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RNASEL (2-5A-dependent ribonuclease) is an enzyme. In the public catalogues the evidence so far is association rather than a proven role. Tied to Prostate cancer.
Endoribonuclease that functions in the interferon (IFN) antiviral response. 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. RNASEL mediated apoptosis is the result of a JNK-dependent stress-response pathway leading to cytochrome c release from mitochondria and caspase-dependent apoptosis.
Open Targets scores its association with cancer at 0.58 (direct and indirect evidence; datatypes literature 0.96, genetic association 0.78, genetic literature 0.61).
In plain words · RNASEL (2-5A-dependent ribonuclease) is an enzyme. In the public catalogues the evidence so far is association rather than a proven role. Tied to Prostate cancer.
RNASEL (2-5A-dependent ribonuclease) is an enzyme. In the public catalogues the evidence so far is association rather than a proven role. Tied to Prostate cancer.
Endoribonuclease that functions in the interferon (IFN) antiviral response.
No product in this corpus aims at RNASEL yet. Inhibitors are shaped to fit the enzyme's active site so the reaction the cancer relies on stops.
First described 1993. Earliest sequence paper UniProt cites for the protein: Zhou et al, Cell, 1993, "Expression cloning of 2-5A-dependent RNAase: a uniquely regulated mediator of interferon action". Source.
Sources: HGNC HGNC:10050 (approved symbol, name, aliases, locus and cross-references (hgnc_complete_set.txt)); UniProt Q05823 (protein name, function text, keywords and locations (REST API)); Open Targets ENSG00000135828 (association with cancer (MONDO_0004992) 0.58; per-cancer scores at or above 0.5: prostate cancer 0.56 (GraphQL API, CC0))
Endoribonuclease that functions in the interferon (IFN) antiviral response. 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. RNASEL mediated apoptosis is the result of a JNK-dependent stress-response pathway leading to cytochrome c release from mitochondria and caspase-dependent apoptosis. Therefore, activation of RNASEL could lead to elimination of virus infected cells under some circumstances. 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. Might play a central role in the regulation of mRNA turnover. Location: Cytoplasm; Mitochondrion (UniProt). Locus 1q25.3 (HGNC).
Query for this target: (TITLE:"RNASEL" OR ABSTRACT:"RNASEL" OR TITLE:"ribonuclease L" OR ABSTRACT:"ribonuclease L" OR TITLE:"2-5A-dependent ribonuclease" OR ABSTRACT:"2-5A-dependent ribonuclease" OR TITLE:"RNS4" OR ABSTRACT:"RNS4" OR TITLE:"PRCA1" OR ABSTRACT:"PRCA1") AND (cancer OR tumor OR tumour OR oncology OR carcinoma OR lymphoma OR leukemia OR leukaemia OR myeloma OR sarcoma OR melanoma OR glioma). Results are unfiltered search hits about RNASEL, not a curated reading list.