The endothelial cell nitric oxide synthase: Is it really constitutively expressed?

D. G. Harrison, R. C. Venema, J. F. Arnal, N. Inoue, Y. Ohara, H. Sayegh, T. J. Murphy

Research output: Contribution to journalArticle

34 Citations (Scopus)

Abstract

During the past two years, the enzyme responsible for production of endothelium-derived nitric oxide, the endothelial cell NO synthase (ecNOS) has been cloned and the gene encoding this enzyme isolated, cloned and its structure characterized. This research has provided direction for a variety of studies of regulation of the ecNOS. Several features of the ecNOS are compatible with a constitutively expressed, poorly regulated gene, including absence of a TATA box and numerous SP-1 sites. The promoter also contains a number of putative binding domains which suggest that it may be regulated by a variety of transcription factor mediated signals. In this review we will discuss evidence to support the concept that the ecNOS is a constitutively expressed gene subject to a modest degree of regulation by important physiological influences.

Original languageEnglish (US)
Pages (from-to)107-117
Number of pages11
JournalAgents and Actions
Volume45
Issue numberSUPPL. I
StatePublished - Jan 22 1995

Fingerprint

Nitric Oxide Synthase Type III
Endothelial cells
Nitric Oxide Synthase
Endothelial Cells
Genes
TATA Box
Gene encoding
Enzymes
Nitric Oxide
Transcription Factors
Research

ASJC Scopus subject areas

  • Toxicology
  • Pharmacology (medical)

Cite this

Harrison, D. G., Venema, R. C., Arnal, J. F., Inoue, N., Ohara, Y., Sayegh, H., & Murphy, T. J. (1995). The endothelial cell nitric oxide synthase: Is it really constitutively expressed? Agents and Actions, 45(SUPPL. I), 107-117.

The endothelial cell nitric oxide synthase : Is it really constitutively expressed? / Harrison, D. G.; Venema, R. C.; Arnal, J. F.; Inoue, N.; Ohara, Y.; Sayegh, H.; Murphy, T. J.

In: Agents and Actions, Vol. 45, No. SUPPL. I, 22.01.1995, p. 107-117.

Research output: Contribution to journalArticle

Harrison, DG, Venema, RC, Arnal, JF, Inoue, N, Ohara, Y, Sayegh, H & Murphy, TJ 1995, 'The endothelial cell nitric oxide synthase: Is it really constitutively expressed?', Agents and Actions, vol. 45, no. SUPPL. I, pp. 107-117.
Harrison DG, Venema RC, Arnal JF, Inoue N, Ohara Y, Sayegh H et al. The endothelial cell nitric oxide synthase: Is it really constitutively expressed? Agents and Actions. 1995 Jan 22;45(SUPPL. I):107-117.
Harrison, D. G. ; Venema, R. C. ; Arnal, J. F. ; Inoue, N. ; Ohara, Y. ; Sayegh, H. ; Murphy, T. J. / The endothelial cell nitric oxide synthase : Is it really constitutively expressed?. In: Agents and Actions. 1995 ; Vol. 45, No. SUPPL. I. pp. 107-117.
@article{463675268f4f476e90ed0722ca008d9e,
title = "The endothelial cell nitric oxide synthase: Is it really constitutively expressed?",
abstract = "During the past two years, the enzyme responsible for production of endothelium-derived nitric oxide, the endothelial cell NO synthase (ecNOS) has been cloned and the gene encoding this enzyme isolated, cloned and its structure characterized. This research has provided direction for a variety of studies of regulation of the ecNOS. Several features of the ecNOS are compatible with a constitutively expressed, poorly regulated gene, including absence of a TATA box and numerous SP-1 sites. The promoter also contains a number of putative binding domains which suggest that it may be regulated by a variety of transcription factor mediated signals. In this review we will discuss evidence to support the concept that the ecNOS is a constitutively expressed gene subject to a modest degree of regulation by important physiological influences.",
author = "Harrison, {D. G.} and Venema, {R. C.} and Arnal, {J. F.} and N. Inoue and Y. Ohara and H. Sayegh and Murphy, {T. J.}",
year = "1995",
month = "1",
day = "22",
language = "English (US)",
volume = "45",
pages = "107--117",
journal = "Inflammation Research",
issn = "1023-3830",
publisher = "Birkhauser Verlag Basel",
number = "SUPPL. I",

}

TY - JOUR

T1 - The endothelial cell nitric oxide synthase

T2 - Is it really constitutively expressed?

AU - Harrison, D. G.

AU - Venema, R. C.

AU - Arnal, J. F.

AU - Inoue, N.

AU - Ohara, Y.

AU - Sayegh, H.

AU - Murphy, T. J.

PY - 1995/1/22

Y1 - 1995/1/22

N2 - During the past two years, the enzyme responsible for production of endothelium-derived nitric oxide, the endothelial cell NO synthase (ecNOS) has been cloned and the gene encoding this enzyme isolated, cloned and its structure characterized. This research has provided direction for a variety of studies of regulation of the ecNOS. Several features of the ecNOS are compatible with a constitutively expressed, poorly regulated gene, including absence of a TATA box and numerous SP-1 sites. The promoter also contains a number of putative binding domains which suggest that it may be regulated by a variety of transcription factor mediated signals. In this review we will discuss evidence to support the concept that the ecNOS is a constitutively expressed gene subject to a modest degree of regulation by important physiological influences.

AB - During the past two years, the enzyme responsible for production of endothelium-derived nitric oxide, the endothelial cell NO synthase (ecNOS) has been cloned and the gene encoding this enzyme isolated, cloned and its structure characterized. This research has provided direction for a variety of studies of regulation of the ecNOS. Several features of the ecNOS are compatible with a constitutively expressed, poorly regulated gene, including absence of a TATA box and numerous SP-1 sites. The promoter also contains a number of putative binding domains which suggest that it may be regulated by a variety of transcription factor mediated signals. In this review we will discuss evidence to support the concept that the ecNOS is a constitutively expressed gene subject to a modest degree of regulation by important physiological influences.

UR - http://www.scopus.com/inward/record.url?scp=0028843225&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028843225&partnerID=8YFLogxK

M3 - Article

C2 - 7536382

AN - SCOPUS:0028843225

VL - 45

SP - 107

EP - 117

JO - Inflammation Research

JF - Inflammation Research

SN - 1023-3830

IS - SUPPL. I

ER -