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. Author manuscript; available in PMC: 2016 Dec 15.
Published in final edited form as: Cell Mol Gastroenterol Hepatol. 2015 Oct 13;2(1):63–76.e5. doi: 10.1016/j.jcmgh.2015.08.008

Figure 7. Loss of UGT1A potentiates ER stress induced by actinomycin D, etoposide, or DSS treatment.

Figure 7

LS180 and HT29 cells were pretreated with UGT1A siRNA or non-specific siRNA for 48 hours and then incubated with actinomycin D (ActD, 40 nM) or etoposide (Eto, 80 μM) for 36 hours. Ugt1ΔIEC and Ugt1F/F mice were treated with 3% DSS in drinking water and colon tissues were collected. Expression of ER stress-responsive genes was quantitated by Q-PCR.