scholarly journals Analysis of the Association of A Heat Shock Protein70-1 Gene Promoter Polymorphism With Myocardial Infarction and Coronary Risk Traits

1998 ◽  
Vol 13 (4) ◽  
pp. 227-235 ◽  
Author(s):  
M.K. Bolla ◽  
G.J. Miller ◽  
D.M. Yellon ◽  
A. Evans ◽  
G. Luc ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heat Shock ◽  
Coronary Disease ◽  
Strong Association ◽  
Gene Promoter ◽  
Promoter Polymorphism ◽  
Base Substitution ◽  
Nucleotide Position ◽  
Heat Shock Element ◽  
The Common

Heat shock proteins (HSP) are induced during coronary ischaemia, and abnormal expression of one HSP gene may cause hypertension in rats, We examined association of a promoter polymorphism in the major stress-inducible hsp70 gene (hsp70-1 or HSP70A1) on chromosome 6 (p21.3) with coronary disease traits, This C→A base substitution (AAACCCC) is at nucleotide position -110 in the heat shock transcription factor binding site (heat shock element, HSE). The first study sample (ECTIM), recruited from Belfast and three centres in France, consisted of 578 myocardial infarction cases and 698 agematched controls. The frequency of the A-110allele was 0.381 (95% CI=0.35-0.41) and 0.384 (95% CI=0.36-0.41) in cases and controls respectively, Homozygotes for the rarer A-110allele had a higher BMI (27.3 kg/m2±3.9) compared with homozygotes for the common C-110allele (26.3 kg/m2±3.3), The rarer homozygotes were shorter and heavier than the common homozygotes. A follow-up study involved 1431 healthy, middle aged men from the UK (NPHSII group). The frequency of the A-110allele was 0.385 (95% CI=0.37 -0.40), and there was no association of genotype with BMI. Thus there appears to be no strong association of the Hsp70-1 promoter polymorphism with risk of myocardial infarction, BMI or any coronary disease traits analysed here.

Modular recognition of 5-base-pair DNA sequence motifs by human heat shock transcription factor

1991 ◽  
Vol 11 (7) ◽  
pp. 3504-3514
Author(s):  
N F Cunniff ◽  
J Wagner ◽  
W D Morgan
Keyword(s):  
Transcription Factor ◽  
Heat Shock ◽  
Gene Promoter ◽  
Heat Shock Transcription Factor ◽  
Heat Shock Gene ◽  
Gene Promoters ◽  
Sequence Motifs ◽  
Binding Modes ◽  
Heat Shock Element

We investigated the recognition of the conserved 5-bp repeated motif NGAAN, which occurs in heat shock gene promoters of Drosophila melanogaster and other eukaryotic organisms, by human heat shock transcription factor (HSF). Extended heat shock element mutants of the human HSP70 gene promoter, containing additional NGAAN blocks flanking the original element, showed significantly higher affinity than the wild-type promoter element for human HSF in vitro. Protein-DNA contact positions were identified by hydroxyl radical protection, diethyl pyrocarbonate interference, and DNase I footprinting. New contacts in the mutant HSE constructs corresponded to the locations of additional NGAAN motifs. The pattern of binding indicated the occurrence of multiple DNA binding modes for HSF with the various constructs and was consistent with an oligomeric, possibly trimeric, structure of the protein. In contrast to the improved binding, the extended heat shock element mutant constructs did not exhibit dramatically increased heat-inducible transcription in transient expression assays with HeLa cells.

scholarly journals Expression of a constitutively active mutant of heat shock factor 1 under the control of testis-specific hst70 gene promoter in transgenic mice induces degeneration of seminiferous epithelium.

2003 ◽  
Vol 50 (2) ◽  
pp. 535-541 ◽  
Author(s):  
Wiesława Widłak ◽  
Konrad Benedyk ◽  
Natallia Vydra ◽  
Magdalena Głowala ◽  
Dorota Scieglińska ◽  
...  
Keyword(s):  
Heat Shock ◽  
Transgenic Mice ◽  
Target Genes ◽  
Gene Promoter ◽  
Basic Mechanism ◽  
Seminiferous Epithelium ◽  
High Rate ◽  
Heat Shock Factor 1 ◽  
Heat Shock Element ◽  
Constitutively Active

Heat shock activates in somatic cells a set of genes encoding heat shock proteins which function as molecular chaperones. The basic mechanism by which these genes are activated is the interaction of the specific transcription factor HSF1 with a regulatory DNA sequence called heat shock element (HSE). In higher eukaryotes HSF1 is present in unstressed cells as inactive monomers which, in response to cellular stress, aggregate into transcriptionally competent homotrimers. In the present paper we showed that the expression of a transgene encoding mutated constitutively active HSF1 placed under the control of a spermatocyte-specific promoter derived from the hst70 gene severely affects spermatogenesis. We found the testes of transgenic mice to be significantly smaller than those of wild-type males and histological analysis showed massive degeneration of the seminiferous epithelium. The lumen of tubules was devoid of spermatids and spermatozoa and using the TUNEL method we demonstrated a high rate of spermatocyte apoptosis. The molecular mechanism by which constitutively active HSF1 arrests spermatogenesis is not known so far. One can assume that HSF1 can either induce or repress so far unknown target genes involved in germ cell apoptosis.

scholarly journals Regulation of human heme oxygenase-1 gene expression under thermal stress

Blood ◽  
1996 ◽  
Vol 87 (12) ◽  
pp. 5074-5084 ◽  
Author(s):  
S Okinaga ◽  
K Takahashi ◽  
K Takeda ◽  
M Yoshizawa ◽  
H Fujita ◽  
...  
Keyword(s):  
Gene Expression ◽  
Thermal Stress ◽  
Heat Shock ◽  
Transient Expression ◽  
Reporter Gene ◽  
Heme Oxygenase ◽  
Gene Promoter ◽  
Heme Oxygenase 1 ◽  
Heat Shock Element ◽  
Hsp70 Mrna

Heme oxygenase-1 is an essential enzyme in heme catabolism, and its human gene promoter contains a putative heat shock element (HHO-HSE). This study was designed to analyze the regulation of human heme oxygenase-1 gene expression under thermal stress. The amounts of heme oxygenase-1 protein were not increased by heat shock (incubation at 42 degrees C) in human alveolar macrophages and in a human erythroblastic cell line, YN-1–0-A, whereas heat shock protein 70 (HSP70) was noticeably induced. However, heat shock factor does bind in vitro to HHO-HSE and the synthetic HHO-HSE by itself is sufficient to confer the increase in the transient expression of a reporter gene upon heat shock. The deletion of the sequence, located downstream from HHO-HSE, resulted in the activation of a reporter gene by heat shock. These results suggest that HHO-HSE is potentially functional but is repressed in vivo. Interestingly, heat shock abolished the remarkable increase in the levels of heme oxygenase-1 mRNA in YN-1–0-A cells treated with hemin or cadmium, in which HSP70 mRNA was noticeably induced. Furthermore, transient expression assays showed that heat shock inhibits the cadmium-mediated activation of the heme oxygenase-1 promoter, whereas the HSP70 gene promoter was activated upon heat shock. Such regulation of heme oxygenase-1 under thermal stress may be of physiologic significance in erythroid cells.

scholarly journals The Heat-Shock Element Is a Functional Component of the Arabidopsis APX1 Gene Promoter

1998 ◽  
Vol 118 (3) ◽  
pp. 1005-1014 ◽  
Author(s):  
Sergei Storozhenko ◽  
Pascal De Pauw ◽  
Marc Van Montagu ◽  
Dirk Inzé ◽  
Sergei Kushnir
Keyword(s):  
Heat Shock ◽  
Gene Promoter ◽  
Heat Shock Element ◽  
Functional Component

scholarly journals Modular recognition of 5-base-pair DNA sequence motifs by human heat shock transcription factor.

1991 ◽  
Vol 11 (7) ◽  
pp. 3504-3514 ◽  
Author(s):  
N F Cunniff ◽  
J Wagner ◽  
W D Morgan
Keyword(s):  
Transcription Factor ◽  
Heat Shock ◽  
Gene Promoter ◽  
Heat Shock Transcription Factor ◽  
Heat Shock Gene ◽  
Gene Promoters ◽  
Sequence Motifs ◽  
Binding Modes ◽  
Heat Shock Element

We investigated the recognition of the conserved 5-bp repeated motif NGAAN, which occurs in heat shock gene promoters of Drosophila melanogaster and other eukaryotic organisms, by human heat shock transcription factor (HSF). Extended heat shock element mutants of the human HSP70 gene promoter, containing additional NGAAN blocks flanking the original element, showed significantly higher affinity than the wild-type promoter element for human HSF in vitro. Protein-DNA contact positions were identified by hydroxyl radical protection, diethyl pyrocarbonate interference, and DNase I footprinting. New contacts in the mutant HSE constructs corresponded to the locations of additional NGAAN motifs. The pattern of binding indicated the occurrence of multiple DNA binding modes for HSF with the various constructs and was consistent with an oligomeric, possibly trimeric, structure of the protein. In contrast to the improved binding, the extended heat shock element mutant constructs did not exhibit dramatically increased heat-inducible transcription in transient expression assays with HeLa cells.

scholarly journals Association of matrix metalloproteinase-2 gene promoter polymorphism with myocardial infarction susceptibility in a Mexican population

2009 ◽  
Vol 88 (2) ◽  
pp. 249-252 ◽  
Author(s):  
Ivan Delgado-Enciso ◽  
Nelida A. Gonzalez-Hernandez ◽  
Luz M. Baltazar-Rodriguez ◽  
Rebeca O. Millan-Guerrero ◽  
Oscar Newton-Sanchez ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Matrix Metalloproteinase ◽  
Gene Promoter ◽  
Promoter Polymorphism ◽  
Mexican Population ◽  
Matrix Metalloproteinase 2 ◽  
Gene Promoter Polymorphism

scholarly journals IGF-I gene promoter polymorphism is a predictor of survival after myocardial infarction in patients with type 2 diabetes

2006 ◽  
Vol 155 (5) ◽  
pp. 751-756 ◽  
Author(s):  
Mojgan Yazdanpanah ◽  
Fakhredin A Sayed-Tabatabaei ◽  
Joop A M J L Janssen ◽  
Ingrid Rietveld ◽  
Albert Hofman ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Type 2 Diabetes ◽  
Gene Promoter ◽  
Population Based ◽  
Promoter Polymorphism ◽  
Increased Risk ◽  
Igf I ◽  
Genetically Determined

Objective: Previously we observed that non-carriers of the most common alleles of an IGF-I promoter polymorphism have low circulating IGF-I levels and an increased risk of developing myocardial infarction (MI), particularly in patients with type 2 diabetes. Design: We investigated whether this IGF-I promoter polymorphism is associated with survival of type 2 diabetes in a Caucasian population aged 55 years and older. Methods: The study was embedded in the Rotterdam Study, a prospective population-based cohort study. At baseline, 668 patients with type 2 diabetes were diagnosed, among which, 55 incident MI were ascertained during follow-up. For the present study, we used two genotype groups: non-variant carriers (homozygous for 192, 194, or 192/194 bp genotypes), and variant carriers. Results: During a median follow-up of 8.8 years, 396 out of the 668 patients with type 2 diabetes (59.3%) died of various causes. The frequency of type 2 diabetes variant carrier and non-variant carriers was 28.7 and 71.3% respectively. The survival in patients with type 2 diabetes without an MI did not differ between the IGF-I genotype groups (hazard ratio (HR) = 0.8, 95% confidence interval (CI): 0.7–1.1, P = 0.1). In contrast, in those who developed an MI, variant carriers had a 2.4 times higher risk of mortality than non-variant carriers (95% CI: 1.2–4.8, P = 0.01). Conclusion: Our study suggests that genetically determined low IGF-I activity is an important determinant of survival in patients with type 2 diabetes who developed an MI. The IGF-I promoter polymorphism, therefore, may help to predict the future mortality risk in this group of patients.

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