IFI16 Mouse Monoclonal Antibody
- Known as:
- IFI16 Mouse Monoclonal Antibody
- Catalog number:
- BIN-003428-M02
- Product Quantity:
- 0.05mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- IFI16 Mouse Monoclonal Antibody
Related genes to: IFI16 Mouse Monoclonal Antibody
- Gene:
- IFI16 NIH gene
- Name:
- interferon gamma inducible protein 16
- Previous symbol:
- -
- Synonyms:
- IFNGIP1, PYHIN2
- Chromosome:
- 1q23.1
- Locus Type:
- gene with protein product
- Date approved:
- 1993-09-29
- Date modifiied:
- 2016-10-05
Related products to: IFI16 Mouse Monoclonal Antibody
Related articles to: IFI16 Mouse Monoclonal Antibody
- Genomic instability is increased in patients with inflammatory bowel disease (IBD), yet whether it contributes directly to disease pathogenesis remains unclear. Here, we identify RADX, a structural antagonist to RAD51 and a key regulator of replication fork stability, as a critical suppressor of intestinal inflammation by limiting innate immune sensing of replication-associated DNA damage. RADX deficiency exacerbates experimental colitis, with macrophages serving as the principal mediators of this phenotype. Mechanistically, RADX competes with the DNA sensor IFI16 for binding to single-stranded DNA (ssDNA). Loss of RADX promotes ssDNA accumulation, triggering IFI16-dependent activation of NF-κB signaling and inflammasome assembly, thereby driving intestinal inflammation. Consistent with these findings, two RADX variants identified in patients with IBD associate with reduced RADX protein expression, increased DNA damage signaling, and elevated IL-1β levels. Pharmacological inhibition of RAD51 with RI-1 alleviated colitis in both wild-type and Radx-deficient mice. Together, these findings establish a mechanistic link between genome instability and intestinal inflammation, identify a RADX-IFI16 checkpoint that restrains pathogenic innate immune activation, and nominate modulation of replication stress as a therapeutic strategy for IBD. - Source: PubMed
Publication date: 2026/07/24
Xian HuifangHuang WanmingChen ZhanghuaLi LiliXiong LiyaZhu JianhengJin HaolanLi XiaotianSong LizhiChen PeiyuRen LuWang WeiFang RongliChen XixiLei WenZhang DengfengLiao WeiliangHuang YuxinLew Andrew MCui JunGong SitangHuang JunRosa Duque Jaime SZhi MinGeng LanlanZhou WenhaoZhang Yuxia - Autoimmune thyroiditis (AIT) ranks among the most common autoimmune disorders globally. Adherence to a healthy lifestyle may substantially offset the risk conferred by a high transcriptomic risk profile. - Source: PubMed
Publication date: 2026/06/24
Li Chun-HuLiu Yu-HangYue Zong-YuZeng Xiang-KunZhang Ze-XuLi XuanLiu Yi-HangLi Ya-HuiZhao TongLiu Peng - About 1.5-2 billion years ago, an endosymbiosis between aerobic α-proteobacteria and anaerobic archaeal cells generated mitochondria, i.e., organelles capable of producing oxidative energy. The bacterial genome was fundamentally reduced and a circular mitochondrial genome evolved containing mainly the genes coding for the subunits of the electron transport chain. Before the symbiotic event, there existed a virus-host co-evolution which involved the development of sensors for detecting dangerous viral DNA/RNA molecules. Endosymbiosis supplied eukaryotic cells not only with an oxidative powerhouse to allow the evolution of more complex multicellular organisms but it also meant that cells now housed an organelle which was able to generate reactive oxygen species (ROS) and to leak mitochondrial DNA (mtDNA) and double-stranded RNA (dsRNA) into the cytoplasm. There is now abundant evidence that during aging and age-related diseases mitochondria are prone to release both mtDNA and dsRNA. In the cytoplasm, mtDNA/dsRNA molecules activate a number of cytosolic nucleic acid sensors leading to the secretion of type-1 interferons (IFN) and many other cytokines which promote an age-related proinflammatory state. Currently, it is known that mtDNA can activate the cGAS-STING pathway, AIM2 inflammasomes, IFI16 receptors, and ZBP1 sensors and in addition mitochondrial dsRNA stimulates RIG-1/MDA5 signaling. Interestingly, there is abundant evidence that all these receptors are drivers of cellular senescence and inflammaging. For decades, there has been mounting evidence that mitochondria have a crucial role in the aging process. We will examine this question from the perspective of evolution and propose that mitochondrial evolution created an endogenic source for the leakage of dangerous mtDNA/dsRNA which subsequently stimulated cytosolic DNA/RNA sensors, an evolutionarily conserved viral defence mechanism. It seems that these two evolutionary events provided not only the basis for the inevitable process of aging but also ensuring the death of parental organisms. - Source: PubMed
Publication date: 2026/07/07
Salminen AnteroKaarniranta KaiKauppinen Anu - Osteoporosis, a prevalent metabolic bone disease, often leads to pathological fractures. Identifying causative relationships between proteins, genetic loci, and osteoporosis can highlight potential therapeutic targets. - Source: PubMed
Hu CongleiWang RuiLi ShitingWang ChunXu YunYu XuekeYe ZhaoChen ShichaoLi GangLi GuangwenLi Hui - The PYHIN (pyrin and HIN domain-containing) gene family encodes central cytosolic DNA sensors, including AIM2 and IFI16, that activate inflammasome and type I interferon pathways during infection. While these pathways are critical for antiviral and antimicrobial defense, how ecological pressures shape their evolution remain unclear. The PYHIN gene family varies across mammals, and bats have completely lost all PYHIN genes. Here, we integrate phylogenomic, comparative genomic, and phylogenetically controlled analyses across more than 150 mammalian species to investigate PYHIN evolutionary dynamics. We show that PYHIN genes form a tightly linked genomic cassette within a conserved chromosomal interval flanked by SPTA1 and CADM3, a pattern we describe as an Anchored Gene Cluster Pulsation mechanism characterized by coordinated expansion, contraction, and loss. Across mammals, the genomic distance between these anchor genes correlates with PYHIN copy number. In bats, phylogenetic logistic regression identifies powered flight and inverted roosting as traits statistically associated with PYHIN loss, whereas echolocation and hibernation show no association. Olfactory receptor genes within the same region are retained, indicating targeted loss of DNA-sensing immune genes rather than generalized genome contraction. These findings support a model in which bat immunity is associated with ecological specialization favoring immune tolerance and provide a framework for understanding immune gene family evolution as integrated genomic modules. - Source: PubMed
Publication date: 2026/05/28
Ziemann ChanaseiStreicher MadelineSicks AllyssaZhang ChiZhang Luwen