RNASEL

2-5A-dependent ribonuclease

Endoribonuclease that functions in the interferon (IFN) antiviral response (PubMed:11585831, PubMed:26263979). In INF treated and virus infected cells, RNASEL probably mediates its antiviral effects through a combination of direct cleavage of single-stranded viral RNAs, inhibition of protein synthesis through the degradation of rRNA, induction of apoptosis, and induction of other antiviral genes (PubMed:11585831, PubMed:26263979). RNASEL mediated apoptosis is the result of a JNK-dependent stress-response pathway leading to cytochrome c release from mitochondria and caspase-dependent apoptosis (PubMed:11585831, PubMed:26263979). Therefore, activation of RNASEL could lead to elimination of virus infected cells under some circumstances (PubMed:11585831, PubMed:26263979). In the crosstalk between autophagy and apoptosis proposed to induce autophagy as an early stress response to small double-stranded RNA and at later stages of prolonged stress to activate caspase-dependent proteolytic cleavage of BECN1 to terminate autophagy and promote apoptosis (PubMed:26263979). Might play a central role in the regulation of mRNA turnover (PubMed:11585831). Cleaves 3' of UpNp dimers, with preference for UU and UA sequences, to sets of discrete products ranging from between 4 and 22 nucleotides in length. Involved in intercellular immune signaling (PubMed:40010341). Cross-activated by 2',5'-oligoadenylates (2-5A) previously generated in RNA virus-infected cells, triggers type I interferon signaling in uninfected neighboring cells to limit local spread of infection (PubMed:40010341)