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)

The aim of the study was to establish an association between the viroimmunological status of HIV positive patients and their levels of the 70-kD heat shock protein (Hsp70). The longitudinal retrospective case study involved 61 patients at the University Hospital in Granada (Spain) from 1999 to 2002. Twenty-five patients were viroimmunologically stable, while the other 36 patients had suffered virological failure. A minimum of three blood samples were taken at intervals of at least 3 months for the patients who were stable virologically and immunologically, whereas four samples were taken for the virological failure group: two previous to the onset of virological failure, a third corresponding to the time of virological failure, and a fourth at least 3 months after remission of virological failure. Blood samples were also obtained from 20 healthy control subjects; Hsp70 levels in all were determined by enzyme immunoassay. The mean concentration of Hsp70 was 145.4 ng/ml in the HIV-infected patients as opposed to 72.1 ng/ml in the controls. While the viroimmunologically stable group showed levels similar to those of the controls (66.5 ng/ml), the mean value of Hsp70 in the virological failure group was nearly four times as high (249.1 ng/ml), yet this difference was not statistically significant. The patients treated with reverse transcriptase inhibitors were found to have significantly higher levels of Hsp70 than the other subjects. The transformed variable Hsp70/CD4(+) presents less variability than the Hsp70 value itself, giving a higher degree of statistical significance, and may be considered a useful parameter for diagnostic, prognostic, and therapeutic management of HIV positive patients.
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PMID:Levels of HSP70 in HIV(+) patients in different viroimmunological states. 1641 24

Metalloproteinases (MMPs) are proteolytic enzymes that function in the extracellular matrix to degrade connective tissues. While it is clear that certain induced skeletal muscle pathologies promote increased expression of MMP-2 and heat shock protein- 72 (HSP-72), the relationship between muscle disuse and expression of MMP-2 and HSP-72 in muscles is unknown. These experiments tested the hypothesis that knee immobilization induced expression of MMP-2 and HSP-72 is disuse-dependent in a way that short-term joint immobilization increases HSP-72 expression, whereas long-term joint immobilization increases MMP-2 expression in skeletal muscles. Male rats (8 months old) completed 1, 2, 3, and 4 weeks of knee joint immobilization. Muscle mRNA and protein levels of MMP-2 and HSP-72 were assessed in Gastrocnemius (Gast), Superficial and Deep Quadriceps, and Soleus (Sol) muscles by reverse transcriptase-polymerase chain reaction and western blotting, respectively. Results reveal that during the first two weeks of immobilization there is increased protein levels of HSP-72 and expression of mRNA of HSP-72 mainly in slow twitch muscle fibers. However, 3 and 4 weeks of joint immobilization increased both mRNA and protein levels of MMP-2 in skeletal muscles containing a high percentage of fast type II fibers (i.e., Gast and superficial quadriceps). These results support the hypothesis that different periods of muscle disuse induced different proteins expression, and that the influence of joint immobilization on the expression of HSP-72 in the short-term, and MMP-2 in the long ran is associated to fiber types.
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PMID:Expression of matrix metalloproteinase 2 and heat shock protein-72 in immobilized muscle in rats. 1667 93

Produced by dietary fiber, butyrate is a potential chemopreventive agent against colon cancer. It stimulates proliferation of normal colonic epithelial cells but induces growth inhibition, differentiation, apoptosis, or a combination of effects in colon carcinoma cells. In this study, we used cDNA membrane arrays and real-time reverse transcriptase-polymerase chain reaction to identify stress genes that were differentially regulated by sodium butyrate (NaB) in HT 29 human colon carcinoma cells. The results indicated that a group of heat shock protein (hsp) genes were upregulated by 3 mM NaB within the first 24 hours of exposure. Because the transcription of hsp genes is under the control of heat shock factors (HSFs), we measured the effects of overexpressed HSF-1 on the responses of HT 29 cells to NaB. Overexpression of HSF-1 inhibited NaB-induced differentiation as measured by alkaline phosphatase activity and carcinoembryonic antigen expression. These results suggest that increased expression of HSFs and Hsps might render colon carcinoma cells resistant to the chemopreventive effects of butyrate.
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PMID:Overexpression of heat shock factor 1 inhibits butyrate-induced differentiation in colon cancer cells. 1700 92

The cellular stress response can mediate cellular protection through expression of heat shock protein (Hsp70), which can interfere with the process of apoptotic cell death. Factors regulating renal epithelial cell apoptosis include angiotensin II. In the present study, we have examined the relationship between the Hsp70 expression and the apoptotic pathway in the kidneys from low-protein-fed rats (8% protein). The possible cytoprotective role of Hsp70 has been evaluated during low-protein feeding and after reincorporation of 24% protein in the diet. The effect of angiotensin II AT1 receptor inhibition has also been studied. Rats were fed with a low-protein (LP) diet (8% protein) for 14 days, and then the animals were recovered by means of a normal protein diet (24% protein) (RP) for 14, 21, and 30 days, and control rats received 24% protein (NP) in the diet. LP and NP rats treated with Losartan (10 mg/kg) were also evaluated. The following methods were performed on the kidneys: terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling assay for apoptosis, reverse transcriptase-polymerase chain reaction assay for AT1, Bax, and Bcl-2 messenger ribonucleic acid (mRNA) expression, and immunohistochemical and Western blot for Hsp70 and caspase 3 protein expression and activity. In the LP group, the cells of the medullary ducts (MDs) showed increased apoptosis associated with weak immunoreaction for Hsp70 and decreased Hsp70 protein levels. In these animals, enhanced proapoptotic ratio Bax/Bcl-2 linked to decreased procaspase 3 protein levels with increased caspase 3 activation were demonstrated. A cytoprotection attributed to Hsp70 could be noted in the RP rats after 21 days of reincorporation of the normal diet, and in the LP-fed group treated with Losartan. In these cases, the MD cells displayed decreased apoptosis and increased Hsp70 expression in colocalization staining, and high Hsp70 levels in cytosolic fraction. A decreased proapoptotic ratio Bax/Bcl-2, associated with increased Bcl-2 mRNA, was also observed. Our results provide evidence for an antiapoptotic, cytoprotective effect of Hsp70 in kidney MD cells of rats with LP intake, when the animals were recovered with 24% protein in diet and after angiotensin II AT1 receptor inhibition. Angiotensin II seems to play a role in the pathogenesis of tubule epithelial cell apoptosis during LP feeding.
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PMID:Heat shock protein 70 expression is associated with inhibition of renal tubule epithelial cell apoptosis during recovery from low-protein feeding. 1727 80

1. In a previous study, we demonstrated that heat shock augments vascular contractility through the stress response. 2. The current study was designed to identify differentially expressed genes after heat shock by using a novel annealing control primer (ACP) system, which was developed recently to identify authentic genes. 3. Rat aortic rings were mounted in organ baths, exposed to 42 degrees C for 45 min and harvested 4 h after the end of heat shock. Total RNA were used for amplification by the reverse transcriptase-polymerase chain reaction (RT-PCR) with ACP system. Differentially amplified PCR products were sequenced, searched against the GenBank and confirmed by RT-PCR. 4. Genes for connective tissue growth factor, stress-inducible protein 1 and heat shock protein 25 were upregulated, whereas a gene for interferon regulatory factor 1 was downregulated. Immunohistochemistry revealed upregulation of the phosphorylated form of Hsp25 in aortic rings after heat shock. 5. These results suggest that phosphorylated Hsp25 plays a pivotal role in the augmentation of vascular contraction after heat shock.
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PMID:Identification of differentially expressed genes after heat shock in isolated rat aorta. 1758 Dec 21

A small heat shock protein gene (hsp22.4) was cloned from Chaetomium globosum using rapid amplification of cDNA ends (RACE). The 986-bp full-length hsp22.4 cDNA contains a 609-bp open reading frame encoding a 202-amino-acid protein with an estimated molecular mass of 22.4 kDa. The hsp22.4 gene was amplified using specific primers in the 5' and 3' untranslated regions of the hsp22.4 cDNA. The temporal expression of hsp22.4 was measured in C. globosum by real-time reverse transcriptase-polymerase chain reaction after exposure to heat, cold, Na(2)CO(3), and NaCl. The expression of hsp22.4 was induced by heat and Na(2)CO(3) treatment and inhibited by cold and NaCl treatment. The hsp22.4 gene was inserted into pYES2 containing the inducible GAL1 promoter and transferred into yeast (Saccharomyces cerevisiae) for expression. The hsp22.4 transgenic yeast displayed significantly greater resistance to heat and Na(2)CO(3) stresses than control (yeast cells transformed with empty pYES2), suggesting that the expression of hsp22.4 gene confers not only heat tolerance but also significant alkali (Na(2)CO(3)) stress tolerance.
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PMID:A heat shock protein gene (hsp22.4) from Chaetomium globosum confers heat and Na2CO3 tolerance to yeast. 1794 Jul 62

In the present study, we observed the expression of toll-like receptor 4 (TLR4) and its downstream signal pathway in peripheral blood monocytes (PBMs) from patients with acute cerebral infarct (ACI). The expression of TLR4 and MyD88 by PBMs was determined by flow cytometry and reverse transcriptase-polymerase chain reaction, and nuclear factor-kappaB (NF-kappaB) activity was detected by electrophoretic mobility shift assay. Ischemia/reperfusion injury-induced cerebral edema, infarction area, and neurologic impairment scores were determined in MyD88 gene knockout mice. The results indicated a significant increase in circulating TLR4(+) monocytes in ACI patients as compared with the control group and the transient ischemia attack (TIA) group. This change paralleled an elevation in TLR4mRNA transcription and serum tumor necrosis factor-alpha (TNF-alpha) and interleukin (IL)-6 in the ACI and TIA groups. Correlation analysis showed TLR4 expression to significantly correlate with cytokine levels and stroke severity. MyD88mRNA differed insignificantly among the three groups. Compared with wild-type mice, 6 h of cerebral ischemia followed by 24 h of reperfusion did not significantly change cerebral edema, cerebral infarction area, and neurologic impairment scores in MyD88 gene knockout mice. Compared with the control group, serum heat shock protein (HSP) 60 increased significantly in the ACI and TIA groups, leading to NF-kappaB activation in TLR4/CD14-transfected HEK293 cells. It is suggested that upregulated TLR4 expression on PMBs may act as one of the peripheral mechanisms of inflammatory injury after ACI. Moreover, circulating HSP60 may be a ligand for TLR4, which is involved in the peripheral mechanism of inflammatory injury after ACI, possibly through an MyD88-independent signal pathway.
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PMID:Upregulated expression of toll-like receptor 4 in monocytes correlates with severity of acute cerebral infarction. 1852 39

In the present study, the toxicity of arsenic trioxide and lead acetate was assessed in adult hepatic stem cells induced in the 2-acetyl-aminofluorene/partial hepatectomy rat model. Isolated oval cells were incubated separately for 6 h with 40 muM each of arsenic trioxide and lead acetate. 3-(4,5-Dimethylthiazole-2-yl)-2,5-diphenyltetrazolium bromide assay denoted significant time-dependent cell death in arsenic and lead treated oval cells. The degree of stress imposed by these metals was evidenced by induction of heat shock protein (HSP) 70 and HSP 90. Arsenic and lead were found to trigger apoptosis as revealed by DNA ladder formation, Western blots of apoptotic factors, and reverse transcriptase polymerase chain reaction analyses of bax and bcl-2. Results clearly indicate that both arsenic and lead induced apoptosis is caspase-mediated and accompanied by extracellular signal-regulated kinase (ERK) dephosphorylation. Full-length BH3-interacting-domain death agonist expression in presence of caspase 3 inhibitor unravels a direct involvement of caspase in As and Pb induced apoptosis. Expression patterns of apoptosis inducing factor, B cell lymphoma-2 (Bcl-2) antagonist of cell death, Bcl-2-associated X protein, and Bcl2 also signify mitochondrial regulation of apoptosis effected by lead and arsenic. It is concluded that stimulation of caspase cascade and simultaneous ERK dephosphorylation are the most significant operative pathways directly associated with apoptotic signals triggered by arsenic and lead in the oval cells.
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PMID:Arsenic trioxide and lead acetate induce apoptosis in adult rat hepatic stem cells. 1861 74

Expression profiles of nine rice heat shock protein genes (OsHSPs) were analyzed by semi-quantitative reverse transcriptase polymerase chain reaction (RT-PCR). The nine genes exhibited distinctive expression in different organs. Expression of nine OsHSP genes was affected differentially by abiotic stresses and abscisic acid (ABA). All nine OsHSP genes were induced strongly by heat shock treatment, whereas none of them were induced by cold. The transcripts of OsHSP80.2, OsHSP71.1 and OsHSP23.7 were increased during salt tress treatment. Expression of OsHSP80.2 and OsHSP24.1 genes were enhanced while treated with 10% PEG. Only OsHSP71.1 was induced by ABA while OsHSP24.1 was suppressed by ABA. These observations imply that the nine OsHSP genes may play different roles in plant development and abiotic stress responses.
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PMID:Expression analysis of nine rice heat shock protein genes under abiotic stresses and ABA treatment. 1913 78

T-2 toxin is one of the most potent trichothecenes, and on exposure causes severe human and animal diseases. We investigated the dose- and time-dependent effect of T-2 toxin on certain biochemical variables, oxidative damage in terms of antioxidant enzyme activity, and gene expression profile in mice. Mice treated intraperitoneally with either 1 LD50 or 2 LD50 dose (5.61 and 11.22 mg/kg body weight, respectively) of T-2 toxin showed significant alterations in hepatic alanine amino transferase, aspartate amino transferase, and lactate dehydrogenase. Significant changes in hepatic lipid peroxidation, depletion of glutathione (GSH), and expression of heat shock protein-70 indicated oxidative damage. We also evaluated the activity of antioxidant enzymes and compared the gene expression profile by quantitative real-time reverse transcriptase-polymerase chain reaction. Except for glutathione reductase (GR), there was a significant increase in activity of glutathione-S-transferase (GST), glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase at 1 LD50 dose. At 2 LD50 dose, SOD showed decrease in activity, whereas GST, GPx, and catalase showed significant increase. In contrast, gene expression profile showed downregulation in GR, GPx, GST, and catalase at 1 LD50 dose. At 2 LD50 dose except GSH synthetase, all other genes were downregulated. The results clearly show oxidative stress as one of the mechanisms of T-2 toxin-mediated toxicity.
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PMID:Oxidative damage and gene expression profile of antioxidant enzymes after T-2 toxin exposure in mice. 1952 62


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