Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In Manduca sexta, ecdysteroids coordinate molting and metamorphosis of insects and are produced by the prothoracic glands under the acute control of the brain neuropeptide prothoracicotropic hormone (PTTH). PTTH stimulates rapid ecdysteroidogenesis accompanied by specific increases in the synthesis and accumulation of three proteins, including one with M(r) = 70 kDa. This 70-kDa protein is a constitutively expressed member of the heat shock protein 70 family (hsc 70). Levels of this hsc 70 vary in a prothoracic gland-specific manner during development as does its PTTH-stimulated synthesis when assayed in vitro. The accumulation of hsc 70 may be regulated by abrupt changes in its turnover rate. The PTTH-stimulated increase in hsc 70 synthesis is dependent upon both translational and transcriptional events. Hsc 70 expression in the prothoracic gland may be required for changes in gland growth, e.g., protein content, that underlie alterations in ecdysteroid production.
Mol Cell Endocrinol 1995 Nov 30
PMID:Prothoracicotropic hormone-regulated expression of a hsp 70 cognate protein in the insect prothoracic gland. 867 67

We investigated the role of alpha B-crystallin expression in the development of thermotolerance in murine L929 cells. An initial heat-shock of 10 min at 45 degrees C induced thermotolerance in these cells to a heat challenge at 45 degrees C administered 24 h later. The thermotolerance ratio at 10(-1) isosurvival was 1.7. Expression of alpha B-crystallin gene was not detected during the 24 h incubation at 37 degrees C following heat shock by either northern or western blots. In contrast, inducible HSP70 synthesis was observed during this time period. Thus, this cell line provided an unique system in which to examine the effects of transfected alpha B-crystallin on thermoresistance and thermotolerance. Cells stably transfected with alpha B-crystallin under the control of an inducible promoter did not show a significant increase in the ability to develop thermotolerance. However, a stably transfected L929 clone expressing high levels of constitutive alpha B-crystallin exhibited an approximately 50% increase in thermal resistance over parental and control cells. Though expression of alpha B-crystallin is not requisite for the development of thermotolerance in L929 cells, overexpression of transfected alpha B-crystallin can contribute to increased thermoresistance.
Mol Cell Biochem 1996 Feb 09
PMID:Thermal response in murine L929 cells lacking alpha B-crystallin expression and alpha B-crystallin expressing L929 transfectants. 871 39

The induction of the heme oxygenase-1 (HO-1) protein, also called HSP32, was compared to HSP70 heat shock protein induction following focal ischemia. Adult Sprague-Dawley male rats (n = 14) were subjected to either 30 min or 2 h of focal cerebral ischemia using the suture, middle-cerebral-artery (MCA) occlusion model. Controls (n = 4) had sham surgery. Following 24 h of reperfusion, subjects were killed and their brains stained immunocytochemically for HO-1 and the HSP70 heat shock proteins. One day following 30 min of ischemia, HO-1 and HSP70 staining in striatum occurred mainly in endothelial cells in infarcts and in glial cells surrounding the areas of infarction. Following the 30 min ischemia HO-1 was not induced in cortex whereas HSP70 was induced in cortical neurons in the MCA distribution. One day following 2 h of MCA ischemia, both HO-1 and HSP70 were induced in neurons in cortex in the MCA distribution. HO-1, however, was induced in glial cells throughout ipsilateral cortex, inside as well as outside the MCA distribution. This suggests that translation and/or transcription of the HO-1 and HSP70 genes are blocked in neurons and glia destined to die within infarcts, whereas translation of these stress genes continues in the endothelial cells. The duration of ischemia required to induce HSP70 in cortical neurons appears to be less than that required to induce HO-1 in cortical glia. Prolonged spreading depression and/or diffuse hemispheric ischemia may induce HO-1 in glia throughout the ipsilateral cortex via immediate early gene activation of the AP-1 site in the HO-1 promoter. Since HO-1 degrades heme, a pro-oxidant, to antioxidant molecules, the induction of HO-1 may augment oxidative defense mechanisms compromised by cerebral ischemia.
Brain Res Mol Brain Res 1996 Apr
PMID:Heme oxygenase-1 (HO-1) protein induction in rat brain following focal ischemia. 873 52

Stress proteins, including the 70 kD heat shock protein (HSP70), are induced in injured cells. The present study was designed to characterize the cells injured by global ischemia in rat brain. Adult rats were subjected to forebrain ischemia using bilateral carotid occlusion and systemic hypotension. HSP70 protein immunostaining of brain sections was performed using the C92 monoclonal antibody one day later. HSP70 immunoreactive cells were found in many brain regions including cortex. HSP70 positive neurons in cortex were found in certain laminae, especially layers 2 and 3. Acid fuchsin positive neurons, cells presumed to be dead, were located only in the layers of cortex where HSP70 immunoreactive neurons were found and were infrequent compared to the large number of HSP70 positive neurons. HSP70 immunoreactive glial cells were detected at the margins of ischemic areas, and were mostly OX42 immunoreactive microglia plus some GFAP immunoreactive astrocytes. In some animals HSP70 stained bipolar cells were detected in the striatum and in white matter which may be type 2 astrocytes. These findings confirm that global ischemia injures microglia and astrocytes, and that cells in a given ischemic region sustain varying degrees of injury--from the HSP70 stained neurons that likely survive the ischemia to acid fuchsin stained cells that die.
Brain Res Mol Brain Res 1995 Dec 28
PMID:HSP70 heat shock protein induction following global ischemia in the rat. 875 Aug 37

Polyomavirus large T-antigen transgenic mice develop cardiac hypertrophy characterized by an increase in atrial natriuretic factor and beta-myosin heavy chain isoform expression. The aim of this study was to examine changes in proto-oncogene expression in hypertrophied hearts from the transgenic mice. Expression of early growth response-1 (Egr-1) mRNA was detected in hearts from all 15 transgenic mice, but was not detectable in 13 control mice. Reverse transcriptase-polymerase chain reaction experiments using Egr-1-specific primers confirmed the increase in Egr-1 mRNA in enlarged hearts from the transgenic mice. Expression of c-jun, junD and Ha-ras mRNAs was increased in the transgenic hearts 3, 17 and 2.8-fold respectively. Western blots showed an increase in c-myc, c-jun and ras protein in hypertrophied transgenic hearts. Immunofluorescence analyses confirmed an increase in Egr-1 and c-jun protein in transgenic cardiomyocytes. Proliferating cell nuclear antigen, Ki-ras and HSP 90 mRNAs were decreased 22, 2.7 and 3-fold, respectively in the transgenic hearts. Not altered in most hypertrophied hearts was expression of c-fos, junB, p53, c-neu, c-myc, HSP70, HSP27, TGF-beta or IGF 1 mRNAs. Proto-oncogene and growth factor gene expression in hypertrophy induced by PVLT expression is modulated with some proto-oncogenes increased and others decreased in expression.
Mol Cell Biochem 1995 Nov 22
PMID:Molecular remodelling in hypertrophied hearts from polyomavirus large T-antigen transgenic mice. 875 Nov 59

Perturbations in keratin intermediate filament organization and Mallory body (MB) formation are associated with alcoholic hepatitis. Inducible heat shock proteins (HSPs) are expressed in a variety of liver diseases including alcoholic liver disease. Therefore, we investigated whether heat shock protein induction can lead to MB formation. Mice were primed by a 5-month feeding of griseofulvin (GF) or diethyl 1,4-dehydro-2,4,6-trimethyl-3,5-pyridinedicarboxylate (DDC) followed by drug withdrawal for 1 month. The animals were then subjected to an in vivo heat shock treatment or sham heat treatment. Liver morphology, HSP expression, liver regeneration (PCNA-labeled nuclei), and MB formation were monitored during a 7-day posttreatment period. Numerous MBs developed in the livers of mice exposed to GF or DDC for 5 months, but very few small MBs remained after 1-month withdrawal of either drug. No MBs were found at Day 1 post heat shock, whereas numerous MBs were observed at Day 7. The frequency of PCNA-labeled nuclei increased during the same period. At Day 1 posttreatment, a variable liver centrilobular necrosis was observed accompanied by a prominent increase in HSP-25 and HSP70 expression, but HSP-90 expression was not increased. In drug-primed mouse liver, a heat shock treatment induces the expression of specific HSPs prior to the formation of MBs, indicating that HSP expression may play a role in the pathogenesis of MB formation. We speculate that this role is through the protein unfolding function of HSP, which leads to the aggregation of the cytokeratins to form MBs as well as to polyubiquitin binding to these proteins in a manner analogous to amyloid formation.
Exp Mol Pathol 1995 Aug
PMID:Heat shock in vivo induces Mallory body formation in drug primed mouse liver. 875 55

This study has shown that the maximal activation of the IP3-DAG regulatory circuit is observed on the 14th day of adaptation to repeated stresses. This activation is characterized by increased activity of phospholipase C and of the positive inotropic response of isolated heart to an alpha-agonist. Simultaneously, this activation is accompanied by the accumulation of five heat shock protein 70 (hsp70) isoforms. The IP3-DAG circuit activation and the hsp70 accumulation are accompanied by a significant increase in the cardiac resistance to post-ischemic reperfusion, as evidenced by a considerable decrease in the contracture, arrhythmias and the creatine kinase release into the perfusate. Continuation of the adaptation to repeated stresses for 28 days leads to complete reversal of the observed shifts.
J Mol Cell Cardiol 1996 May
PMID:The role of hsp70 and IP3-DAG mechanism in the adaptive stabilization of structures and heart protection. 876 23

The genes and proteins of the HSP70 family, are involved in important processes in cells and organelles at normal temperature and after heat stress. Constitutive Hsc70 and heat-inducible Hsp70 genes are known in all organisms including plants. The goal of our present investigation was to generate an Hsp70 mutation in Arabidopsis thaliana. In a transgenic approach a heat-inducible antisense Hsp70 gene was constructed, plants were transformed and screened for lack of heat-inducible HSP70 mRNA; two such lines were further investigated. In these plants the Hsp70 gene was not induced by heat shock, and the level of HSC70 RNA was also greatly reduced. This negative antisense effect was specific for genes of the HSP70 family and the induction of mRNAs encoding the small HSP18 class of heat shock protein (HSP) was not affected. The level of HSP70/HSC70 proteins was significantly reduced in transgenic plants, but HSP18 was induced to the same level in different transgenic lines and in untransformed plants. The acquisition of thermotolerance was negatively affected in artisense plants, the survival temperature being 2 degrees C below the survival temperature of the wild type and other transgenic lines. Another major effect concerning the regulation of the endogenous heat shock transcription factor HSF was detected by testing the ability to form heterotrimers between authentic HSF and recombinant HSF-GUS (beta-glucuronidase) proteins. The shut-off time, required to turn of HSF activity during recovery from heat stress, was significantly prolonged in antisense plants compared with wild-type and other transgenic lines. Our results imply a dual role of HSP70 in plants, a protective role in thermotolerance and a regulatory effect on HSF activity and hence the autoregulation of the heat shock response.
Mol Gen Genet 1996 Aug 27
PMID:An Hsp70 antisense gene affects the expression of HSP70/HSC70, the regulation of HSF, and the acquisition of thermotolerance in transgenic Arabidopsis thaliana. 880 99

Transient expression of the luciferase gene, under transcriptional control of several heterologous promoters, was obtained in heart primary cell cultures of the Pacific oyster, Crassostrea gigas. Drosophila heat shock protein 70 promoter (hsp70), cytomegalovirus, and simian virus early promoters, controlling the luciferase gene, were transfected into the cell cultures using liposomes. Two culture media were used to establish primary cell cultures and tested as transfection media. Parameters such as the quantity of DNA and the ratio of DNA to liposome were analyzed to define the best transfection conditions. In oysters, the Drosophila inducible hsp70 promoter behaved in a way similar to that observed in other animal species. Moreover, for this study, hsp70 was more efficient than the cytomegalovirus and simian virus promoters.
Mol Mar Biol Biotechnol 1996 Sep
PMID:Transient expression of luciferase reporter gene after lipofection in oyster (Crassostrea gigas) primary cell cultures. 881 24

The flanking sequences of several genes have been shown to direct a position independent expression of transgenes. Attempts to completely identify the insulating sequences have failed so far. Some of these sequences contain a matrix attached region (MAR) located in the flanking part of the genes. This article will show that the MARs in cultured cells located in the 3' OH region of the human apolipoprotein B100 (Apo B100) and within the SV40 genome were unable to stimulate and insultate transgene expression directed by the promoters from a rabbit whey acidic protein (WAP) gene or from human cytomegalovirus (hCMV) early genes. In transgenic mice, the MAR from the Apo B100 and SV40 genes did not enhance the expression of a transgene containing the rabbit whey acid protein (WAP) promotor, the late gene SV40 intron (VP1 intron), the bovine growth hormone (bGH) cDNA and the SV40 late gene terminator. This construct was even toxic for embryos. Similarly, the specialized chromatin structure (SCS) from the Drosophila 87A7 HSP70 gene reduced chloramphenicol acetyl transferase (CAT) activity when added between a cytomegalovirus (CMV) enhancer and a Herpes simplex thymidine kinase (TK) gene promoter. This inhibitory action was almost complete when a second SCS sequence was added before the CMV enhancer. Sequences from the firefly luciferase and from the human gene cathepsin D cDNA used as control unexpectedly showed a similar inhibitory effect when added to the CMVTKCAT construct instead of SCS. When added before the CMV enhancer and after the transcription terminator in the CMVTKCAT construct, the SCS sequence was unable to insulate the integrated gene as seen by the fact that the level of CAT in cell extracts were by no means correlated with the number of copies in individual clones. From these data, it is concluded that i) a MAR containing the canonical AT rich sequences does not amplify the expression of all gene constructs ii) At rich MAR sequences do not have per se an insulating effect iii) Drosophila SCS from the 87A7 HSP70 gene has no insulating effect in all gene constructs (at least in mammalian cells) iv) and the addition of a DNA fragment between an enhancer and a promoter in a gene construct cannot be used as a reliable test to evaluate its insulating property.
Mol Biol Rep
PMID:The effect of matrix attached regions (MAR) and specialized chromatin structure (SCS) on the expression of gene constructs in cultured cells and in transgenic mice. 885 71


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