April 2020 Nsp3 abcam ab181620 Nucleocapsid Sino Biological 40143-MM05 Validation Commercial antibodies validated as per manufacturers website: Beta actin Sigma A5441 Immunoblot on chicken fibroblast cell extracts Spike Abcam Ab252690 Validated by ELISA on free peptide from SARS-CoV-1 Nsp3 abcam ab181620 Validated by western blot on SARS-CoV-1 infected cells Nucleocapsid Sino Biological 40143-MM05 Validated by western blot with corresponding viruses Eukaryotic cell lines Policy information about cell lines Cell line source(s) VeroE6 cells were obtained from ATCC, Calu-3 cells were obtained from Manfred Frey, originally from ATCC. Authentication Cells were not further authenticated Mycoplasma contamination Cells have been tested and are free of mycoplasma.

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Background and Purpose-We observed recently that elevated plasma cysteine levels are associated with poor clinical outcome in acute stroke patients. In a rat stroke model, cysteine administration increased the infarct volume apparently via its conversion to hydrogen sulfide (H 2 S). We therefore investigated the effects of H 2 S and the inhibition of its formation on stroke. Methods-Cerebral ischemia was studied in a rat stroke model created by permanent occlusion of the middle cerebral artery (MCAO). The resultant infarct volume was measured 24 hours after occlusion. Results-Administration of sodium hydrosulfide (NaHS, an H 2 S donor) significantly increased the infarct volume after MCAO. The NaHS-induced increase in infarct volume was abolished by the administration of dizolcilpine maleate (an N-methyl-D-aspartate receptor channel blocker). MCAO caused an increase in H 2 S level in the lesioned cortex as well as an increase in the H 2 S synthesizing activity. Administration of 4 different inhibitors of H 2 S synthesis reduced MCAO-induced infarct volume dose dependently. The potency of these inhibitors in effecting neuroprotection in vivo appeared to parallel their potency as inhibitors of H 2 S synthesis in vitro. It also appeared that most of the H 2 S synthesizing activity in the cortex results from the action of cystathionine ␤-synthase. Conclusions-The present results strongly suggest that H 2 S plays a part in cerebral ischemic damage after stroke.Inhibition of H 2 S synthesis should be investigated for its potential as a novel neuroprotective stroke therapy.