DNAS1_RABIT DNASE1 ELISA tesk kit
- Known as:
- DNAS1_RABIT DNASE1 Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen15128
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- Other suppliers
- Gene target:
- DNAS1_RABIT DNASE1 ELISA tesk kit
Related genes to: DNAS1_RABIT 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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- Neutrophil extracellular traps (NETs) are essential components of antimicrobial defense, but excessive or persistent NET accumulation can promote inflammation, tissue injury, thrombosis, and disease progression. DNase I is a major extracellular nuclease involved in the degradation of NETs and extracellular DNA, thereby contributing to immune homeostasis. Genetic variation in DNASE1 may influence this clearance capacity. Among DNASE1 polymorphisms, the Q222R substitution, designated DNASE1*2, is a common functional variant associated with reduced DNase I enzymatic activity. This reduction may limit NET degradation under conditions of increased extracellular DNA burden, such as inflammation and malignancy. Clinical studies have linked DNASE1*2 or DNase I phenotype 2 with myocardial infarction, adverse cardiovascular outcomes, and several malignancies. This review summarizes current evidence supporting DNASE1*2 as a potential genetic modifier of DNase I activity, NET clearance, and disease susceptibility. The review also discusses the possible clinical relevance of DNASE1*2 in disease risk, prognosis, and future genotype-informed therapeutic strategies, which require further validation. - Source: PubMed
Publication date: 2026/08/26
Razia SultanaKimura-Kataoka KaoriInoue KenTakeshita Haruo - To explore how neutrophil extracellular traps (NETs) mediate neuropathic pain in primary Sjögren's syndrome-associated peripheral neuropathy (pSS-PN). - Source: PubMed
Publication date: 2026/09/04
Xu LiyingWei JiyingChen DonghuaXu BihuaLiu YuxinFu XiangmingyangZheng JiamanTang LingLin JunhaoYang YiLi WeiYuan Chao - Prostate cancer (PCa) and Alzheimer's disease (AD) are age-related disorders with a complex epidemiological association and limited therapeutic options. Identifying shared molecular drivers may reveal new treatment targets. - Source: PubMed
Publication date: 2026/08/20
Wang MengxueQian YanrongHuang EnyaoChu ChunyanGao TianChen ShengrongZhao NaLuo CaichenLiu YifanZheng XiejunhaoHu HaowenHan BowenChen MingMao WeipuLi Wenchao - Fracture healing is an evolutionarily conserved process that depends on the complex interplay of osteogenic, angiogenic, and inflammatory responses. Impaired bone healing is observed in up to 10 to 15% of patients with fractures and can lead to nonunion, which is the absence of bone healing. Here, we explore a role of neutrophil extracellular traps (NETs) in fracture healing and their association with nonunion. In both mice and humans, skeletal injury triggers rapid but transient NET formation at the fracture site. The combined genetic deletion of enzymes essential for NET clearance, and , initially favors callus mineralization in the early healing phase. However, sustained NET elevation subsequently leads to impaired bone regeneration and fracture nonunion over the course of healing. Conversely, additional deletion of the NET-generating enzyme improves bone regeneration and lowers nonunion rates. Mechanistically, NETs up-regulate cGas-Sting signaling, thereby collapsing the formation of type-H vessels, which couple osteogenesis to angiogenesis in the fracture callus. Pharmacological inhibition of cGas-Sting restored type-H vessels, enhanced bone healing, and prevented nonunion in -deficient but not -deficient mice. In patients, serum NET markers declined during normal healing but were elevated in nonunion, correlating with excessive NET and STING accumulation in the callus. Therapeutically, the inhibition of NET formation with the Pad4 inhibitor GSK484 or the promotion of NET clearance with dornase alfa (recombinant DNase1) accelerated bone repair and prevented nonunion in preclinical models. These findings identify sustained NETs as a disruptor of fracture healing and a potential target for enhancing bone regeneration. - Source: PubMed
Publication date: 2026/09/02
Xie WeixinAlbertsen Lilly-CharlotteEis-Janzyk GesineKühlwein CharlotteJiang ShanSchlickewei CarstenKleinertz HolgerAugustin RubenSevecke JanSchröder SaskiaRickert MaylaWeisselberg SamiraDonat AntoniaPan HaoyanKnapstein PaulFischer VerenaHaffner-Luntzer MelanieBay AnnikaAmling MichaelRolvien TimKrause MatthiasRenné ThomasFrosch Karl-HeinzBaranowsky AnkeKeller Johannes - 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