scholarly journals Tumor necrosis factor-alpha genetic polymorphism may contribute to progression of bovine leukemia virus-infection

2006 ◽  
Vol 8 (8) ◽  
pp. 2163-2171 ◽  
Author(s):  
Satoru Konnai ◽  
Tatsufumi Usui ◽  
Manabu Ikeda ◽  
Junko Kohara ◽  
Toh-ichi Hirata ◽  
...  
Keyword(s):  
Genetic Polymorphism ◽  
Tumor Necrosis Factor ◽  
Virus Infection ◽  
Tumor Necrosis Factor Alpha ◽  
Bovine Leukemia Virus ◽  
Tumor Necrosis ◽  
Leukemia Virus ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Necrosis Factor

Genetic Polymorphisms of Tumor Necrosis Factor Alpha and Susceptibility to Dengue Virus Infection in a Mexican Population

2017 ◽  
Vol 30 (8) ◽  
pp. 615-621 ◽  
Author(s):  
Marina Sánchez-Leyva ◽  
Jorge Guillermo Sánchez-Zazueta ◽  
Juan Fidel Osuna-Ramos ◽  
Horacio Rendón-Aguilar ◽  
Rafael Félix-Espinoza ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Virus Infection ◽  
Dengue Virus ◽  
Genetic Polymorphisms ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Dengue Virus Infection ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Necrosis Factor

scholarly journals Stimulus-Specific Assembly of Enhancer Complexes on the Tumor Necrosis Factor Alpha Gene Promoter

2000 ◽  
Vol 20 (6) ◽  
pp. 2239-2247 ◽  
Author(s):  
James V. Falvo ◽  
Adele M. Uglialoro ◽  
Brigitta M. N. Brinkman ◽  
Menie Merika ◽  
Bhavin S. Parekh ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Virus Infection ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Calcium Flux ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACT The human tumor necrosis factor alpha (TNF-α) gene is rapidly activated in response to multiple signals of stress and inflammation. We have identified transcription factors present in the TNF-α enhancer complex in vivo following ionophore stimulation (ATF-2/Jun and NFAT) and virus infection (ATF-2/Jun, NFAT, and Sp1), demonstrating a novel role for NFAT and Sp1 in virus induction of gene expression. We show that virus infection results in calcium flux and calcineurin-dependent NFAT dephosphorylation; however, relatively lower levels of NFAT are present in the nucleus following virus infection as compared to ionophore stimulation. Strikingly, Sp1 functionally synergizes with NFAT and ATF-2/c-jun in the activation of TNF-α gene transcription and selectively associates with the TNF-α promoter upon virus infection but not upon ionophore stimulation in vivo. We conclude that the specificity of TNF-α transcriptional activation is achieved through the assembly of stimulus-specific enhancer complexes and through synergistic interactions among the distinct activators within these enhancer complexes.

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