Association of hepatic ?2-adrenergic receptor gene transcript destabilization during postnatal development in the sprague-dawley rat with a Mr 85,000 protein that binds selectively to the ?2-adrenergic receptor mRNA 3?-untranslated region

Publisher Website
Google Scholar
Abstract
In the liver, transcript destabilization contributes to the decrease in steady-state levels of β2-adrenergic receptor mRNA that occurs during early postnatal development in the rat. From genomic DNA, polymerase chain reaction (PCR) was used to amplify a 718-basepair (bp) fragment of the β2-adrenergic receptor gene including the entire 3′-untranslated region. Results from SDS-gel electrophoresis and autoradiography demonstrated a Mr 85,000 cellular factor present in postnatal day 60, but not fetal day 18 rat liver that was ultraviolet (UV) light-crosslinked to in vitro transcribed β2-adrenergic receptor RNA 3′-untranslated region. Unlabeled β2-adrenergic receptor RNA 3′-untranslated region, but not mouse β-actin RNA, competed with labeled β2-adrenergic receptor RNA 3′-untranslated region for binding to the Mr 85,000 protein. Cross-linking of the β2-adrenergic receptor RNA 3′-untranslated region to the Mr 85,000 protein was inhibited by the ribohomopolymer poly(U), with poly(A), poly(C) and poly(G) having little or no effect. Thus, a Mr 85,000 protein has been identified in adult male rat liver that may interact with U-rich sequences in the 3′-untranslated region of the β2-adrenergic receptor mRNA and may account for the decreased stability of hepatic β2-adrenergic receptor gene transcripts that occurs during development.