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)

A procedure is presented for the preparation of a (3)H-labeled complementary DNA (cDNA) specific for the mRNA coding for alpha(2u)-globulin, a male rat liver protein under multihormonal control that represents approximately 1% of hepatic protein synthesis. Rat liver polysomes are incubated with monospecific rabbit antiserum to alpha(2u)-globulin, which binds to the nascent alpha(2u)-globulin chains on the polysomes. These antibody-polysome complexes are then adsorbed to goat antiserum to rabbit IgG that is covalently linked to p-aminobenzylcellulose. mRNA preparations are thus obtained that contain 30-40% alpha(2u)-globulin mRNA. A labeled cDNA is made to this alpha(2u)-globulin-enriched mRNA preparation by using RNA-dependent DNA polymerase (reverse transcriptase). To remove the non-alpha(2u)-globulin sequences, this cDNA preparation is hybridized to an RNA concentration x incubation time (R(0)t) of 1000 mol of ribonucleotide per liter x sec with female rat liver mRNA, which, though it shares the vast majority of mRNA sequences with male liver, contains no alpha(2u)-globulin mRNA sequences. The cDNA remaining single-stranded is isolated by hydroxylapatite chromatography and is shown to be specific for alpha(2u)-globulin mRNA by several criteria. Good correlation was found in all endocrine states studied between the hepatic level of alpha(2u)-globulin, the level of functional alpha(2u)-globulin mRNA as assayed in a wheat germ cell-free translational system, and the level of alpha(2u)-globulin mRNA sequences as measured by hybridization to the alpha(2u)-globulin cDNA. Thus, the hormonal control of hepatic alpha(2u)-globulin synthesis by sex steroids and thyroid hormone occurs through modulation of the cellular level of alpha(2u)-globulin mRNA sequences, presumably by hormonal control of transcriptive synthesis.
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PMID:Multihormonal induction of hepatic alpha2u-globulin mRNA as measured by hybridization to complementary DNA. 7 84

Attempts were made to elucidate whether thyroid hormone upregulates renal pro-epidermal growth factor (pro-EGF) gene expression, biosynthesis and release in adult rats which were rendered hypothyroid. Predominantly pro-EGF was detected in renal cortex, whereas pro-EGF and its degraded species were found in urine. We demonstrated that T3 increased pro-EGF levels in renal cortex to 2.2 +/- 0.17, 2.37 +/- 0.19, 2.73 +/- 0.25, and 3.10 +/- 0.45 fold within day 1, 2, 4 and 8, respectively following treatment. Immunoreactive EGF, assessed by immunohistochemical methods, was confined in the distal convoluted tubule and thick ascending limb of Henle. T3 markedly enhanced the density of irEGF in these nephrons. T3 augmented the concentration of urinary irEGF to 2.1, 2.2, 2.8 and 3.6 fold within day 1, 2, 4 and 8 and the abundance of urine pro-EGF to 2.53 +/- 1.39, 3.8 +/- 0.70, 3.59 +/- 1.48 fold within day 1, 2, 4, respectively. Moreover, we employed reverse transcriptase/polymerase chain reaction method to analyze relative abundance of pro-EGF mRNA in kidneys of various thyroid states and found T3 markedly increased pro-EGF mRNA levels after treatment of 1, 2 and 4 days. These results indicated that thyroid hormone augmented the gene expression, biosynthesis and excretion of pro-EGF in adult rat kidney.
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PMID:Thyroid hormone upregulates gene expression, synthesis and release of pro-epidermal growth factor in adult rat kidney. 756 92

We studied the effects of thyroid hormone (T3) on GH, TSH, and T3 receptor (TR) gene expression as well as deiodinase activities during rat pituitary development. By reverse transcriptase-polymerase chain reaction, GH and TSH beta transcripts were detectable on fetal day 15. Although with certain differences, the expression of both GH and TSH beta genes was under T3 control during fetal and neonatal life. Differences in plasma, but not pituitary, TSH concentrations were observed between control and hypothyroid animals throughout the period studied. Both TR alpha and TR beta genes were expressed in the fetal pituitary. TR alpha 1, TR beta 2, and c-erbA alpha 2 transcripts displayed a developmental profile different from that of TR beta 1. Thyroid hormone repressed TR alpha 1, TR beta 2, and c-erbA alpha 2 and stimulated TR beta 1. Type I and type II deiodinase activities (5'DI and 5'DII, respectively) had different ontogenic patterns; 5'D-II was the predominant activity in fetuses, with levels similar to those in adults, whereas the level of 5'D-I was low and increased with age. T3 stimulated 5'D-I and decreases 5'D-II. These results demonstrate that in somatotroph and thyrotroph cells, the mechanisms responsible for T3 action are mature and active very early in development and suggest an involvement of this hormone in the establishment and/or maintenance of the somatotroph and thyrotroph phenotype.
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PMID:Effect of perinatal hypothyroidism on the developmental regulation of rat pituitary growth hormone and thyrotropin genes. 766 53

The present study was performed to examine whether renal expression of the renin gene is regulated by thyroid hormone. Thirty male Sprague-Dawley rats were divided into hypothyroid, control, and hyperthyroid groups by use of daily intraperitoneal administration of methimazole, saline vehicle, or thyroxine, respectively. Each group was further subdivided into sympathetic innervated and sympathetic denervated subgroups by use of intraperitoneal administration of saline vehicle or 6-hydroxydopamine. Plasma renin activity and renal levels of renin were measured by radioimmunoassays after 8 wk. Renal expression of renin mRNA was evaluated by a semiquantitative reverse transcriptase-polymerase chain reaction. Compared with control animals, plasma renin activity, renal level of renin, and renal expression of renin mRNA were reduced (82, 94, and 71%, respectively) in hypothyroid animals and elevated (155, 1,182, and 152%, respectively) in hyperthyroid animals. Sympathetic denervation had no independent effect on these renin values. Our results indicate that thyroid hormone stimulates renin synthesis without involving the sympathetic nervous system.
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PMID:Thyroid hormone stimulates renin synthesis in rats without involving the sympathetic nervous system. 912 27

Nonfunctioning tumors (NFTs) of the anterior pituitary often express elevated levels of the glycoprotein hormone alpha-subunit, which, under normal physiological conditions, is under negative feedback control by thyroid and gonadal steroid hormones. We postulate that inappropriately elevated levels of expression of alpha-subunit in the face of normal levels of these target organ hormones may reflect an abnormality of thyroid hormone receptors (TRs) and/or gonadal steroid receptors in NFTs. Using immunocytochemistry and Western blotting we have examined TR and estrogen receptor (ER) protein expression in normal human anterior pituitary glands and NFTs. Pretranslational expression of these receptors was examined using semiquantitative reverse transcriptase-PCR. Expression of all TR variant and ER proteins was reduced in pituitary tumors compared with that in normal pituitaries. The expression of messenger ribonucleic acids encoding the TR beta1 and TR beta2 isoforms and ER was also significantly reduced in tumors compared with normal tissues, although there was no difference between tumors and normals in the level of expression of TR alpha1 and alpha2 messenger ribonucleic acids. We suggest that reduced expression of TRs and ER may account for inappropriate expression of the glycoprotein hormone alpha-subunit gene in some NFTs and may contribute to uncontrolled tumor growth.
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PMID:Thyroid hormone and estrogen receptor expression in normal pituitary and nonfunctioning tumors of the anterior pituitary. 917 14

A gene responsive to thyroid hormone (TH) has been identified in the adult rat brain cerebral tissue. A cDNA probe differentially expressed in euthyroid, hypothyroid and hyperthyroid rat cerebral tissue, generated by reverse transcriptase-PCR differential display of mRNA, was used to screen the rat brain cDNA library. A 3.4 kb positive clone hybridized in Northern blots with a 3.8 kb mRNA that proved to be TH responsive (THR). The remaining coding sequence and a part of the 5' untranslated region of this cDNA were obtained by 5' rapid amplification of cDNA ends. The deduced amino acid sequence revealed that THR protein (THRP), a 68 kDa moiety, has 83% sequence similarity with c-Abl interactor protein (Abi-2), which is a substrate for tyrosine kinase activity of c-Abl. The extensive similarity between the two proteins suggests a potential role for THRP as a substrate for c-Abl. Northern analysis showed that the expression of THR mRNA in hyperthyroid rats is 6-fold that in euthyroid rats. There is also a 4-6-fold increase in the concentration of THRP, as analysed by Western analysis. Owing to the extensive similarity between rat THRP and human Abi-2, a polyclonal anti- (human Abi-2) antibody was successfully used for Western analysis of proteins from the rat tissues. The observed increase in both the mRNA and the protein did not decline after beta-adrenergic system blockade with propranolol, suggesting that the action of TH on the expression of this gene is not mediated through the beta-adrenergic system. Immunohistochemical studies revealed that neuronal cells were particularly rich in THRP. Both THR mRNA and THRP are rapidly induced in vivo after intravenous administration of thyroxine. Tissue distribution studies indicated that the cerebral tissue was particularly enriched with THR mRNA and 68 kDa THRP. A cDNA clone for a THR gene could provide a useful tool to study the molecular mechanisms of TH effects on cerebral tissue in adult animals.
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PMID:Cloning and characterization of a complementary DNA for a thyroid hormone-responsive protein in mature rat cerebral tissue. 935 37

The effects of thyroid hormone on renin secretion, renin content, and renin mRNA levels in juxtaglomerular (JG) cells harvested from rat kidneys were determined by radioimmunoassays and reverse transcriptase-polymerase chain reaction. Despite a lack of immediate effect, incubation with triiodothyronine dose dependently increased renin secretion during the first 6 h and elevated renin content and renin mRNA levels during the subsequent period. Simultaneous incubation with triiodothyronine and the calcium ionophore A-23187 abolished the increase in renin secretion and attenuated the increase in renin content but did not affect the increase in renin mRNA levels. During simultaneous incubation with triiodothyronine and the adenylate cyclase inhibitor SQ-22536 or membrane-soluble guanosine 3',5'-cyclic monophosphate (cGMP), the increases in renin secretion, content, and mRNA were similar to those observed in the presence of triiodothyronine alone, except for a cGMP-induced attenuation of the increase in renin secretion. These findings suggest that thyroid hormone stimulates renin secretion by JG cells through the calcium-dependent mechanism, whereas the stimulation of renin gene expression by thyroid hormone does not involve intracellular calcium or cyclic nucleotides.
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PMID:Differential effects of thyroid hormone on renin secretion, content, and mRNA in juxtaglomerular cells. 948 51

Thyrotropin (TSH)-secreting pituitary adenomas cause hyperthyroxinemia in the presence of "inappropriately" elevated concentrations of TSH. TSH production under these circumstances escapes the normal negative feedback effect of thyroid hormone. We propose that this defective negative feedback is mediated by an abnormality of thyroid hormone receptor (TR) expression. Two TSH-secreting pituitary adenomas were analyzed by immunocytochemistry for TR isoform protein expression and by semiquantitative reverse transcriptase polymerase chain reaction (RT-PCR) for TR isoform mRNA expression. The results obtained from these tumors were compared with the findings from six normal human pituitaries. Neither tumor examined expressed detectable levels of nuclear TRalpha or TRbeta proteins, in contrast to the normal pituitaries studied, which expressed all TR isoforms. Application of RT-PCR, however, revealed mRNAs encoding each TR isoform in all tumorous and normal tissues examined. Semiquantitative RT-PCR revealed similar levels of expression of TRalpha and TRbeta isoform mRNAs in tumors and normal tissue, in contrast to the observed difference in TR proteins. Absent TRalpha and TRbeta protein expression, in association with normal mRNA levels, implies a post-transcriptional defect in TR mRNA processing in TSH-secreting adenomas. Reduced TR expression in these tumors may explain defective negative feedback of thyroid hormone on TSH production, and may also contribute to uncontrolled tumor growth.
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PMID:An abnormality of thyroid hormone receptor expression may explain abnormal thyrotropin production in thyrotropin-secreting pituitary tumors. 949 47

It is well known that renal hypertrophy is induced by hyperthyroidism; however, the mechanism is not fully understood. We recently reported that cardiac hypertrophy in hyperthyroidism is mediated by enhanced cardiac expression of renin mRNA. The present study addresses the hypothesis that renal hypertrophy in hyperthyroidism is mediated by amplification of renal expression of renin mRNA. Twenty Sprague-Dawley rats were divided into control (n=5) and hyperthyroid groups by daily intraperitoneal injections of saline vehicle or thyroxine. The hyperthyroid group was subdivided further into hyperthyroid-vehicle (n=5), hyperthyroid-losartan (n=5), and hyperthyroid-nicardipine (n=5) groups by daily intraperitoneal injections of saline vehicle, losartan, or nicardipine. All rats were killed at 4 weeks, and the blood and kidneys were collected. The kidney-to-body weight ratio increased in the hyperthyroid groups (+34%). Radioimmunoassays and reverse transcriptase-polymerase chain reaction revealed increased renal renin (+91%) and angiotensin II (+65%) levels and enhanced renal renin mRNA expression (+113%) in the hyperthyroid groups. Losartan and nicardipine decreased systolic blood pressure to the same extent, but only losartan caused regression of thyroxine-induced renal hypertrophy. These results suggest that thyroid hormone activates the intrarenal renin-angiotensin system via enhancement of renal renin mRNA expression, which then leads to renal hypertrophy.
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PMID:Mechanism of hyperthyroidism-induced renal hypertrophy in rats. 979 36

We have reported previously that thyroid hormone activates the circulating and tissue renin-angiotensin systems without involving the sympathetic nervous system, which contributes to cardiac hypertrophy in hyperthyroidism. This study examined whether the circulating or tissue renin-angiotensin system plays the principal role in hyperthyroidism-induced cardiac hypertrophy. The circulating renin-angiotensin system in Sprague-Dawley rats was fixed by chronic angiotensin II infusion (40 ng/min, 28 days) via mini-osmotic pumps. Daily i.p. injection of thyroxine (0.1 mg/kg per day, 28 days) was used to mimic hyperthyroidism. Serum free tri-iodothyronine, plasma renin activity, plasma angiotensin II, cardiac renin and cardiac angiotensin II were measured with RIAs. The cardiac expression of renin mRNA was evaluated by semiquantitative reverse transcriptase-polymerase chain reaction. Plasma renin activity and plasma angiotensin II were kept constant in the angiotensin II and angiotensin II+thyroxine groups (0.12+/-0.03 and 0.15+/-0.03 microgram/h per liter, 126+/-5 and 130+/-5 ng/l respectively) (means+/-s.e.m.). Despite stabilization of the circulating renin-angiotensin system, thyroid hormone induced cardiac hypertrophy (5.0+/-0.5 vs 3.5+/-0.1 mg/g) in conjunction with the increases in cardiac expression of renin mRNA, cardiac renin and cardiac angiotensin II (74+/-2 vs 48+/-2%, 6.5+/-0.8 vs 3.8+/-0.4 ng/h per g, 231+/-30 vs 149+/-2 pg/g respectively). These results indicate that the local renin-angiotensin system plays the primary role in the development of hyperthyroidism-induced cardiac hypertrophy.
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PMID:Local renin-angiotensin system contributes to hyperthyroidism-induced cardiac hypertrophy. 985 75


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