental systems, it also induces M1-type tumor-associated macrophages (TAMs) polarization and reduces TAM infiltration. RNF5 and TRIM56 are known to mediate K48/K63-linked ubiquitination of STING. Here, we demonstrate LAMP2 modulates this ubiquitination pattern in BLCA. Via virtual screening, we discover MRGPRX4 modulator-2 (Mm-2), a LAMP2-binding small molecule with anti-tumor activity against BLCA. Combined with gemcitabine (GEM), Mm-2 blocks autophagic flux and activates STING signaling. It also alters TAM phenotypes in our in vitro and in vivo models. The LAMP2-STING-TAMs axis shows potential as a therapeutic target for modulating the tumor immune microenvironment (TME) and affecting drug response in BLCA. - Source: PubMed
Publication date: 2026/09/23
Lv YueYin QiangLi WuhengDeng LeihongLiu JiashengLv HaolongZhang PengQiu YihangGuo DifengTao RuiGan XiuguoXu FanghuaLiu ZanWang Yongquan - Acute Myocardial infarction (AMI) continues to be a severe deadly disease with a high case-fatality rate and great psychological and economic costs. Despite the development of new therapies, early diagnosis and treatment optimization still are problematical. Here we applied the integrated bioinformatics strategy to screen potential new diagnosis biomarkers for AMI based on the inflammation-related cGAS-STING pathway. By integrating differentially expressed genes (DEGs), weighted gene co-expression network analysis (WGCNA), and cGAS-STING gene set from high-throughput RNA sequencing, we obtained a total of 11 candidate genes from 914 DEGs, which enriched mainly for inflammatory and immune response pathways. Further refining them in machine learning algorithms, we identified core genes with diagnostic values. Subsequent test shows the AUC values of PFKFB3 and TLR2 both were more than 0.7 and their promising diagnostic values were verified. Based on the immune infiltration analysis, expression of PFKFB3 and TLR2 were very significantly associated with a large number of immune cells, such as monocytes, neutrophils and dendritic cells. As for single cell sequencing analysis, they were mainly found expressed on macrophages. Overall, we show that PFKFB3 and TLR2 are possible biomarkers of AMI which have not been reported so far. Thus they may open a path for new diagnostics and personalized therapy. Validation in independent populations is needed. - Source: PubMed
Publication date: 2026/09/18
Li JuyingChen HongkuiHuang YihaoZhi YupengChen ChunGuo Yansong - The cyclic GMP-AMP synthase-stimulator of interferon genes (STING) pathway is essential for antiviral immunity, and its dysregulation causes inflammatory disease. The mechanism underlying STING activation, including its essential endoplasmic reticulum-to-Golgi translocation, has remained elusive. Here, we identify a dedicated actin-based transport system licensed by the smooth muscle actin isoform ACTA2 via in vitro reconstitution. Superresolution live imaging reveals STING becomes punctate and activated while moving along ACTA2 filaments. This ACTA2-directed network is required for antiviral interferon responses against HSV-1. Strikingly, it also drives pathological interferon production and lethal autoimmunity in mice, where its genetic or pharmacological disruption rescues disease. Furthermore, ACTA2 expression correlates with proinflammatory cytokine levels in peripheral blood mononuclear cells from systemic lupus erythematosus patients, and its downregulation ameliorates this inflammatory signature. Our work defines a specific cytoskeletal network that governs STING-dependent inflammatory responses to both foreign and self-DNA, thereby establishing stimulus-directed organelle trafficking as a central control point in innate immune signaling. - Source: PubMed
Publication date: 2026/09/15
Hou XiantengWu QingDu YangtingWang ChangwanZhu JunyanJiang YingboChen SheZhou LishaWu XiaoyuWang HongyanYang HuiHou Fajian