Aliases for OAS1 Gene
External Ids for OAS1 Gene
Previous HGNC Symbols for OAS1 Gene
Previous GeneCards Identifiers for OAS1 Gene
This gene is induced by interferons and encodes a protein that synthesizes 2',5'-oligoadenylates (2-5As). This protein activates latent RNase L, which results in viral RNA degradation and the inhibition of viral replication. Alternative splicing results in multiple transcript variants with different enzymatic activities. Polymorphisms in this gene have been associated with susceptibility to viral infection and diabetes mellitus, type 1. A disease-associated allele in a splice acceptor site influences the production of the p46 splice isoform. This gene is located in a cluster of related genes on chromosome 12. [provided by RefSeq, Feb 2016]
GeneCards Summary for OAS1 Gene
OAS1 (2'-5'-Oligoadenylate Synthetase 1) is a Protein Coding gene. Diseases associated with OAS1 include Diabetes Mellitus, Insulin-Dependent and Hand, Foot And Mouth Disease. Among its related pathways are Type II interferon signaling (IFNG) and Hepatitis C. Gene Ontology (GO) annotations related to this gene include RNA binding and transferase activity. An important paralog of this gene is OAS3.
UniProtKB/Swiss-Prot for OAS1 Gene
Interferon-induced, dsRNA-activated antiviral enzyme which plays a critical role in cellular innate antiviral response. In addition, it may also play a role in other cellular processes such as apoptosis, cell growth, differentiation and gene regulation. Synthesizes higher oligomers of 2-5-oligoadenylates (2-5A) from ATP which then bind to the inactive monomeric form of ribonuclease L (RNase L) leading to its dimerization and subsequent activation. Activation of RNase L leads to degradation of cellular as well as viral RNA, resulting in the inhibition of protein synthesis, thus terminating viral replication. Can mediate the antiviral effect via the classical RNase L-dependent pathway or an alternative antiviral pathway independent of RNase L. The secreted form displays antiviral effect against vesicular stomatitis virus (VSV), herpes simplex virus type 2 (HSV-2), and encephalomyocarditis virus (EMCV) and stimulates the alternative antiviral pathway independent of RNase L.