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
- DNA cross-linking agents remain a cornerstone of cancer chemotherapy. While their efficacy was traditionally attributed to direct genotoxicity, blocking DNA replication and transcription to induce cell death, recent evidence suggests that their therapeutic activity also involves innate immune activation. Aberrant repair of DNA lesions generates cytosolic DNA fragments, which are sensed by cyclic GMP-AMP synthase (cGAS). This activates the cGAS-STING (stimulator of interferon genes) pathway, driving the production of type I interferons and proinflammatory cytokines, thereby eliciting antitumor immunity. This review traces the molecular trajectory from DNA lesions formation to immune stimulation. We summarize the chemistry of classical and emerging DNA cross-linking agents, the replication stress they impose, and DNA damage response (DDR) generating cytosolic DNA as a trigger for innate immune activation. We then highlight key mechanistic insights into cGAS-STING signaling. Finally, we discuss therapeutic opportunities in their combinations with STING agonists for more effective immune activation. Collectively, this framework reframes DNA cross-linking agents from simple cytotoxins into in situ vaccines that harness DNA damage-driven immunity. - Source: PubMed
Li JingaoWang LuoMao XuqingHu DongmeiLu QinyueShi ChengyiWang YifengMeng ZhaoweiFan HeliSun Huabing - Multiple sclerosis (MS) is a chronic neuroinflammatory disorder characterized by oligodendrocyte injury and demyelination. The disease progresses from peripheral immune attacks to compartmentalized central nervous system (CNS) inflammation, culminating in irreversible neurodegeneration. Although current immunotherapies suppress peripheral relapses, they inadequately address compartmentalized CNS inflammation and progressive neurodegeneration. - Source: PubMed
Hu ShengfeiXiao XiaCheng XiHuang YiyingCui TingtingShen ShishiCui ChunpingXiao LiTan HanzhangQiu WeiZhao YipengLi Rui - Defence against viral infection is a conserved feature of all cellular life. From single-cell bacteria to humans and complex multicellular animals, constitutive and inducible forms of immunity are required to inhibit viruses and safeguard cellular fitness. Recent studies reveal that the components of human antiviral immunity are surprisingly ancient, originating billions of years ago in bacteria as pathways that defend against phage replication. The unification of previously disparate fields of human and bacterial immunity creates a foundation to explain key features of host-virus interactions. This Review defines principles of pathogen recognition, signal amplification and immune effector function that shape mechanisms of antiviral immunity that are shared across kingdoms of life. Shared forms of immunity, including cGAS-STING, inflammasomes, argonautes and viperin, reveal ancient features of antiviral defence. Similarly, direct comparisons of pattern recognition receptors and interferon-stimulated genes in human cells with CRISPR immunity and anti-phage defence systems in bacteria explain prevalent strategies to effectively sense and inhibit viral replication. Cross-kingdom analysis reveals universal rules that control host-virus interactions and highlights open questions in understanding of antiviral immunity. - Source: PubMed
Publication date: 2026/08/12
Kranzusch Philip J - The cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) pathway is an essential cytosolic DNA-sensing system that plays an important role in the regulation of innate immune and inflammatory responses in the central nervous system (CNS). It was first discovered as a promising antiviral defense cascade and has since been shown to execute broader functions in neuroinflammation and neurodegeneration. The pathway can become hyperactive with the release of endogenous DNA from damaged nuclei, mitochondria, or genomic instability, leading to chronic production of type I interferon (TI-IFN), various pro-inflammatory cytokines, and eventually contributing to chronic neuroinflammatory diseases. Recent studies have found that dysregulated cGAS-STING signaling is associated with several neurological disorders, such as Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), amyotrophic lateral sclerosis (ALS), traumatic brain injury (TBI), stroke, and age-related neurodegeneration. In the CNS, chronic activation of this pathway leads to activation of microglia, oxidative stress, breakdown of the blood-brain barrier (BBB), impaired function of the synapses, and neuronal death. Mitochondrial dysfunction and cytosolic release of mitochondrial DNA (mtDNA) further promote inflammatory signaling, thus perpetuating neurodegeneration. This review highlights the molecular and pathological mechanisms of cGAS-STING signaling in a broader aspect of neurological disorders and appraises the novel therapeutics already under development to inhibit this pathway to regulate neuroinflammation and enhance neurological outcomes. - Source: PubMed
Publication date: 2026/08/12
Rahim AbdulZubair Shaik MahammadAhamed MustakDas SoumiPatel RoyalDebnath BiplabPorel Pratyush - Mapping mutations to cellular outcomes reveals the molecular mechanisms underlying STING activity. - Source: PubMed
Publication date: 2026/08/11
Foley John F