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:2.7.7.49 (reverse transcriptase)
31,746 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although fetal growth is generally considered to be independent of pituitary growth hormone (GH), it is possible that pituitary GH plays a modulatory role in organ development or that a GH-like substance of non pituitary origin may influence fetal growth through the GH receptor. Accordingly, we have used immunohistochemistry, northern blot analysis, the reverse transcriptase-polymerase chain reaction and solution hybridization to study the ontogeny of the GH receptor/binding protein (BP) from the 12-day-old embryo (E12) to the E18 rat fetus. GH receptor/BP immunoreactivity was observed in all major organ systems of the E18 rat fetus and was not preferentially associated with any germ layer derivative. A general increase in GH receptor/BP immunoreactivity was evident from E12 to E18, with a marked increase occurring between E16 and E18. Hemangioblastic tissue was, however, strongly or intensely immunoreactive at all stages of development, as was the placenta. Most noteworthy of the other tissues expressing GH receptor/BP immunoreactivity by day 18 were skeletal and smooth muscle, chondroprogenitor cells, epithelial lining cells, neuronal ganglia, ependymal cells and the adrenal cortex. In the placenta, the most prominent immunoreactivity was associated with decidual cells. Total RNA was isolated from E12 to E18 rat fetuses and adult rat liver. Northern hybridization with a 35S-labelled rat GH receptor cRNA probe revealed that 3.9 kb and 1.2 kb transcripts complementary to the rat GH receptor riboprobe are present from at least E16. The existence of GH receptor mRNA at E12 and E14 was demonstrated by the polymerase chain reaction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prenatal expression of the growth hormone (GH) receptor/binding protein in the rat: a role for GH in embryonic and fetal development? 161 49

Twenty-eight human pituitary adenomas were analyzed for the expression of Pit-1 messenger ribonucleic acid (mRNA) by using reverse transcriptase-polymerase chain reaction analysis of frozen-section mRNA. Pit-1 mRNA was detected in all functioning tumors and in 9 of 11 nonfunctioning tumors. Pit-1 beta, which is a more active isoform of transcriptional factor for growth hormone than Pit- alpha and which arises from an alternative splicing mechanism, was detected in 14 of 17 functioning tumors and in 5 of 11 nonfunctioning tumors. The transcript that corresponds to Pit-1T, which increases thyroid-stimulating hormone beta promoter activity in rat thyrotropic tumor cells, was not found. There was no significant difference in the total Pit-1 (alpha+beta) mRNA expression level between functioning tumors and nonfunctioning tumors. Growth hormone-producing tumors and other pituitary adenomas also showed no significant difference in the Pit-1 beta/Pit-1 alpha expression ratio. Our data suggest that the major role of Pit-1 gene in pituitary adenoma might not be involved in the regulation of hormone production.
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PMID:Expression and alternative splicing of Pit-1 messenger ribonucleic acid in pituitary adenomas. 886 65

Growth hormone (GH) receptor mRNA is found within the corpus luteum and endometrium of cattle. However, binding sites for placental lactogen (PL) but not GH are found within these tissues. The objectives were to isolate cDNA for the GH receptor within the reproductive tissues of cattle and to examine these cDNA as potential variants of the GH receptor that bind PL. Ten cDNA clones were isolated from a bovine endometrial cDNA library with a 32P-labeled cDNA of the GH receptor extracellular domain. On the basis of restriction enzyme digestion, 2 of the 10 cDNA clones contained exon 1. The DNA sequence of these clones was determined by dideoxy nucleotide sequencing. The exon 1 DNA sequence of each clone (exon 1B) was different from the previously reported exon 1 for the bovine GH receptor cDNA isolated from liver (exon 1A). Analyses of these cDNA sequences showed that exon 1B contained significant homology with placental forms of the GH receptor found in mouse and human. Unlike the human cDNA, the bovine cDNA isolated from endometrium contained an intact third exon. Amplification of GH receptor mRNA by reverse transcriptase polymerase chain reaction, with exon 1A- and 1B-specific forward primers, showed that exon 1B was expressed in liver, corpus luteum, ovary, endometrium, and myometrium. Exon 1A was found almost exclusively in liver, and little was found in reproductive tissues. The predicted initiation of protein coding for the GH receptor was within the second exon and was not changed by the splicing of the alternate first exon. This suggests that the alternate mRNA results in the expression of intact GH receptor protein that is similar to that found within liver. Alternative promoters (1B) may control the expression of the receptor outside the liver. Furthermore, mechanisms other than the differential splicing of GH receptor protein may dictate the specificity of PL binding within the endometrium and corpus luteum.
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PMID:Expression of alternate growth hormone receptor messenger RNA in ovary and uterus of cattle. 888 95

We have examined whether alterations in the growth hormone/insulin-like growth factor-1 axis play a role in the pathogenesis of psoriasis. Serum, urine, full skin biopsies, and suction blister roofs were obtained from patients with psoriasis and from healthy controls. Serum concentrations of insulin-like growth factor-1 and insulin-like growth factor binding protein-3 were measured by radioimmunoassay. Growth hormone-binding protein was measured by ligand-mediated immunofunctional assay. Growth hormone concentration in urine was measured by an immunometric assay, and growth hormone receptor-gene expression was measured by RNase protection assay or by quantitative reverse transcriptase polymerase chain reaction in total RNA isolated from epidermal suction blister roofs. Serum concentrations of insulin-like growth factor-1 (249 +/- 12 micrograms per liter, mean +/- SEM, n = 42, and 277 +/- 21 micrograms per liter, n = 9, for psoriatic patients and controls, respectively), insulin-like growth factor binding protein-3 (3.1 +/- 0.08 mg per liter, n = 42, and 3.3 +/- 0.22 mg per liter, n = 9), growth hormone-binding protein (344 +/- 65 pmol per liter, n = 10, and 311 +/- 83 pmol per liter, n = 9), urinary growth hormone excretion during 24 h (12.8 +/- 2.7 microIU per 24 h, n = 12, and 12.3 +/- 1.6 microIU per 24 h, n = 9), and epidermal growth hormone receptor gene expression [32 +/- 12 x 10(3) mRNA transcripts per microgram total RNA (involved skin), n = 11, and 47 +/- 14 x 10(3) mRNA transcripts per microgram total RNA, n = 9] were similar in patients and controls. For insulin-like growth factor-1 and insulin-like growth factor binding protein-3 the values in psoriatic patients were also similar to those in larger control groups, n = 195 and n = 400, respectively. In addition, we found no evidence of local expression of growth hormone or prolactin in full skin punch biopsies from psoriatic involved skin by reverse transcriptase polymerase chain reaction. In conclusion, our results suggest that alterations in the growth hormone/ insulin-like growth factor-1 axis do not play a major role in the pathogenesis of psoriasis.
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PMID:No evidence for involvement of the growth hormone/insulin-like growth factor-1 axis in psoriasis. 934 96

The hGH-V gene codes for a variant of human pituitary growth hormone (hGH-N) named placental growth hormone (hPGH). hPGH shares 93% amino acid identity with hGH-N. Until now the hGH-V gene was considered to be exclusively expressed in human placenta, where it replaces maternal circulating hGH-N at the end of pregnancy. In this study we investigated by reverse transcriptase-polymerase chain reaction (RT-PCR) analysis hGH-N, and hGH-V, gene expression in PBMC in men, women and pregnant women. We have demonstrated that hGH-N and hGH-V transcripts are simultaneously produced by PBMC in both men and women as well as pregnant women. The PBMC of a PIT-1-negative woman expressed only the hGH-V transcript, but not the hGH-N one as expected. In conclusion, hGH-V mRNA is expressed by cells other than the syncytiotrophoblast, is not regulated by PIT-1, and may be involved in immune regulation, as is pituitary GH.
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PMID:Both pituitary and placental growth hormone transcripts are expressed in human peripheral blood mononuclear cells (PBMC). 936 22

Growth hormone (GH) increases the amount of insulin-like growth factor-I (IGF-I) mRNA in rat skeletal muscle, but this effect has not been demonstrated in human muscle. An autocrine effect of IGF-I produced in muscle may be an important determinant of the increased muscle mass associated with GH therapy. Thus, we examined IGF-I mRNA abundance in skeletal muscle biopsy samples taken 10 h after a subcutaneous injection of GH (0.03 mg/kg, n = 6) or placebo (normal saline, n = 5) in men and women over 60 years of age. Relative tissue concentrations of IGF-I mRNA were evaluated with a competitive reverse transcriptase-polymerase chain reaction assay. Mean plasma IGF-I concentrations rose steadily after the GH injection, and were 74% higher in the GH group than in the control group at the time of the muscle biopsies. There was no consistent difference between the GH and control groups in muscle IGF-I mRNA abundance when expressed in relation to total RNA or polyadenylated RNA. However, one GH-treated subject had three times more IGF-I mRNA, relative to polyadenylated RNA, than the average control subject. There was no effect of GH on levels of mRNAs encoding the most abundant myofibrillar proteins, actin and myosin heavy chain. These data do not support the hypothesis that increased IGF-I mRNA abundance in skeletal muscle is required for the anabolic effect of GH in people over 60 years of age.
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PMID:Insulin-like growth factor-I, actin, and myosin heavy chain messenger RNAs in skeletal muscle after an injection of growth hormone in subjects over 60 years old. 939 11

Growth hormone (GH) is produced in progestin-induced hyperplastic ductular mammary epithelia in dogs. Progestins also induce the development of cystic endometrial hyperplasia (CEH) in this species. The study reported here investigated whether GH gene expression could also be demonstrated in progestin-induced hyperplastic epithelium in the canine uterus. Eight beagle bitches were treated with 10 mg medroxyprogesterone acetate (MPA) kg-1 body mass s.c. at intervals of 3 weeks, for a total of five times in four dogs (group I) and for a total of 13 times in the other four dogs (group II). Blood samples were collected twice during each 3 week period for measurement of plasma concentrations of GH, insulin-like growth factor I (IGF-I) and IGF-II. At the end of the series of injections uterine tissue was obtained by ovario-hysterectomy. Histological examination confirmed that CEH was present in all uteri after MPA treatment; the changes in the dogs of group I were less marked than those in group II. Immunohistochemical examination of the uterine tissues showed that immunoreactive(i) GH was present in a number of uteri with CEH. iGH was usually located in the cytoplasm of glandular epithelial cells. However, reverse transcriptase PCR using GH-specific primers failed to demonstrate mRNA encoding GH in the uterine tissue of all dogs. It is concluded that local production of GH is not involved in progestin-induced hyperplasia of uterine epithelial cells in dogs.
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PMID:Lack of association of progestin-induced cystic endometrial hyperplasia with GH gene expression in the canine uterus. 940 6

A P1 cloned insert of about 85.5 kilobases (kb) was isolated, containing four members of the human growth hormone/chorionic somatomammotropin (GH/CS) gene family and the thyroid hormone receptor interacting protein (TRIP-1) gene. The presence of the CS-like, CS-A, GH-variant and, most downstream, CS-B gene was confirmed by DNA blotting and sequence analysis. The TRIP-1 gene was detected 40 kb downstream of the CS-B gene and in the reverse transcriptional orientation to all the GH/CS genes. The TRIP-1 gene is highly homologous to the SUG-1 gene in yeast and is evolutionarily conserved among several species. Based on the common location of the GH and TRIP-1 (or homologue) genes on the same chromosome in the human, pig and rat genomes, we suggest that these loci are physically linked. Previously, it was reported that a muscle-specific sodium channel (SCN4A) gene is located immediately upstream of the pituitary growth hormone (GH-N) gene, and is linked to the GH gene locus in both humans and rats. This suggests a further linkage between the SCN4A, GH and TRIP-1 loci. Also, deoxyribonuclease hypersensitive sites have been reported in and around these loci and were associated with an important locus control region for the GH/CS genes. Unlike the GH/CS genes, we show, using reverse transcriptase-polymerase chain reaction that the TRIP-1 gene is expressed ubiquitously and, through RNA blotting, as a 1.4-kb transcript. This implies an open and active chromatin structure. The possible effect of this structure on the adjacent human GH/CS gene locus is discussed.
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PMID:Physical linkage of the human growth hormone gene family and the thyroid hormone receptor interacting protein-1 gene on chromosome 17. 966 65

Growth hormone (GH) and placental lactogen (PL) gene transcription patterns in testicular germ cell tumors (GCT) and normal testicular tissue were comparatively investigated to identify GH/PL gene products associated with the development of GCT. This was done by nondiscriminative reverse transcriptase-polymerase chain reaction (RT-PCR), amplifying all major transcripts of any of the 5 GH/PL genes--GH-N(ormal), GH-V(ariant), PL-A, PL-B, PL-L(ike)--and subsequent analytical restriction enzyme analyses of 5'-end radioactively labeled cDNA. Surprisingly, all nonseminomatous GCT (NSGCT; n = 9) expressed GH-N, PL-A/B, and PL-L transcripts (9 of 9). Seminoma (n = 7) showed a distinctly unique pattern of GH-N and PL-A/B. GH-V products, which are hallmarks of the normal healthy testis, were not detected in any testicular cancer specimen (0 of 16). The fact that both seminomatous and NSGCT showed alterations in the same gene cluster indicates a pathogenetic relationship. Two choriocarcinoma cell lines of conceptus origin, BeWo and JAR, clearly differing from the male counterparts, exhibited a placental-derived pattern of PL-A/B and GH-V. Obviously, profound differences exist between conceptus and male germ cell GH/PL gene cluster transcription. In summary, the unique testicular pattern of GH/PL gene expression changes significantly and in directed ways with malignancy. Loss of GH-V gene expression in testicular GCT compared with normal testis and loss (seminoma) or mutation (NSGCT) of PLL gene products might have significance in terms of the relationship between these tumors and for testicular GCT development.
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PMID:The testis-specific expression pattern of the growth hormone/placental lactogen (GH/PL) gene cluster changes with malignancy. 1053 68

Although effective treatment of antiretroviral-associated metabolic abnormalities ultimately depends on understanding the mechanisms involved, clinicians facing these problems are beginning to feel compelled to do something now to manage treatment-related metabolic complications. Diet and exercise should not be overlooked, because both can be effective in managing these complications without causing further side effects. Fibric acid derivatives such as gemfibrozil and statins can lower HIV-associated cholesterol and triglyceride levels, although further data are needed on problematic interactions between statins and protease inhibitors (PIs). Hypoglycemic agents may have some role in managing glucose abnormalities, although troglitazone cannot be recommended for fat abnormalities alone and metformin may cause lactic acidosis. Growth hormone and anabolic steroids may have some role in treating lipodystrophy, but the cost of growth hormone is prohibitive for many patients and definitive data on efficacy are lacking. Replacing a PI with a reverse transcriptase inhibitor has improved lipid and glucose levels in some studies. However, that strategy begs the question of how the nucleosides might contribute to lipodystrophy.
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PMID:How to manage metabolic complications of HIV therapy: what to do while we wait for answers. 1075 16


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