Browse our anti-OAS2 (OAS2) Antibodies

Human 2'-5'-Oligoadenylate Synthetase 2, 69/71kDa (OAS2) interaction partners

1. OAS2 rs739901 5'-flanking C/A genetic polymorphisms involve the susceptibility to EV71 infection, and A allele might be a risk factor of the susceptibility to EV-71 infection.

2. Mx1 and OAS1-2 polymorphisms were associated with the severity of liver disease in HIV/HCV-coinfected patients, suggesting a significant role in the progression of hepatic fibrosis.

3. Epigenetic regulation of OAS2 shows disease-specific DNA methylation profiles at individual CpG sites.

4. we characterized the functional consequences of the Neandertal haplotype in the transcriptional regulation of OAS genes at baseline and infected conditions. We found that cells from people with the Neandertal-like haplotype express lower levels of OAS3 upon infection, as well as distinct isoforms of OAS1 and OAS2

5. Suggest 2'5'-oligoadenylate synthetase 2 mediates T-cell receptor CD3-zeta chain down-regulation via caspase-3 activation in oral cancer.

6. Data obtained suggest that the OAS2 rs1293762 and CD209 rs2287886 SNPs are associated with predisposition to chronic hepatitis C in Russian population.

7. Primary mononuclear cells from patients with systemic sclerosis have increased basal levels of OASL and OAS2 genes.

8. The results suggest that OAS1-OAS3-OAS2 haplotypes are associated with differential susceptibility to clinical outcomes of dengue infection.

9. The data suggest a possible association between OAS2 and OAS3 single nucleotide polymorphisms and the outcome of tick-borne encephalitis virus infection in a Russian population.

10. 2'-5'-oligoadenylate synthetase type 2 (OAS2), a dsRNA binding protein involved in the pathway that activates RNase-L, is identified as a new binding partner for NOD2.

Mouse (Murine) 2'-5'-Oligoadenylate Synthetase 2, 69/71kDa (OAS2) interaction partners

1. A non-synonymous mutation in Oas2 (I405N) in the viral sensor Oas2 was found and the mutation caused post-partum failure of lactation in healthy mice with otherwise normally developed mammary glands, characterized by greatly reduced milk protein synthesis coupled with epithelial cell death, inhibition of proliferation and a robust interferon response. The mutation activates the OAS2 pathway.

Pig (Porcine) 2'-5'-Oligoadenylate Synthetase 2, 69/71kDa (OAS2) interaction partners

1. Endogenous expression of the porcine OAS2 gene could be promoted by interferon (IFN)-beta or PRRSV infection in porcine alveolar macrophages. Knockdown of porcine OAS2 led to increases in PRRSV replication, and OAS2 expression suppressed replication of PRRSV in a retinoic acid inducible gene I (RIG-I)-dependent manner, anti-PRRSV activity of porcine OAS2 would be lost if RNase L and OAS2 were both silenced.