scholarly journals T-box transcription factor eomesodermin/Tbr2 in Atlantic cod (Gadus morhua L.): Molecular characterization, promoter structure and function analysis

2019 ◽  
Vol 93 ◽  
pp. 28-38
Author(s):  
Heng Chi ◽  
Kristian Gillebo Sørmo ◽  
Jing Diao ◽  
Roy Ambli Dalmo
2021 ◽  
Vol 534 ◽  
pp. 206-211
Author(s):  
Jianzhong Huang ◽  
Xiaoqiu Wu ◽  
Kaiting Sun ◽  
Zhiyong Gao

2021 ◽  
Vol 35 (1) ◽  
pp. 862-872
Author(s):  
Chunliu Li ◽  
Dejia Hou ◽  
Lin Zhang ◽  
Xiaohong Li ◽  
Jiangbo Fan ◽  
...  

2021 ◽  
Author(s):  
Marta Eide ◽  
Xiaokang Zhang ◽  
Odd André Karlsen ◽  
Jared V. Goldstone ◽  
John Stegeman ◽  
...  

Abstract How an organism copes with chemicals is largely determined by the genes and proteins that collectively function to defend against, detoxify and eliminate chemical stressors. This integrative network includes receptors and transcription factors, biotransformation enzymes, transporters, antioxidants, and metal- and heat-responsive genes, and is collectively known as the chemical defensome. Although the types of defensome genes are generally conserved in animals, there are important differences in the complement and function of specific genes between species. Teleost fish is the largest group of vertebrate species and can provide valuable insights into the evolution and functional diversity of defensome genes.In this study, we compared the genes comprising the chemical defensome of five fish species that span the teleosteii evolutionary branch often used as model species in toxicological studies and environmental monitoring programs: zebrafish (Danio rerio), Atlantic cod (Gadus morhua), medaka (Oryzias latipes), Atlantic killifish (Fundulus heteroclitus) and three-spined stickleback (Gasterosteus aculeatus). Genome miningrevealed evolved differences in the number and composition of defensome genes that can have implication for how these species sense and respond to environmental pollutants. The results indicate that knowledge regarding the diversity and function of the defensome will be important for toxicological testing and risk assessment studies.


2009 ◽  
Vol 71 (4-5) ◽  
pp. 469-481 ◽  
Author(s):  
Xiaoxia Dai ◽  
Changjun You ◽  
Lei Wang ◽  
Guoxing Chen ◽  
Qifa Zhang ◽  
...  

2017 ◽  
Vol 121 (suppl_1) ◽  
Author(s):  
Gobinath Shanmugam ◽  
Madhusudhanan Narasimhan ◽  
Jolyn Fernandes ◽  
Kevin Whitehead ◽  
Silvio H Litovsky ◽  
...  

Background: Heart failure is a growing cause of human morbidity and mortality. Supplementations of free radical scavenging antioxidants have largely failed to protect the myocardium from oxidative stress diseases. While endogenous transcriptional activation of antioxidants appears to be promising, their chronic effects are unknown. Here, we tested a hypothesis that chronic activation of antioxidant system will result in reductive stress (RS) and lead to pathological cardiac hypertrophy. Methods: Novel transgenic (TG) mice expressing constitutively active Nrf2 in the heart (α-MHC-caNrf2-TG) and their littermates were used to study the effects on structure and function of the myocardium. Myocardial glutathione redox state (GSH/GSSG), transcript levels (qPCR), and protein (immunoblotting) for Nrf2-related antioxidants and structure and function analysis (echocardiography - Vevo2100 Imager) in Non-transgenic (NTg), TG-low and TG-high mice (n=6-12/gp.) were performed at 6-8 months of age. Further, changes in cardiomyocytes and rate of survival in TG mice were analyzed. Results: Kaplan-Meier survival plots demonstrated 10 and 40% mortality in TG-low and TG-high, respectively, compared to NTG by 60 weeks of age. The myocardial glutathione and its redox ratio (GSH/GSSG) were significantly increased (p<0.05) in the TG-low and TG-high compared with NTg mice indicates development of RS. A significant increase in Nrf2-ARE (promoter) binding with increased expression of antioxidant genes and proteins (p<0.05) were noted in TG vs. NTg mice. Increased heart-to-body weight and heart weight to tibia length ratios were prominent in TG-high relative to NTg or TG-low mice. Histological analyses (WGA, H&E staining) showed increased cardiomyocyte size, ventricular wall thickening and decreased chamber volume in TG mice. Echocardiography analyses revealed significant hypertrophic cardiomyopathy with abnormally increased ejection fraction (HCM i EF) due to chronic reductive stress. Conclusion: Thus, basal attenuation of the obligatory oxidative signaling with chronic activation of Nrf2-antioxidants could shift the redox equilibrium to “reductive” side and thereby causing pathological cardiac remodeling.


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