Differential regulation of ZFAS1 splice variants by endoplasmic reticulum stress in hepatocyte cell lines.

Indeed, we demonstrate that levels of ZFAS1 and its variants were resistant to an 18‐h treatment with the Pol II inhibitor ACTD; treatment with the Pol II and CK2 inhibitor DRB in fact showed a trend toward increased abundance.

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Testing for the abundance of UPR effectors, ZFAS1 suppression reduced BiP expression only under steady‐state conditions, although the effect was small and did not reach statistical significance at the protein level.

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