Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.27.1 (RNase)
16,360 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During brain maturation, histone H1(0) accumulates in both nerve and glial cells. The expression of this "linker" histone, the role of which still remains unclear, is a complex process, having both transcriptional and post-transcriptional regulatory components. In particular, the expression of H1(0) in rat cortical neurons is regulated mainly at the post-transcriptional level, and unknown cellular proteins are likely to affect H1(0) mRNA stability and/or translation. In looking for such factors, we tested the ability of rat brain extracts to protect H1(0) RNA probe from degradation by T1 RNase. The results reported here demonstrate that rat brain contains at least one major (p40) and two minor (p110 and p70) binding factors, specific for H1(0) RNA, all of which are much more or exclusively expressed in adult rat brain, when compared with other tissues. The binding of the factors is confined to a portion of the 3'-untranslated region (3'-UTR), which is highly conserved among murine and human H1(0) mRNAs. These findings suggest that the proteins identified play a critical role in regulating the expression of H1(0) histone in the brain of mammals.
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PMID:H1(0) RNA-binding proteins specifically expressed in the rat brain. 971 12

There is increasing evidence that the 5'UTR of mRNAs affects regulation of gene expression in eukaryotic cells. We examined the overexpression of the mu-opioid receptor in High Five insect cells, employing rat mu-receptor cDNA linked to variable lenghts of their native 5'UTR. The sequences employed consist of either 209 nucleotides (termed ,,long") upstream the translation initiation site of the mu-receptor mRNA, or a truncated 5'UTR comprising only 11 nucleotides (,,short"). These constructs served to generate recombinant baculovirus for the expression of mu-receptor protein in High Five insect cells. 48 hours after baculovirus infection cells were harvested for mu-receptor characterization or RNA analysis. Scatchard analysis of radioligand binding consistently revealed three to four fold higher concentrations of the mu-opioid receptors expressed with the ,,long" over the ,,short" UTR containing baculovirus. The distinct expression rates of mu-receptors paralleled the amounts of mRNAs determined by RNase protection assay. Regardless of the distinct 5'UTR regions, the expressed opioid receptors displayed identical high affinity binding characteristics for the opioid antagonist diprenorphine and similar EC50 values to inhibit forskolin (10(-5) M) stimulated cAMP synthesis. Our results demonstrate that the native 5'UTR of the mu-opioid receptor has an enhancing effect on expression in the baculovirus/insect cell system.
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PMID:Mu-opioid receptor expression in High Five insect cells is regulated by 5' untranslated region (5'UTR). 1020 40

In sunflower, PET1-cytoplasmic male sterility is correlated with the presence of a novel mitochondrial gene (orf522) located 3' to the atpA gene. The dicistronic atpA-orf522 transcripts are preferentially destabilized in male florets of 'restored to fertility' plants as compared with sterile plants. In this report, we show that atpA-orf522 transcripts may be polyadenylated in vivo at their 3' termini and that a tissue-specific increase in the level of polyadenylated atpA-orf522 transcripts correlates with the tissue-specific instability of atpA-orf522 mRNAs in male florets of the restored hybrid plants. In addition, we have identified two distinct ribonuclease activities in sunflower mitochondria, one of which preferentially degrades polyadenylated as compared with non-polyadenylated RNA substrates corresponding to the 3' UTR of atpA-orf522 transcripts. These in vivo and in vitro results show that polyadenylation is involved in the degradation pathway of the mitochondrial atpA-orf522 transcripts and that polyadenylation can be developmentally regulated by a nuclear gene(s) upon restoration of fertility.
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PMID:Polyadenylation accelerates the degradation of the mitochondrial mRNA associated with cytoplasmic male sterility in sunflower. 1039 90

In the mouse, GH-binding protein (GHBP) and GH receptor (GHR) are encoded by a single gene via alternative splicing. We previously demonstrated that the steady-state levels of the GHR and GHBP mRNAs are significantly elevated in mouse liver during pregnancy. Hepatic GHR and GHBP mRNAs are associated primarily with one of two different 5' untranslated regions (5' UTRs), designated 5' UTR Liver1 (L1) and Liver2 (L2). Distinct promoters associated with each of these 5' UTRs have recently been characterized. In the present study, we have investigated the role of transcriptional activation in the pregnancy-induced upregulation of GHR and GHBP mRNAs in liver. We also report on the relative contribution of the 5' UTR L1 and 5' UTR L2 promoters to the hepatic expression of the GHR/GHBP gene in the liver. Our approach was to compare, by ribonuclease protection assay (RPA), GHR/GHBP transcript levels in hepatic nuclear and total cellular RNA samples from virgin and late-pregnant mice. In these RPAs we utilized riboprobes that were complementary to the coding region of GHR/GHBP transcripts, as well as to the two noncoding, alternative first exons 5' UTR L1 and L2. When employing the coding region probe, RPAs revealed that the gestational increase in the levels of nuclear GHR/GHBP transcripts were statistically comparable with the increase in GHR/GHBP transcript levels in total cellular RNA. This finding suggests that enhanced transcriptional activity, rather than increased cytoplasmic half-life, is responsible for the upregulation of GHR/GHBP RNA in the pregnant liver. In RPAs utilizing the noncoding region probes, both nuclear and total cellular GHR/GHBP transcripts associated with 5' UTR L1 were significantly upregulated in late-pregnant as compared with virgin mice. In contrast, the levels of both nuclear and total GHR/GHBP transcripts associated with 5' UTR L2 were comparable between nonpregnant and pregnant animals. Moreover, 5' UTR L2-containing transcripts were present at levels that were only 3-5% of the 5' UTR L1-associated transcripts in the late-pregnant liver. Thus, we conclude that the gestational upregulation of the GHR/GHBP gene in the mouse liver can be ascribed to the significantly enhanced transcriptional activity of the 5' UTR L1 promoter.
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PMID:Transcriptional upregulation of hepatic GH receptor and GH-binding protein expression during pregnancy in the mouse. 1042 50

The AMPA (alpha-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid)-preferring receptor is one of the pharmacologically defined ionotropic glutamate receptors, which mediate fast excitatory synaptic transmission in the central nervous system of vertebrates. Here, we report the mapping of the transcriptional start points and identification of the intron-exon boundaries of the teleost AMPA receptor subunit gene fGluR2 beta. fGluR2 beta and the mouse GluR2 share a similar genomic organization, having identical intron insertion sites and a large intron 2; however, fGluR2 beta has an extra exon encoding an alternate 5'-UTR. Results of RT-PCR and RNase protection analyses indicate that mature fish brain expresses two types of fGluR2 beta transcripts with different 5' ends. Transcriptions of these two fGluR2 beta transcripts started from two chromosomal regions separated by at least 10 kb. Only the transcript starting from the region more upstream on the chromosome was spliced. Moreover, transcript initiated from the downstream region was more abundant than that initiated from the upstream region.
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PMID:Genomic organization of the Oreochromis mossambicus glutamate receptor subunit 2 beta gene (fGluR2 beta): presence of two different 5'-untranslated regions. 1052 56

Gamma-aminobutyric acid (GABA) type A receptors are multisubunit ligand-gated ion channels which mediate inhibition in the brain. The GABA(A) receptor alpha3 subunit gene exhibits extensive variation in its developmental and regional expression, but the detailed mechanisms governing the expression patterns of this gene remain unknown. We have cloned and begun to characterize the murine alpha3 subunit gene Gabra3. All but one of the 10 exons and the intron-exon boundaries have been sequenced; the first intron is in the 5' untranslated region (5'UTR) of the alpha3 mRNA. Rapid amplification of the cDNA 5'-end (5'-RACE) and RNase protection indicated many transcription start sites, with the major site (=+1) corresponding to a 5'UTR of 178 bases. Most sites were in or just downstream of a region of 55 (mouse) and 25 (human) GA repeats in the proximal promoter, as revealed by genome walking of Gabra3 and the human gene GABRA3. No canonical TATA or CAAT boxes or initiator (Inr) sites were found in either promoter, but both contained conserved consensus sites for several transcription factors. Progressive deletion of the mouse promoter produced positive or negative effects on expression of reporter (luciferase) constructs, with the highest observed activity in several types of transiently transfected cells for a construct containing bases -320 to +35. The GA repeats and a much shorter nearby series of four GC repeats, the first three of which are part of a consensus E2F site, appear to contribute significantly to mouse promoter activity. Upstream GA repeats enhanced activity of the SV40 promoter, and the GA repeat sequence bound nuclear proteins from several tissues.
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PMID:The mouse GABA(A) receptor alpha3 subunit gene and promoter. 1058 10

The murine gastrin-releasing peptide receptor (mGRP-R) is a member of the G protein-coupled receptor family and mediates important physiological actions of its specific ligand, the gastrointestinal hormone/neurotransmitter GRP, including mitogenic properties in the mouse Swiss 3T3 fibroblasts. Glucocorticoids and increases in intracellular cAMP are reported to alter GRP-R gene transcription, but the molecular basis for these effects is unknown. To begin to identify possible gene regulatory mechanisms that are responsible for modifying mGRP-R expression, we determined its structure and investigated its basal promoter activity. We isolated and characterized genomic bacteriophage P1 clones encoding the mouse gastrin-releasing peptide receptor (mGRP-R). By DNA sequencing and Southern blot analyses, we determined the protein coding region to be contained in three exons interrupted by two introns 20 and 2kb in length. The open reading frame of the putative GRP-R gene encodes for a 384-amino-acid protein which demonstrates 48% identity with the mouse BRS-3 protein and 53% identity with the mouse NMB-R protein. The mGRP-R gene locus extends over 29kb and was mapped to the X-chromosome (DXMit20) utilizing a minisatellite polymorphism in the 5' UTR and by fluorescent in-situ hybridization (FISH). In Swiss 3T3 cells, which natively express mGRP-R, two gene-specific mRNA species of 3 and 7kb can be detected by Northern blot analysis. With RNase protection assays, and independently with inverse PCR of 5' RACE clones, common mRNA initiation sites were identified clustered between 21 and 61bp downstream of a TTTAAA motif, which is located 450bp upstream of the ATG translation start site. However, different polyadenylation sites are utilized. A 2kb genomic DNA fragment extending from 2147 to 141 bases 5' to the ATG translation start was cloned into a luciferase reporter plasmid and shown to contain promoter activity in Swiss 3T3 and COS-7 cells. Progressive promoter truncations and mutations of a cyclic AMP response element (CRE) located 83bp upstream of the TTTAAA motif demonstrate that transcriptional mGRP-R activation in Swiss 3T3 cells only occurs when both the TTTAAA motif and the intact CRE site are retained. With the availability of the full structure of the mGRP-R gene and the minimal promoter sequences reported in this study, it will be possible in future studies to investigate the molecular basis for transcriptional regulation of the mGRP-R gene by glucocorticoids, cAMP and other factors.
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PMID:Molecular organization of the mouse gastrin-releasing peptide receptor gene and its promoter. 1068 96

During evaluation of follicle-stimulating hormone-beta (FSHB) expression in anterior pituitary glands by an RNase protection assay (RPA), the expected fragment of 205 nucleotides at positions 759-963 was not detected in one boar that had moderate plasma and pituitary FSH concentrations. After subcloning and sequencing, mRNA from this boar lacked an 11-bp fragment (5'-CATTTGGAAAC-3') at nucleotide positions 807-817 of the 3'-untranslated region (3'-UTR, D allele). Wild-type FSHB (WT allele) was present in pituitary RNA and genomic DNA in both Meishan (MS) and White Composite (WC) pigs; whereas the D allele was present only in MS pigs (P < 0.01; 5/6 MS vs. 0/6 WC). Also, we found the D allele in five other Chinese breeds but absent in ten American Landrace, 11 Yorkshire and 17 Berkshire pigs. Additionally, the D allele had one silent nucleotide change in the coding region plus six, single nucleotide changes in the 3'-UTR.
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PMID:Identification and characterization of a new allele for the beta subunit of follicle-stimulating hormone in Chinese pig breeds. 1069 Mar 58

Regulation of pituitary vasopressin V1b receptors plays a critical role in regulating pituitary adrenocorticotropic hormone (ACTH) secretion during adaptation to stress. The objective of this study was to isolate the promoter regulatory region of the V1b receptor gene to better understand the molecular mechanisms involved in V1b receptor regulation. Screening of a rat genomic library using probes directed to the coding region and to the 5'UTR of the rat V1b receptor resulted in the isolation of several clones containing the 5'upstream regions of the V1b receptor cDNA. Sequencing of an 11.2 Kb fragment revealed 8.2 Kb upsteam of the reported cDNA sequence, which contains a putative promoter regulatory region. The 3' end of the clone contained 1472 base pairs corresponding to the recognized cDNA sequence, followed by 1506 bp of unknown sequence located at the end of the sixth transmembrane domain, probably corresponding to an intron, characteristic of these family of receptors. An additional 161 bp intron was found in the 5'UTR, similar to that described in the rat oxytocin receptor gene. 5'RACE and RNase protection analysis mapped two major putative transcription start points at -830 and -861 bp from the starting methionine. Analysis of the putative promoter region showed no indication of a proximal TATA box, but the presence of a CACA box, a GAGA box, several AP-1 and AP-2 sites and a cluster of Sp1 sites upstream of the AP-2 sites. A luciferase construct containing a 2.1-kb of putative promoter, and part of the 5'UTR including the first intron, showed promoter activity when transfected into COS-7, CHO and PC12 cell lines but not in AtT-20 cells. A similar construct without the intron and distal 5'UTR sequence has no promoter activity in the same cell lines. In summary, the V1b receptor gene contains at least 3 exons and 2 introns. The 5'flanking sequence contains several potential sites for transcriptional regulation, and induced luciferace activity only in constructs containing intron 1, suggesting that the latter is important for receptor gene activation. The data provide bases for future analysis of the regulatory elements controlling V1b receptor transcription.
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PMID:Isolation and characterization of the promoter region of the rat vasopressin V1b receptor gene. 1079 83

Quakingviable (qk(v)) is a well known dysmyelination mutation. Recently, the genetic lesion of qk(v) has been defined as a deletion 5' to the qkI gene, which results in the severe reduction of the qkI-encoded QKI RNA-binding proteins in myelin-producing cells. However, no comprehensive model has been proposed regarding how the lack of QKI leads to dysmyelination. We hypothesized that QKI binds to myelin protein mRNAs, and the lack of QKI causes posttranscriptional misregulation, which in turn leads to the loss of the corresponding myelin proteins. To test this hypothesis, we developed an RNase protection assay to directly measure the mRNA isoforms encoding the myelin basic proteins (MBPs) in the brain. Our result suggested that isoform-preferential destabilization of MBP mRNAs in the cytoplasm was responsible for the reduced MBPs in the qk(v)/qk(v) brain during early myelination. In addition, we detected markedly reduced MBP mRNAs in the qk(v)/qk(v) myelin fraction with concomitant accumulation of MBP mRNAs associated with membrane-free polyribosomes. Presumably, the impaired localization of MBP mRNAs to the myelin membrane may cause insufficient incorporation of the newly synthesized MBPs into the myelin sheath. Finally, we observed interactions between QKI and MBP mRNAs, and removing MBP 3'UTR significantly reduced QKI-binding. Taken together, these observations suggest that misregulation at multiple posttranscriptional steps is responsible for the severe reduction of MBPs in qk(v) dysmyelination, presumably because of the lack of interactions between MBP mRNAs and the QKI RNA-binding proteins.
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PMID:Destabilization and mislocalization of myelin basic protein mRNAs in quaking dysmyelination lacking the QKI RNA-binding proteins. 1086 52


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