Endothelial cell nitric oxide synthase, although considered a constitutively expressed gene, is subject to regulation by various physiological and pathophysiological signals.
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Questions strictly constitutive ecNOS view; leaves open dynamic regulation in endothelial function and disease.
Recent studies have provided insight into how the expression of endothelial cell nitric oxide synthase (ecNOS) is regulated. 2. The promoter of ecNOS has several features that are compatible with a constitutively expressed, so-called 'house keeping' gene. These include absence of a TATA box and the presence of Sp1 binding sites located near the transcription start site. The promoter also contains a number of putative binding domains which suggests that it may be regulated by a variety of transcription factor mediated signals. 3. Studies of cultured endothelial cells suggest that ecNOS expression is modulated by shear stress, transforming growth factor beta, inhibition of protein kinase C and the state of proliferation. These experiments indicate that although the ecNOS is a 'constitutively expressed' gene, its content in the endothelium is subject to modest degrees of regulation that may have important physiological and pathophysiological implications.
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Harrison et al. (1996) studied this question.
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