DNAS1_BOVIN DNASE1 ELISA tesk kit
- Known as:
- DNAS1_BOVIN DNASE1 Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen15099
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- Other suppliers
- Gene target:
- DNAS1_BOVIN DNASE1 ELISA tesk kit
Related genes to: DNAS1_BOVIN DNASE1 ELISA tesk kit
- Gene:
- DNASE1 NIH gene
- Name:
- deoxyribonuclease 1
- Previous symbol:
- DNL1
- Synonyms:
- -
- Chromosome:
- 16p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1992-07-08
- Date modifiied:
- 2016-07-18
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- The recognition of mislocalized DNA and RNA by cGAS-STING, RIG-I/MDA5, the OAS-RNase L axis, and endosomal TLR3/7/8 has emerged as a unifying paradigm linking cancer, autoinflammation, and antiviral immunity. Counterbalancing these sensors is a structurally heterogeneous nuclease repertoire whose distinct substrate specificities, subcellular compartments and pH optima constrain ligand availability in space and time. Disruption of this equilibrium drives disease through two mirror-image mechanisms. In cancer, DNASE1 is inactivated by tumor-derived G-actin, DNASE1L3 is transcriptionally silenced in hepatocellular, colorectal and lung adenocarcinomas, and DNASE2 is upregulated in immunologically "cold" tumors, together permitting neutrophil-extracellular-trap-mediated exclusion of cytotoxic T cells and suppression of cytosolic DNA sensing. In autoimmunity, biallelic loss of DNASE1L3, TREX1, RNase H2, ADAR1 or RNase T2 produces the interferonopathies of systemic lupus and Aicardi-Goutières syndrome. Diagnostically, nuclease-specific cleavage signatures have matured into cell-free DNA fragmentomics validated across 13 cancer types in a 3,021-patient cohort; therapeutically, the field now spans engineered actin-resistant DNASE1/DNASE1L3 biologics, selective TREX1 and ADAR1 inhibitors entering first-in-human evaluation, STING-activating nanomedicines, RNase Fc-fusions such as RSLV-132 in phase 2a lupus, and JAK1/2 inhibition as standard of care in Aicardi-Goutières syndrome. We synthesize this evidence as a two-fate problem: whether an endogenous nucleic acid accumulates at these sensors to drive autoinflammation or is cleared by nucleases before detection is set by the balance between sensor engagement and clearance capacity. The therapeutic corollary acts on the ligand rather than the enzyme, restoring ligand availability where disease is malignant and restoring clearance where disease is self-directed. - Source: PubMed
Publication date: 2026/08/06
Xia LintaoWang YixiYan XiuliZhang Hui - The formation of extracellular traps (ETs) through ETosis has emerged as a key mechanism in immunothrombosis. However, the temporal dynamics and clinical significance of ETosis in coronary thrombi of ST-elevation myocardial infarction (STEMI) patients remain incompletely understood. We investigated whether ETosis burden increases with thrombus age and is associated with and genetic variants as well as impaired myocardial reperfusion. Thrombus aspirates from 81 STEMI patients undergoing primary percutaneous coronary intervention were histologically classified as fresh ( = 41) or lytic ( = 40). ETosis was quantified by citrullinated histone H3 (CitH3) immunohistochemistry and digital image analysis, complemented by multiplex staining for myeloperoxidase (MPO), CD68, caspase 3, and CD61. Plasma ET-related markers and genotyping of (rs1053874) and (rs11797) were also performed. CitH3-positive cells were present in all thrombi but were more abundant in lytic (older) thrombi compared with fresh thrombi (1348 vs. 591 cells/mm, < 0.001). Increased ETosis was associated with neutrophil and macrophage infiltration, apoptosis, prolonged ischemia time, elevated systemic inflammation (neutrophil-lymphocyte ratio and C-reactive protein), and impaired myocardial reperfusion (lower TIMI flow grades). Moreover, the GG genotype was associated with higher densities of MPO- and CD68-positive cells, whereas the CC genotype was associated with increased densities of CitH3-, MPO-, and CD68-positive cells. This study demonstrates that ETosis increases with coronary thrombus maturation and is associated with local inflammation and impaired reperfusion in STEMI. Genetic variants in and may modulate inflammatory cell accumulation within thrombi. These findings suggest ETosis as a potential therapeutic target, particularly in patients with delayed presentation. - Source: PubMed
Publication date: 2026/07/03
Pangonytė DaliaŠimonytė SandritaLesauskaitė VaivaSiratavičiūtė VitalijaBakšytė GiedrėMarcinkevičienė JolantaStanionienė ZitaUtkienė LinaJusienė LinaRadikė RedaJaruševičius GediminasUnikas RamūnasVitkauskienė AstraDobilienė Olivija - This study aimed to investigate the mechanisms underlying impaired oral wound healing in aged individuals, with a focus on the roles of neutrophil extracellular traps (NETs) and NLRP3 inflammasome activation. - Source: PubMed
Publication date: 2026/07/01
Wang DongyangBai FuweiWang ZhanqiHe JunningLi HaiyunZhou FengChen TaoXiang LinMan YiWu Yingying - Antiphospholipid syndrome (APS) is an immunothrombotic disorder, frequently attributed to autoantibodies that bind β2-glycoprotein I (β2GPI). A study showed that the platelet-specific chemokine, platelet factor 4 (PF4), binds to β2GPI, enhancing recognition of β2GPI by APS antibodies. APS antibodies induce the release of neutrophil extracellular traps (NETs), webs of decondensed chromatin that bind both PF4 and b2GPI. We propose that PF4 bridges β2GPI to NETs (and other PF4-targeted polyanions), leading to the formation of prothrombotic PF4:b2GPI:NET immunotargets in APS. Dynamic light-scattering studies of isolated IgGs from four patients with triple-positive APS show formation of PF4:β2GPI:NET complexes that bind APS antibodies. NETs released in a microfluidic system bound b2GPI, but only in the presence of PF4, forming a multimolecular APS antigenic target. Whole blood infused through a photochemically-injured, endothelium-lined microfluidic channel formed platelet-, fibrin-, and complement- rich thrombi that bound APS antibody only in the presence of PF4. Thrombi were reduced in size if either ADAMTS13 or DNase1 was infused. In a murine APS model, wildtype and transgenic mice expressing platelet human PF4 ± FcgRIIA developed more intense neutrophil rolling along veins, and more extensive thrombus formation following laser injury to cremaster arterioles and venules, whereas mice lacking PF4 did not. Three antigenically distinct anti-hPF4 monoclonal antibodies blocked thrombosis in vitro, and neutrophil rolling and thrombosis in vivo. Our studies provide new insights into the basis of APS that has mechanistic parallels to other known PF4 immunothrombotic disorders and offer potential diagnostic and non-anticoagulant therapeutic strategies for clinical management. - Source: PubMed
Publication date: 2026/06/30
Field Conroy OSarkar AmritaBdeir KhalilKim HyunjunYadav Santosh KumarOberg JennaZhao GuohuaJiang StevenGumedelli ManasMcCrae Keith RArepally Gowthami MRollin JérômeGruel YvesOrtel Thomas LKowalska M AnnaCines Douglas BGollomp KandaceRauova LubicaPoncz Mortimer - After musculoskeletal injury, a considerable proportion of patients develop heterotopic ossification (HO), the formation of bone at ectopic sites. Traumatic HO is a disabling condition, potentially resulting in loss of joint function and compression of neurovascular structures. Available treatment options are often unsuccessful, frequently necessitating surgical resection of HO lesions with a high risk of recurrence. Given that myeloid cells, including neutrophils and macrophages, are among the first cell types to infiltrate injured tissue, the present study explored the relationship of extracellular traps (ETs) with HO formation in humans and mice. Human HO sample analysis revealed the presence of different stages of ETosis, which are clinically associated with increased ET concentrations in the blood. Experimentally, genetic impairment of ET resolution through combined and deficiency led to increased traumatic HO in mice, whereas HO was strongly attenuated by additional deletion of the ET generator . Neutrophil depletion impaired local ET formation, reduced HO formation, and blunted genotype-specific differences in HO outcome. In osteogenic precursors, ETs promoted matrix mineralization, and inhibition of ETosis or degradation of cell-free DNA, a major ET component, resulted in reduced osteogenesis. Pharmacological facilitation of ET clearance by dornase alfa, a US Food and Drug Administration-approved recombinant DNase1, or inhibition of ETs by the PADI4 inhibitor GSK484, resulted in inhibition of traumatic HO formation in mice without adversely affecting systemic bone remodeling. Together, our clinical and experimental findings demonstrate that traumatic HO is mediated by targetable neutrophil-dependent mechanisms, with altered ET formation contributing to these effects. - Source: PubMed
Publication date: 2026/05/06
Jiang ShanEis-Janzyk GesineAugustin RubenKleinertz HolgerSchröder SaskiaSevecke JanXie WeixinPan HaoyanBehrens IsabellWeisselberg SamiraAlbertsen Lilly-CharlotteMüller Elenavon Kroge SimonAlimy Assil-RaminFal MiladAmling MichaelTolosa EvaRenné ThomasFrosch Karl-HeinzMader KonradRolvien TimBaranowsky AnkeKeller Johannes