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- W2020165052 abstract "Hepatic responsiveness to beta 2-adrenergic stimulation is dynamically regulated during early development as well as following hepatic injury and disease. In the present study, the molecular mechanisms that underlie the decline in the steady-state levels of hepatic beta 2-adrenergic receptor mRNA that occurs during development in the male rat were investigated. As determined by nuclear run-on assays, an age-associated reduction in beta 2-adrenergic receptor gene transcription was observed. The transcription rate of the beta 2-adrenergic receptor gene in postnatal day 18 liver was approximately 50% lower than that of fetal liver. Stability of beta 2-adrenergic receptor gene transcripts was highest (t1/2 approximately 6h) in hepatocytes isolated from fetal rats and was lowest (t1/2 approximately 6h) in hepatocytes from postnatal day 14 rats. In fetal hepatocytes, but not postnatal day 2 hepatocytes, cycloheximide appeared to stabilize beta 2-adrenergic receptor gene transcripts in the presence of actinomycin D. These findings establish the molecular basis of reduced steady-state levels of beta 2-adrenergic receptor mRNA in liver during early postnatal development and suggest multilevel regulatory control of hepatic beta 2-adrenergic receptor gene expression." @default.
- W2020165052 created "2016-06-24" @default.
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- W2020165052 date "1993-10-01" @default.
- W2020165052 modified "2023-09-27" @default.
- W2020165052 title "Transcriptional and posttranscriptional regulation of hepatic ?2-adrenergic receptor gene expression during development" @default.
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- W2020165052 doi "https://doi.org/10.1002/jcp.1041570109" @default.
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