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Treatment of primary hepatocytes with the ER stressor tunicamycin (TM) upregulated UPR-responsive mRNAs, whereas etomoxir cotreatment suppressed this effect (Figure 1A)
As shown in Table 1, AID significantly improved almost all CGM metrics compared to MDI
Jakubowski and collaborators have recently reported that cells efficiently convert homocysteine into homocysteine thiolactone by methionyl-tRNA synthetase (Jakubowski et al, 2000b)
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