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Glutathione-s-transferase M1 and T1 polymorphisms and associations with type 1 diabetes age-at-onset.

Bekris, L M; Shephard, C; Peterson, M; Hoehna, J; Van Yserloo, B; Rutledge, E; Farin, F; Kavanagh, T J and Lernmark, Åke LU (2005) In Autoimmunity 38(8). p.567-575
Abstract
Type 1 diabetes (T1D) is an autoimmune disease characterized by pancreatic beta cell destruction involving auto-reactive T-cells, pro-inflammatory cytokines, reactive oxygen species (ROS) and loss of insulin. Monozygotic twin studies show a 20-60% concordance with T1D indicating there may be an environmental component to the disease. Glutathione (GSH) is the major endogenous antioxidant produced by the cell. GSH participates directly in the neutralization of free radicals and plays a role in the immune response. Glutathione-s-transferases (GSTs) conjugate GSH to free-radicals or xenobiotics. GST activity depletes GSH levels and may either detoxify or enhance the toxicity of a compound. Glutathione-s-transferase mu 1 (GSTM1) and... (More)
Type 1 diabetes (T1D) is an autoimmune disease characterized by pancreatic beta cell destruction involving auto-reactive T-cells, pro-inflammatory cytokines, reactive oxygen species (ROS) and loss of insulin. Monozygotic twin studies show a 20-60% concordance with T1D indicating there may be an environmental component to the disease. Glutathione (GSH) is the major endogenous antioxidant produced by the cell. GSH participates directly in the neutralization of free radicals and plays a role in the immune response. Glutathione-s-transferases (GSTs) conjugate GSH to free-radicals or xenobiotics. GST activity depletes GSH levels and may either detoxify or enhance the toxicity of a compound. Glutathione-s-transferase mu 1 (GSTM1) and glutathione-s-transferase theta 1 (GSTT1) have polymorphic homozygous deletion (null) genotypes resulting in complete absence of enzyme activity. GSTM1 and GSTT1 null genotypes in Caucasian populations have frequencies of approximately 40-60% and 15-20%, respect (Less)
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author
publishing date
type
Contribution to journal
publication status
published
subject
keywords
glutathione-s-transferase, Type 1 diabetes, polymorphism, GSTT1, GSTM1, age-at-onset
in
Autoimmunity
volume
38
issue
8
pages
567 - 575
publisher
Taylor & Francis
external identifiers
  • scopus:30844448323
ISSN
0891-6934
DOI
10.1080/08916930500407238
language
English
LU publication?
no
id
f2d892ec-bd5a-4cc6-b616-5a8577f83995 (old id 1133056)
date added to LUP
2008-06-25 14:15:49
date last changed
2017-06-25 04:19:29
@article{f2d892ec-bd5a-4cc6-b616-5a8577f83995,
  abstract     = {Type 1 diabetes (T1D) is an autoimmune disease characterized by pancreatic beta cell destruction involving auto-reactive T-cells, pro-inflammatory cytokines, reactive oxygen species (ROS) and loss of insulin. Monozygotic twin studies show a 20-60% concordance with T1D indicating there may be an environmental component to the disease. Glutathione (GSH) is the major endogenous antioxidant produced by the cell. GSH participates directly in the neutralization of free radicals and plays a role in the immune response. Glutathione-s-transferases (GSTs) conjugate GSH to free-radicals or xenobiotics. GST activity depletes GSH levels and may either detoxify or enhance the toxicity of a compound. Glutathione-s-transferase mu 1 (GSTM1) and glutathione-s-transferase theta 1 (GSTT1) have polymorphic homozygous deletion (null) genotypes resulting in complete absence of enzyme activity. GSTM1 and GSTT1 null genotypes in Caucasian populations have frequencies of approximately 40-60% and 15-20%, respect},
  author       = {Bekris, L M and Shephard, C and Peterson, M and Hoehna, J and Van Yserloo, B and Rutledge, E and Farin, F and Kavanagh, T J and Lernmark, Åke},
  issn         = {0891-6934},
  keyword      = {glutathione-s-transferase,Type 1 diabetes,polymorphism,GSTT1,GSTM1,age-at-onset},
  language     = {eng},
  number       = {8},
  pages        = {567--575},
  publisher    = {Taylor & Francis},
  series       = {Autoimmunity},
  title        = {Glutathione-s-transferase M1 and T1 polymorphisms and associations with type 1 diabetes age-at-onset.},
  url          = {http://dx.doi.org/10.1080/08916930500407238},
  volume       = {38},
  year         = {2005},
}