Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.30.1 (S1 nuclease)
 3,660 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The rate of response to thyroid hormone on cardiac growth, heart rate, and the relative changes in messenger RNA (mRNA) coding for alpha- and beta-myosin heavy chain (MHC), slow sarcoplasmic reticulum calcium-adenosine triphosphatase, and thyroid hormone receptors in ventricular tissue of hypothyroid rats was investigated. Hypothyroid rats had significantly smaller hearts, with slower heart rates and expressed no alpha-MHC mRNA as analyzed by an S1 nuclease protection assay when compared to euthyroid animals that expressed 79% alpha-MHC. Twelve hours after treating hypothyroid rats with 20 micrograms of L-T4, detectable levels of alpha-MHC mRNA were present and the shift to alpha-MHC mRNA was complete by 72 h of treatment. Northern blot analysis showed that hypothyroidism resulted in a 60% decrease in the level of sarcoplasmic reticulum calcium-adenosine triphosphatase mRNA which increased after 12 h of T4 administration and was 2.5-fold (P less than 0.05) greater than euthyroid levels after 72 h. In contrast, thyroid hormone receptor mRNA levels measured in poly(A)+ RNA were elevated in hypothyroid rats and decreased to euthyroid levels within 24 h after thyroid hormone treatment. These changes in cardiac gene expression occurred simultaneously with changes in both cardiac size and heart rate. The current studies characterize the coordinated changes and the time course for gene expression that occur in the hypothyroid heart after acute T4 administration.
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PMID:Time course of the in vivo effects of thyroid hormone on cardiac gene expression. 131 35

The developmental regulation of the expression of nerve growth factor (NGF) was studied in the mouse submandibular gland (SMG). Having demonstrated that, in the neonatal mouse, maturation of the SMG can be accelerated by treatment with thyroid hormones, with the resulting induction in SMG content of NGF, studies were undertaken to further examine the locus of thyroid hormone action. Because of the sexual dimorphism of the SMG, both male and female neonatal mice were used. NGF messenger RNA levels were undetectable in SMGs from untreated immature mice, while hybridization to total RNA from T4-treated mice was easily observable for NGF complementary DNA. Treatment for 14 days compared to 7 days resulted in a 7-fold increase in SMG NGF mRNA levels. A signal was obtained in 21-day-old control mice using S1 nuclease protection analysis; T4 increased NGF mRNA levels by 100-fold in both male and female immature mice. Heteronuclear RNA levels were induced 20-fold by T4. No sex differences were readily observable. Determination of the effect of thyroid hormone treatment on SMG NGF gene expression by nuclear run-on assay demonstrated a significant transcriptional effect of T4. Initial experiments using the pmngf6 vector, which is a pBR322-derived probe containing the full length NGF cDNA, showed a 2.5-fold induction of gene transcription. When an internal fragment of pmngf6 was subcloned into pTZ18R, thus removing the dC/dG tails contained in pmngf6, the background hybridization was considerably reduced and a 12.5-fold induction in NGF gene transcription was obtained after T4 treatment of neonatal mice. The results show that thyroid hormones increase NGF gene expression in the SMG of the immature male and female mouse. This effect is due in part to a significantly enhanced rate of gene transcription.
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PMID:Thyroid hormones precociously increase nerve growth factor gene expression in the submandibular gland of neonatal mice. 154 29

Carboxypeptidase-H (CPH) is a metallocarboxypeptidase implicated in the processing of peptide hormones. Consistent with such a role, the gene for CPH is expressed in cells that secrete regulatory peptides, such as those of the brain and endocrine tissues. In the rat brain, CPH is transcribed from a single transcriptional start site associated with the initiator-type element first described in the gene encoding lymphocyte-specific terminal deoxynucleotidyltransferase. We have used a combination of Northern blot analysis and S1 nuclease protection mapping to describe the expression and transcription initiation pattern of the gene for CPH in the peripheral tissues and brain regions of the normal rat. The single transcriptional start site is used in all tissues examined, except the pituitary, where two additional specific initiation sites are found. The expression of the CPH gene is up-regulated in the anterior pituitary gland as a consequence of systemic thyroid hormone depletion, and this increase is associated with a preferential utilization of the novel upstream transcriptional initiation sites. Thus, the use of different major transcriptional initiation sites of the CPH gene in the pituitary gland is subject to differential direct or indirect thyroid hormone regulation.
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PMID:Pituitary-specific transcriptional initiation sites of the rat carboxypeptidase-H gene and the influence of thyroid hormone status. 160 81

Genomic clones containing the 5'-flanking region and exon 1 of the human and rat Na,K-ATPase alpha 3 isoform gene have been isolated and characterized. The nucleotide sequences of 1.6 kb of the rat gene and 2.8 kb of the human gene in the 5'-flanking region were determined. Mapping of transcription initiation sites by primer extension and S1 nuclease protection analyses indicates that transcription is initiated in the same region in both genes although the rat gene has a greater number of initiation sites. Neither gene has a canonical TATA box, having instead a ATAT sequence preceding the transcription initiation sites. There is a perfect CCAAT sequence, in the reverse orientation, approximately 30 bp upstream of the potential TATA box in both genes. We have identified potential binding sites for transcription factors Sp-1, AP-1, AP-2, and AP-4, as well as for glucocorticoid and thyroid hormone receptors in the 5'-flanking regions. These are conserved in both human and rat alpha 3 isoform genes.
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PMID:Characterization of the 5'-flanking region of the human and rat Na,K-ATPase alpha 3 gene. 217 44

Genomic clones for 2287 nucleotides of the 5' flanking region, 135 nucleotides of the first exon, and 283 nucleotides of the first intron of the hepatic lipase gene were characterized. The predominant start site for transcription was identified by primer extension and S1 nuclease analyses to be 50 bases upstream of the ATG initiation codon. Based on the location of the major transcription start site, the functional TATA box is located 29 nucleotides upstream. Putative response elements for AP-2, cAMP, OCT-1, C/EBP, estrogen, glucocorticoids, sterols and thyroid hormone were located in this gene. Also a putative liver-specific element for apolipoproteins, C3P, was identified.
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PMID:Isolation and characterization of clones for the rat hepatic lipase gene upstream regulatory region. 232 83

Androgens mediate their effects through an intracellular receptor that is a member of the steroid/thyroid hormone family of receptors. The expression of this protein is tightly regulated in different tissues and among cell types within a single tissue. To define the mechanisms controlling the expression of the androgen receptor, we have isolated and characterized the promoter of the androgen receptor gene in the human prostate cell line LNCaP. The major site of transcription initiation is approximately 1.1 kilobases upstream of the initiator methionine of the androgen receptor protein. The promoter region lacks typical "TATA" and "CAAT" sequence motifs but lies in a GC-rich region and contains a putative Sp1 binding site characteristic of a "housekeeping" promoter and a 44-base segment composed of alternating adenosine and guanosine residues. S1 nuclease protection analyses indicate that the same promoter is employed both in human tissues (prostate, testes), in genital skin fibroblasts, in T47D and MCF-7 breast cancer cells, and in LNCaP prostate cancer cells.
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PMID:Expression of the human androgen receptor gene utilizes a common promoter in diverse human tissues and cell lines. 238 Jan 87

A region of the rat growth hormone gene and 5' flanking DNA has been identified which promotes accurate, thyroid hormone-regulated transcriptional initiation. GC rat pituitary tumor cells were transfected with chimaeric plasmids containing various lengths of rat growth hormone gene and 5' flanking DNA fused to the coding region of the dominant selectable marker gene neo. Thyroid hormone induction of rGH-neo RNA was observed by Northern and dot blot analysis of cells transfected with rGH-neo chimaeric genes sharing the rat growth hormone gene and upstream regions from -235 to +11. Initiation of rGH-neo transcription was mapped by S1 nuclease protection to the in vivo initiation site of the natural growth hormone gene. Transcription of the most deleted thyroid hormone responsive construct involved an induction-attenuation cycle qualitatively similar to the response of the natural gene. However, the 3,5,3'-triiodo-L-thyronine responsiveness of this deleted construct was approximately 2- to 3-fold less than that of less deleted rGH-neo genes tested. These results suggest that, at a minimum, the sequences required for the cyclic 3,5,3'-triiodo-L-thyronine transcriptional response are located within the region of the gene from -235 to +11. Other sequences essential for full responsiveness appear to be located elsewhere in the 5'-flanking DNA. Rat growth hormone promoter utilization appears to be strongly cell-type dependent. We obtained stable transfectants with rGH-neo constructs only in GC cells.
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PMID:Thyroid hormone regulation of the transfected rat growth hormone promoter. 242 Jul 97

The human thyrotropin beta-subunit gene was isolated and characterized from two genomic libraries and found to contain three exons separated by two introns of 3.9 and 0.45 kilobase pairs. Exons 2 and 3 in the mouse thyrotropin beta-subunit gene are not found in humans due to a lack of consensus sequences important in exon splicing. Moreover, using primer extension, RNA sequencing, and S1 nuclease analysis, we determined, in a thyrotropin-producing pituitary adenoma, that exon 1 in humans contains only one transcriptional start site and is 37 base pairs in length. This is unlike both the rat and mouse thyrotropin beta-subunit genes which contain two transcriptional start sites. Changes in the genomic structure of the more 5' "TATA box" and surrounding "CAAT box" might explain why the more 5' start site in humans is apparently not utilized. Moreover, the first exon in humans is longer than the corresponding exon in murine species presumably due to a 9-base pair insertion between the TATA box and transcriptional start site (37 versus 27 nucleotides). Thus, while alternative exon splicing and differential start site utilization in response to thyroid hormone may be important in the regulation of murine thyrotropin beta-subunit genes, they are not found in man.
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PMID:Isolation and characterization of the human thyrotropin beta-subunit gene. Differences in gene structure and promoter function from murine species. 245 86

The appearance of the mRNA for the adult fast IIB myosin heavy chain (MHC) was examined during postnatal development of rats using an S1 nuclease assay. In normal rats, a large increase in the adult MHC mRNA began at 6-7 days after birth, whereas daily injections of newborn rats with 3 micrograms of triiodothyronine (T3) resulted in a precocious increase of the mRNA as early as 3 days after birth. Injection of a range of doses of T3 demonstrated that a large effect was obtained between 30 and 300 ng of T3/day/rat. Fast myosin protein was also precociously induced over the same range of T3 doses. This effect was also seen in denervated muscles, and muscles responded similarly to the different doses of T3 whether they were denervated or not. These results suggest that either thyroid hormone or some circulating factors induced by thyroid hormone are limiting factors in controlling the neonatal-to-adult fast MHC transition and that these factors may act directly on muscle tissue.
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PMID:Thyroid hormone induces a nerve-independent precocious expression of fast myosin heavy chain mRNA in rat hindlimb skeletal muscle. 283 75

Thyroid hormone has a number of effects on cardiovascular and renal function which are shared by the atrial natriuretic peptide (ANP). We attempted to demonstrate a relationship between the two by studying the effects of thyroid hormone on the expression of the ANP gene and the secretion of its encoded protein. Thyroid hormone, when given to thyroidectomized rats, increased plasma ANP levels by approximately 2-fold in both watered and dehydrated animals. Cardiac ANP mRNA in dehydrated animals fell to 25% of that in the water-replete controls. T4 increased cardiac ANP mRNA 3-fold in dehydrated animals, but failed to alter ANP mRNA in those animals allowed free access to water. The effect of thyroid hormone appeared to take place, at least in part, at the level of the ANP-synthesizing cardiocyte. T3, at concentrations ranging from 10(-10)-10(-8) M, increased ANP mRNA levels a maximum of 2-fold in primary cultures of neonatal cardiocytes. Both basal and T3-stimulated ANP transcripts appeared to be identical to their counterparts in the adult atria, as assessed by blot hybridization and S1 nuclease analysis. T3 (10(-8) M) also effected a 2-fold increase in media ANP immunoreactivity. These data indicate that thyroid hormone increases the secretion and genetic expression of ANP in vivo and in vitro and suggests a role for the peptide as a mediator of at least some thyroid hormone effects in the cardiovascular system.
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PMID:Thyroid hormone increases rat atrial natriuretic peptide messenger ribonucleic acid accumulation in vivo and in vitro. 296 52


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