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- W2068030732 abstract "Primer extension and RNase protection analyses of the rat β2-adrenergic receptor (β2AR) gene identify two transcription start points at −64 and −220 nt, respectively. Transient transfections of putative promoter/pCAT constructs into DDT1 MF-2 cells indicate that fragments −36 to −100 (P1) and −186 to −312 (P2) are sufficient to promote transcription, whereas −911 to −1122 contains a negative regulatory element(s). RNase protection analysis of the 3‘ untranslated region (3‘-UTR) indicates the presence of two transcripts with 3‘-UTR of 111 and 604 nt exclusive of the poly(A+) tails. Northern blots of β2AR mRNA using full-length and partial cDNA probes indicate that a major 2.2 kb and a minor 1.6 kb species arise from the use of alternative promoters as well as different polyadenylation signals. DNase I footprinting and DNA mobility shift assays (DMSA) using rat liver nuclear extracts identify a number of transcription factors binding to sequence elements within or upstream from P1 and P2, including Sp1, CRE, CP1, AP-2, NF-1, NF-κB, and C/EBP. Supershift assays using antibodies against C/EBPα and C/EBPβ and mutational analyses indicate that the protein binding to the C/EBP consensus recognition site at −925 to −933 is C/EBPα. The activity of promoter/CAT constructs containing the C/EBP recognition site is significantly decreased by cotransfection of C/EBPα but not C/EBPβ into either DDT1 MF-2 cells or primary rat hepatocytes. Partial hepatectomy causes a transient decrease in C/EBPα, as measured by DMSA, and an increase in β2AR mRNA levels and rate of transcription in the remnant liver. Thus, derepression via C/EBPα is likely involved in the up-regulation of β2AR in the regenerating rat liver." @default.
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- W2068030732 date "1996-01-01" @default.
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- W2068030732 title "DNA Elements and Protein Factors Involved in the Transcription of the β<sub>2</sub>-Adrenergic Receptor Gene in Rat Liver. The Negative Regulatory Role of C/EBPα" @default.
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- W2068030732 doi "https://doi.org/10.1021/bi960844o" @default.
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