Anti-DNASE1L3 / Deoxyribonuclease gamma

In 1X PBS, pH 7.4, with 0.09% sodium azide. DNASE1L3 is a member of the deoxyribonuclease enzyme family, responsible for breaking down DNA molecules into smaller fragments. This process is essential for the clearance of cellular debris, including dying cells and extracellular DNA released during inflammation. Without the action of DNASE1L3, the accumulation of DNA waste can lead to autoimmune diseases and other inflammatory conditions. Research has shown that DNASE1L3 plays a key role in modulating immune responses and protecting against inflammatory damage. By efficiently clearing DNA debris, this enzyme helps to maintain the balance between immunity and tolerance in the body. Dysregulation of DNASE1L3 activity has been linked to various autoimmune disorders, highlighting the importance of this enzyme in immune homeostasis. Furthermore, DNASE1L3 has been identified as a potential therapeutic target for treating autoimmune diseases and inflammatory conditions. By enhancing the activity of this enzyme, researchers hope to restore immune balance and prevent the development of autoimmune reactions. Protein function: Has DNA hydrolytic activity. Is capable of both single- and double-stranded DNA cleavage, producing DNA fragments with 3'-OH ends. Can cleave chromatin to nucleosomal units and cleaves nucleosomal and liposome-coated DNA (PubMed:10807908, PubMed:14646506, PubMed:27293190, PubMed:9070308, PubMed:9714828). Acts in internucleosomal DNA fragmentation (INDF) during apoptosis and necrosis (PubMed:23229555, PubMed:24312463). The role in apoptosis includes myogenic and neuronal differentiation, and BCR-mediated clonal deletion of self-reactive B cells. Is active on chromatin in apoptotic cell-derived membrane-coated microparticles and thus suppresses anti-DNA autoimmunity (PubMed:27293190). Together with DNASE1, plays a key role in degrading neutrophil extracellular traps (NETs). NETs are mainly composed of DNA fibers and are released by neutrophils to bind pathogens during inflammation. Degradation of intravascular NETs by DNASE1 and DNASE1L3 is required to prevent formation of clots that obstruct blood vessels and cause organ damage following inflammation. [The UniProt Consortium]