Substrate In Vitro Evidence:
1. RLI (RNase L inhibitor) expression is not regulated by interferon action. RLI expression in reticulocyte extracts antagonizes the 2-5A binding ability and the nuclease activity of endogenous RNase L. The overexpression of RLI in HeLa cells inhibits IFN activity on encephalomyocarditis. RLI is the first described mediator of the 2-5A/RNase L pathway. Bisbal, C et al. JBC 1995 Jun 2, 270(22):13308-17 PMID 7539425.
2. RLI is induced during HIV-1 infection and downregulates the 2-5A/RNase L pathway in human T cells, leading to an increase in HIV replication. RLI antisense cDNA-expressing clones reverse the inhibition of RNase L activity and leads to a decrease in viral load. Martinand, C et al. J Virol 1999 Jan, 73(1):290-6 PMID 9847332.
3. RLI is transiently induced by dsRNA. Martinand, C et al. J Interferon Cytokine Res 1998 Dec, 18(12):1031-8 PMID 9877446.
Tissue Distribution Evidence:
1. Northern blot shows ubiquitous expression of two transcript forms but differences in levels of expression suggest a tissue-specific regulation. Aubry, F et al. FEBS Lett 1996 Feb 26, 381(1-2):135-9 PMID 8641422.
