Heterogeneity of the glutathione transferase genes encoding enzymes responsible for insecticide degradation in the housefly

1996 ◽  
Vol 43 (3) ◽  
pp. 236-240 ◽  
Author(s):  
Michael Syvanen ◽  
Zonghan Zhou ◽  
Jonathan Wharton ◽  
Claire Goldsbury ◽  
Alan Clark
Keyword(s):  
Glutathione Transferase ◽  
Insecticide Degradation ◽  
Genes Encoding

Heterogeneity of the Glutathione Transferase Genes Encoding Enzymes Responsible for Insecticide Degradation in the Housefly

1996 ◽  
Vol 43 (3) ◽  
pp. 236-240
Author(s):  
Michael Syvanen ◽  
Zonghan Zhou ◽  
Jonathan Wharton ◽  
Claire Goldsbury ◽  
Alan Clark
Keyword(s):  
Glutathione Transferase ◽  
Insecticide Degradation ◽  
Genes Encoding

scholarly journals Identification, characterization and structure of a new Delta class glutathione transferase isoenzyme

2005 ◽  
Vol 388 (3) ◽  
pp. 763-771 ◽  
Author(s):  
Rungrutai UDOMSINPRASERT ◽  
Saengtong PONGJAROENKIT ◽  
Jantana WONGSANTICHON ◽  
Aaron J. OAKLEY ◽  
La-aied PRAPANTHADARA ◽  
...  
Keyword(s):  
Crystal Structure ◽  
Fatty Acids ◽  
Active Site ◽  
Glutathione Transferase ◽  
Putative Promoter ◽  
Anopheles Dirus ◽  
Adult Females ◽  
Genes Encoding ◽  
Supergene Family ◽  
Gst Activity

The insect GST (glutathione transferase) supergene family encodes a varied group of proteins belonging to at least six individual classes. Interest in insect GSTs has focused on their role in conferring insecticide resistance. Previously from the mosquito malaria vector Anopheles dirus, two genes encoding five Delta class GSTs have been characterized for structural as well as enzyme activities. We have obtained a new Delta class GST gene and isoenzyme from A. dirus, which we name adGSTD5-5. The adGSTD5-5 isoenzyme was identified and was only detectably expressed in A. dirus adult females. A putative promoter analysis suggests that this GST has an involvement in oogenesis. The enzyme displayed little activity for classical GST substrates, although it possessed the greatest activity for DDT [1,1,1-trichloro-2,2-bis-(p-chlorophenyl)ethane] observed for Delta GSTs. However, GST activity was inhibited or enhanced in the presence of various fatty acids, suggesting that the enzyme may be modulated by fatty acids. We obtained a crystal structure for adGSTD5-5 and compared it with other Delta GSTs, which showed that adGSTD5-5 possesses an elongated and more polar active-site topology.

scholarly journals Polymorphisms in Genes Encoding Glutathione Transferase Pi and Glutathione Transferase Omega Influence Prostate Cancer Risk and Prognosis

2021 ◽  
Vol 8 ◽  
Author(s):  
Veljko Santric ◽  
Dejan Dragicevic ◽  
Marija Matic ◽  
Milica Djokic ◽  
Marija Pljesa-Ercegovac ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Glutathione Transferase ◽  
Redox Homeostasis ◽  
Prostate Cancer Risk ◽  
Gst Polymorphisms ◽  
Increased Risk ◽  
Genes Encoding ◽  
Gst Polymorphism ◽  
First Time

Considering the pleiotropic roles of glutathione transferase (GST) omega class members in redox homeostasis, we hypothesized that polymorphisms in GSTO1 and GSTO2 might contribute to prostate cancer (PC) development and progression. Therefore, we performed a comprehensive analysis of GSTO1 and GSTO2 SNPs’ role in susceptibility to PC, as well as whether they might serve as prognostic biomarkers independently or in conjunction with other common GST polymorphisms (GSTM1, GSTT1, and GSTP1). Genotyping was performed in 237 PC cases and 236 age-matched controls by multiplex PCR for deletion of GST polymorphisms and quantitative PCR for SNPs. The results of this study, for the first time, demonstrated that homozygous carriers of both GSTO1*A/A and GSTO2*G/G variant genotypes are at increased risk of PC. This was further confirmed by haplotype analysis, which showed that H2 comprising both GSTO1*A and GSTO2*G variant alleles represented a high-risk combination. However, the prognostic relevance of polymorphisms in GST omega genes was not found in our cohort of PC patients. Analysis of the role of other investigated GST polymorphisms (GSTM1, GSTT1, and GSTP1) in terms of PC prognosis has shown shorter survival in carriers of GSTP1*T/T (rs1138272) genotype than in those carrying at least one referent allele. In addition, the presence of GSTP1*T/T genotype independently predicted a four-fold higher risk of overall mortality among PC patients. This study demonstrated a significant prognostic role of GST polymorphism in PC.

scholarly journals Human nuclear pregnane X receptor cross-talk with CREB to repress cAMP activation of the glucose-6-phosphatase gene

2007 ◽  
Vol 407 (3) ◽  
pp. 373-381 ◽  
Author(s):  
Susumu Kodama ◽  
Rick Moore ◽  
Yukio Yamamoto ◽  
Masahiko Negishi
Keyword(s):  
Knockout Mice ◽  
Glutathione Transferase ◽  
Pregnane X Receptor ◽  
Camp Response Element Binding ◽  
Wild Type ◽  
Huh7 Cells ◽  
Genes Encoding ◽  
Element Binding Protein ◽  
Promoter Construct ◽  
Dependent Protein

The nuclear PXR (pregnane X receptor) was originally characterized as a key transcription factor that activated hepatic genes encoding drug-metabolizing enzymes. We have now demonstrated that PXR also represses glucagon-activated transcription of the G6Pase (glucose-6-phosphatase) gene by directly binding to CREB [CRE (cAMP-response element)-binding protein]. Adenoviral-mediated expression of human PXR (hPXR) and its activation by rifampicin strongly repressed cAMP-dependent induction of the endogenous G6Pase gene in Huh7 cells. Using the −259 bp G6Pase promoter construct in cell-based transcription assays, repression by hPXR of PKA (cAMP-dependent protein kinase)-mediated promoter activation was delineated to CRE sites. GST (glutathione transferase) pull-down and immunoprecipitation assays were employed to show that PXR binds directly to CREB, while gel-shift assays were used to demonstrate that this binding prevents CREB interaction with the CRE. These results are consistent with the hypothesis that PXR represses the transcription of the G6Pase gene by inhibiting the DNA-binding ability of CREB. In support of this hypothesis, treatment with the mouse PXR activator PCN (pregnenolone 16α-carbonitrile) repressed cAMP-dependent induction of the G6Pase gene in primary hepatocytes prepared from wild-type, but not from PXR-knockout, mice, and also in the liver of fasting wild-type, but not PXR-knockout, mice. Moreover, ChIP (chromatin immunoprecipitation) assays were performed to show a decreased CREB binding to the G6Pase promoter in fasting wild-type mice after PCN treatment. Thus drug activation of PXR can repress the transcriptional activity of CREB, down-regulating gluconeogenesis.

DNA methylation in satellite repeats disorders

2019 ◽  
Vol 63 (6) ◽  
pp. 757-771 ◽  
Author(s):  
Claire Francastel ◽  
Frédérique Magdinier
Keyword(s):  
Dna Methylation ◽  
Human Genome ◽  
Repetitive Dna ◽  
Dna Sequences ◽  
Satellite Repeats ◽  
Tremendous Progress ◽  
Genes Encoding ◽  
Dna Elements ◽  
Near Future

Abstract Despite the tremendous progress made in recent years in assembling the human genome, tandemly repeated DNA elements remain poorly characterized. These sequences account for the vast majority of methylated sites in the human genome and their methylated state is necessary for this repetitive DNA to function properly and to maintain genome integrity. Furthermore, recent advances highlight the emerging role of these sequences in regulating the functions of the human genome and its variability during evolution, among individuals, or in disease susceptibility. In addition, a number of inherited rare diseases are directly linked to the alteration of some of these repetitive DNA sequences, either through changes in the organization or size of the tandem repeat arrays or through mutations in genes encoding chromatin modifiers involved in the epigenetic regulation of these elements. Although largely overlooked so far in the functional annotation of the human genome, satellite elements play key roles in its architectural and topological organization. This includes functions as boundary elements delimitating functional domains or assembly of repressive nuclear compartments, with local or distal impact on gene expression. Thus, the consideration of satellite repeats organization and their associated epigenetic landmarks, including DNA methylation (DNAme), will become unavoidable in the near future to fully decipher human phenotypes and associated diseases.

Polymorphisms within genes encoding co-stimulatory molecules modulate the susceptibility to Graves' disease and orbitopathy

2014 ◽  
Author(s):  
Jacek Daroszewski ◽  
Edyta Pawlak-Adamska ◽  
Janusz Przemyslaw ◽  
Irena Frydecka ◽  
Lidia Karabon ◽  
...  
Keyword(s):  
Graves Disease ◽  
Genes Encoding
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