GSTT1 Gene

2020 ◽  
Author(s):  
Keyword(s):  
2012 ◽  
Vol 13 (9) ◽  
pp. 4417-4421 ◽  
Author(s):  
Jie Chen ◽  
Liang Ma ◽  
Ning-Fu Peng ◽  
Shi-Jun Wang ◽  
Le-Qun Li

2020 ◽  
Vol 14 (Supplement_1) ◽  
pp. S188-S188
Author(s):  
J H Kim ◽  
J B Ahn ◽  
D H Kim ◽  
S Kim ◽  
H W Ma ◽  
...  

Abstract Background The enzyme glutathione S-transferase theta 1 (GSTT1) is involved in detoxifying chemicals, including reactive oxygen species (ROS). Oxidative stress plays a key role in the pathogenesis of inflammatory bowel disease (IBD). Although mutation of the GSTT1 gene increases IBD susceptibility, the underlying mechanisms remain unexplained. Methods The Gstt1 gene was intrarectally or intraperitoneally delivered to mice with dextran sodium sulphate (DSS)-induced colitis. The GSTT1 gene was knocked down or knocked out using short interfering RNA or genome editing, respectively. Protein and mRNA expression and differentiation of goblet cells were evaluated. Results We identified decreased expression of GSTT1 in inflamed tissues from IBD patients and mice compared with their control counterparts, respectively. We also noted attenuation of colitis through gene transfer of Gstt1 to DSS-treated mice via the interleukin-22 (IL-22) pathway. GSTT1 was differently regulated by pathogens and host immune responses. Down-regulation of GSTT1 reduced innate defence responses and goblet cell differentiation. The GSTT1 mutation in intestinal epithelial cells as well as IBD patients diminished its dimerisation, which was connected to insufficient phosphorylation of signal transducer and activator of transcription 3 and p38/mitogen-activated protein kinase by their common activator, IL-22. Conclusion GSTT1 ameliorated IL-22 in colitis in a dependent manner and contributed as a modulator of goblet cells through sensing pathogens and host immune responses. Its mutations are linked to chronic intestinal inflammation due to its insufficient dimerisation. Our results provide new insights into GSTT1 mutations and their functional consequences in IBDs.


Biomarkers ◽  
2020 ◽  
Vol 25 (6) ◽  
pp. 483-489
Author(s):  
Muhammad Khisroon ◽  
Ajmal Khan ◽  
Asma Ayub ◽  
Ihsan Ullah ◽  
Javeed Farooqi ◽  
...  

2012 ◽  
Vol 77 (04) ◽  
pp. 261-266 ◽  
Author(s):  
Kohei Miyazaki ◽  
Keisuke Sugimoto ◽  
Shoji Tsuji ◽  
Anna Iharada ◽  
Shinsuke Fujita ◽  
...  

2011 ◽  
Vol 2011 (1) ◽  
Author(s):  
Hyunok Choi ◽  
Elaine Hoffman ◽  
Quazi Quamruzzaman ◽  
Mahmuder Rahman ◽  
Golam Mahiuddin ◽  
...  

2011 ◽  
Vol 2 (1) ◽  
pp. 36
Author(s):  
Cassio Cardoso Filho ◽  
Gustavo Lourenço ◽  
Julia Yoriko Shinzato ◽  
Luiz Carlos Zeferino ◽  
Fernando Ferreira Costa ◽  
...  

2018 ◽  
Vol 1 (3) ◽  
pp. 80
Author(s):  
Gang Xiao

Objective To investigate the relationship between the polymorphism of glutathione S transferase M1, T1(GSTM1, GSTT1) gene and the susceptibility to antituberculosis drug induced hepatotoxicity (ATDH) in patients with tuberculosis. Methods GSTM1 and GSTT1 gene polymorphisms in patients with or without liver toxicity after antituberculous treatment were analyzed using multiple PCR method. Results In ATDH group and control group, the proportion of GSTM1 gene deletion was 58.0% and 50.7%respectively, and the difference was not statistically signifcant (OR=1.322, 95%CI=0.921~1.878), the frequencies of GSTT1 deletion were 46.3% and 49.3%, respectively, and there was no signifcant difference between them. There was no signifcant difference in frequency of GSTM1 and GSTT1 variation between case group and control group (P> 0.05), and no synergistic effect of those two gene polymorphism were detected in the occurrence of antituberculosis drug-induced hepatotoxicity. Conclusion The polymorphisms of GSTM1 and GSTT1 genes may not be associated with the risk of ATDH.


2020 ◽  
Vol 21 (8) ◽  
pp. 2251-2257
Author(s):  
Phakarat Tangkhuenkhan ◽  
Kitiphong Harncharoen ◽  
Somchai Thanasitthichai ◽  
Danai Tiwawech ◽  
Wichai Purisa ◽  
...  

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