be traced to known cis (ChORE) and trans (ChREBP) elements (Figure S5G–I), transcriptional activation is significantly weaker than under hyperglycemia, and hence insufficient to account for the robust increases in TXNIP mRNA to their new steady-states under ER stress. This implied either the existence of unidentified trans factors and/or cis elements that stimulate TXNIP transcription under ER stress, or that the induction is also due to processes other than transcription. To test this second possibility, we asked whether the rapid induction of TXNIP upon ER stress is due in part to changes in mRNA stability. By measuring mRNA half-life when transcription is arrested by Actinomycin D (ActD), we find that TXNIP mRNA is inherently labile, but that it becomes significantly stabilized (~ 3 fold) during ER stress (Figure 3A and B).
