Gene Activity Control, Development and Stress Response

Gene Activity Control, Development and Stress Response... 

Gene activity control, development and stress response... 

NF-AT3 also cooperates with GATA-4, a heart-specific transcription factor. When Ca2+ levels rise in a stressed heart, NF-AT3 moves to the nucleus and binds to GATA-4 and both turn on genes responsible for cardiac hypertrophy. The clinical importance of cardiac hypertrophy, which eventually causes heart failure, makes the development of drugs that act like immunosuppressives, preventing nuclear import of NF-AT3, an active area of research into control of cardiac hypertrophy. ... 

Marui et al. clarified the relation between oxidative stress in the arterial wall (in particular, the endothelium) and the development of the inflammatory response [19,25]. Expression of VCAM-1 by hmnan endothelial cells stimulated by cytokines such as interleukin-1 (IL-1) is mediated by redox-sensitive control mechanisms [25]. The redox-sensitive nature of this gene regulation was determined by the use of antioxidants that are active intracellularly. It was reported that the antioxidant pyrolidine dithiocarbamate (PDTC) inhibited the IL-1-induced endothelial expression of mRNA for VCAM-1 and was as effective as a monoclonal antibody against the VCAM-1 counterligand very late antigen-4 (VLA-4) in inhibiting binding of Molt-4 cells, which express VLA-4 [25]. 

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