Matches in Nanopublications for { ?s ?p " To investigate this possibility, we induced endoplasmic reticulum stress by means of amino acid limitation or selective chemicals, and assessed the time course response of ATF5 and CYP2B6. We analyzed ATF5 mRNA and protein levels in HepG2 cells deprived of nutrients by incubation in amino acid-free KRB buffer. Figure 9B shows evidence that, despite no significant ATF5 mRNA changes, there was an important induction of ATF5 protein in human hepatoma cells. We investigated the effect of several stress stimuli in the CYP2B6 expression level and found that the incubation of HepG2 cells with amino acid?free KRB buffer and tunicamycin caused a timedependent increase of the CYP2B6 mRNA level (Fig. 9B), whereas other ER stress-inducing compounds, such as glucosamine, triggered a more modest activation (data not shown).We found a post-transcriptional up-regulation of ATF5 and a parallel induction of CYP2B6 mRNA. " ?g. }
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- _3 value " To investigate this possibility, we induced endoplasmic reticulum stress by means of amino acid limitation or selective chemicals, and assessed the time course response of ATF5 and CYP2B6. We analyzed ATF5 mRNA and protein levels in HepG2 cells deprived of nutrients by incubation in amino acid-free KRB buffer. Figure 9B shows evidence that, despite no significant ATF5 mRNA changes, there was an important induction of ATF5 protein in human hepatoma cells. We investigated the effect of several stress stimuli in the CYP2B6 expression level and found that the incubation of HepG2 cells with amino acid?free KRB buffer and tunicamycin caused a timedependent increase of the CYP2B6 mRNA level (Fig. 9B), whereas other ER stress-inducing compounds, such as glucosamine, triggered a more modest activation (data not shown).We found a post-transcriptional up-regulation of ATF5 and a parallel induction of CYP2B6 mRNA. " provenance.