Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.27.5 (RNase)
 17,967 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Major changes in serum levels of insulin-like growth factor I (IGF-I) and IGF-binding proteins (IGFBPs) occur in children with end-stage liver disease in association with changes in body composition. We hypothesized that these changes would be associated with changes in hepatic messenger RNA (mRNA) expression. Eleven children with end-stage extrahepatic biliary atresia and 11 controls (liver donors) were studied. Serum samples were obtained from the children with biliary atresia immediately before orthotopic liver transplantation. Serum IGF-I, IGFBP-1, and IGFBP-2 levels were measured by radioimmunoassay, and IGFBP-3 by immunoradiometric assay. In both groups, growth hormone receptor mRNA expression was examined by quantitative reverse transcription-polymerase chain reaction, IGF-I mRNA expression by ribonuclease protection assay, and IGFBP-1 to -4 mRNA expression by Northern analysis. Growth hormone receptor and IGF-I mRNA levels were reduced 1.7-fold (P = .003) and 9.6-fold (P = .0001) in biliary atresia compared with levels in controls. Despite increased serum IGFBP-1 levels and reduced IGFBP-3 levels in biliary atresia, there was no change in either IGFBP-1 or IGFBP-3 mRNA expression. In contrast, serum levels and mRNA expression of IGFBP-2 were increased 1.6-fold (P = .003) and twofold (P = .0001), respectively, compared with controls. Gene expression did not correlate with liver dysfunction or body composition. Changes in growth hormone receptor and IGF-I mRNA expression may account for the reduction in serum IGF-I found in pediatric liver disease. In contrast, the marked alteration in circulating IGFBP levels was not accompanied by changes in hepatic IGFBP gene expression, suggesting that posttranslational mechanisms may be important.
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PMID:Hepatic growth hormone receptor, insulin-like growth factor I, and insulin-like growth factor-binding protein messenger RNA expression in pediatric liver disease. 939 4

Growth hormone receptor (GHR) cDNA and gene of the Japanese flounder (Paralicthys olivaceus) were cloned and their molecular structures were characterized. The 641 amino acid sequence predicted from the cDNA sequence showed more than 75% overall sequence similarity with GHRs of other teleosts such as turbot and goldfish, and contained common structural features of vertebrate GHRs. The extracellular domain of flounder GHR had three pairs of cysteines and an FGEFS motif with a replacement E to D. The cytoplasmic domain contained two conserved motifs referred to as box 1 and box 2. The flounder GHR gene was cloned by PCR using primers designed from the sequence of the GHR cDNA. The GHR gene was composed of 10 exons. The sequence of exon 1 corresponded to the 5'-untranslated region of the cDNA, and exons 2-6 encoded most parts of the extracellular domain. The transmembrane domain was found in exon 7, and the intracellular domain was encoded in exons 8-10. Exon 10 also encoded the 3'-untranslated region. Comparison of the flounder GHR gene with the human GHR gene shows that the flounder gene contains no exons corresponding to exon 3 of the human GHR gene, and that the region corresponding to exon 10 in the human GHR gene is encoded by exons 9 and 10 in the flounder GHR gene. These findings indicate that the flounder GHR gene diverged from those of mammalian and avian GHR genes, especially in the organization of the exons encoding the cytoplasmic domain. In addition to the regular form of GHR mRNA, a 3'-truncated form lacking the region derived from exons 9 and 10 was detected as a minor species in the liver by RT-PCR and by RNase protection assay. RT-PCR analysis showed that both the regular and the 3'-truncated GHR mRNAs are expressed in a wide range of flounder tissues with the highest levels being found in the liver. The 5'-flanking region of the flounder GHR gene was cloned by inverse PCR, and three transcription start points were identified with similar frequency by RNase protection assay.
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PMID:Characterization of structure and expression of the growth hormone receptor gene of the Japanese flounder (Paralichtys olivaceus). 1522 40

Growth hormone receptor (GHR) played key roles in human and animal growth. Both human laron type dwarfism and sex linked dwarf chicken were caused by the mutation of GHR gene. In this study, we identified an endogenously expressed long non-coding natural antisense transcript, GHR-AS, which overlapped with the GHR mRNA (GHR-S) in a tail to tail manner. Spatial and temporal expression analyses indicated that GHR-AS were highly expressed in chicken liver and displayed ascending with the development of chicken from E10 to 3 w of age. Interfering GHR-AS caused GHR-S decreasing, accompanied with increasing of the inactive gene indicator, H3K9me2, in the GHR-S promoter regions in LMH cells. RNase A experiment exhibited that GHR-AS and GHR-S can form double strand RNAs at the last exon of GHR gene in vivo and in vitro, which hinted they could act on each other via the region. In addition, the levels of GHR-S and GHR-AS can be affected by DNA methylation. Compared the normal chicken with the dwarfs, the negative correlation trends were showed between the GHR-S promoter methylation status and the GHR-AS levels. This is the first report of that GHR gene possessed natural antisense transcript and the results presented here further highlight the fine and complicated regulating mechanism of GHR gene in chicken development.
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PMID:Chicken GHR natural antisense transcript regulates GHR mRNA in LMH cells. 2771 55