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Thus, activation of RNase L (show RNASEL Proteins) does not require mouse hepatitis virus virus-induced interferon (show IFNA Proteins) but rather correlates with adequate levels of basal Oas (show SMOC1 Proteins) gene expression, maintained by basal interferon (show IFNA Proteins) signaling.
Mouse hepatitis virus Ns2 cleaves 2',5'-oligoadenylate, the product of 2',5'-oligoadenylate synthetase, to prevent activation of the cellular endoribonuclease RNase L (show RNASEL Proteins) and consequently block viral RNA degradation.
Activation of Oas1a gene expression by type I IFN requires both STAT1 (show STAT1 Proteins) and STAT2 (show STAT2 Proteins)
In the absence of a functional OAS1a pathway, herpes simplex virus type 1 antigen expression is more widespread, and the ability of IFN-beta (show IFNB1 Proteins) transgene treatment to reduce infectious HSV-1 in eyes and trigeminal ganglia is lost.
May play a role in mediating resistance to virus infection, control of cell growth, differentiation, and apoptosis.
(2-5')oligo(A) synthase 1A
, (2-5')oligo(A) synthetase 1A
, 2'-5'-oligoadenylate synthase 1A
, 2-5A synthase 1A
, 2-5A synthetase 1A
, p42 OAS