EC Number   |
General Information |
Reference |
|---|
   2.7.7.84 | evolution |
conserved catalytic mechanism for the 2'- and 3'-specific nucleotidyl transferases. specific nucleotidyl transferases. Comparison with structures of other superfamily members indicates that the donor substrates are bound by conserved active site features while the acceptor substrates are oriented by nonconserved regions |
720462 |
| 2.7.7.84 | evolution |
in mice, the OAS gene family locates on chromosome 5 and consists of eight genes of Oas1 (Oas1a through Oas1h), Oas2, Oas3, and two OasL genes (OasL1 and OasL2). Oas1a and Oas1g are only active to convert ATP into di- and tri-2,5A, whereas Oas1b, Oas1c, Oas1d, Oas1e, Oas1f, Oas1h and MSM-derived Oas1b are inactive |
-, 761241 |
| 2.7.7.84 | evolution |
isozyme OAS1 belongs to the 2'-5'-oligoadenylate synthetases (OAS) family of interferon-inducible enzymes that act as pattern recognition receptors (PRR) to bind double-stranded RNA (dsRNA) during viral infection. The C-terminal catalytic domain of OAS2 (DII) shares strong sequence homology and catalytic aspartic acids (D408, D410, D481) with OAS1 |
760514 |
| 2.7.7.84 | evolution |
isozyme OAS2 belongs to the 2'-5'-oligoadenylate synthetases (OAS) family of interferon-inducible enzymes that act as pattern recognition receptors (PRR) to bind double-stranded RNA (dsRNA) during viral infection. The C-terminal catalytic domain of OAS2 (DII) shares strong sequence homology and catalytic aspartic acids (D408, D410, D481) with OAS1iral infection |
760514 |
| 2.7.7.84 | malfunction |
cells transfected with 25 AS antisense oligonucleotides inhibit the antiviral effect of IFN-gamma |
722625 |
| 2.7.7.84 | malfunction |
knockdown of endogenous OAS1 increases the PRRSV ORF7 mRNA level to 1.6 and 1.7times of that in control in 24 and 36 hours post-infection of PRRSV, respectively, and leads to approximate 5.5times increase of the frequency of fluorescence positive cells compared to negative control. Overexpression of OAS1 in Marc-145 cells can inhibit the replication of PRRSV |
760363 |
| 2.7.7.84 | malfunction |
mutation of the conserved Leu3 and Pro7 and of Cys330, Cys331, and Lys332 reduce enzyme activity |
720462 |
| 2.7.7.84 | malfunction |
mutation of the conserved Leu3 and Pro7 and of Cys330, Cys331, and Lys332 reduce enzyme activity. Mutants S62A and S63A display Michaelis-Menten kinetics toward NAD+, the kcat of the Ser62Ala mutant is approximately 3fold lower than the kcat for either the wild-type or the S63A mutant |
720462 |
| 2.7.7.84 | malfunction |
OAS2 knockdown increases ZIKV replication. Overexpression of OAS2 modestly increases the IFN-induced p-STAT1 both with IFN treatment and without IFN treatment compared to control. OAS2 overexpression also increases ISRE activity and some classical ISGs expression including Myxovirus resistance-A (MxA) and interferon-induced protein 2 (IFIT2) |
762508 |
| 2.7.7.84 | malfunction |
the effects of OASL silencing on cytokine and chemokine (MCP-1) secretion in THP-1 macrophages can be summarised as follows: I. TNF-alpha and IL-1beta secretion is enhanced during mycobacterial infection in the presence of OASL, II. OASL enhances MCP-1 production in response to THP-1 infection by pathogenic mycobacteria only, and III. IL-10 production is unaffected by the presence/absence of OASL. Silencing of OASL promotes intracellular replication of pathogenic and non-pathogenic mycobacteria, OASL exerts a suppressive effect on intracellular mycobacterial replication |
761910 |
