An Unprocessed Pseudogene of Inducible Nitric Oxide Synthase Gene in Human

Park, Chang‐Shin; Lee, Hyun-Sil; Lee, Hei-Yung; Krishna, Gopal

doi:10.1006/niox.1997.0138

Cited by 10 publications

(3 citation statements)

References 25 publications

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“…A recent study suggests that the human genome contains at least two loci for the NOS II gene, one of which (NOS II‐1) has been assigned to the proximal region of the long arm (cen q11.2 or 11.2–q12) or to pericentric (p11–q11) regions of chromosome 17. Another pseudogene (NOS II‐2) is mapped to chromosome 17q11.2 site (Park et al , 1997). The human NOS I gene has 29 exons and extends over 160 kb, encoding a protein of c .…”

Section: Generation and Regulation Of No In Immune Systemmentioning

confidence: 99%

The role of nitric oxide in inflammatory reactions

Tripathi

Kashyap

et al. 2007

FEMS Immunology &Amp; Medical Microbiology

416

274

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Nitric oxide (NO) was initially described as a physiological mediator of endothelial cell relaxation, an important role in hypotension. NO is an intercellular messenger that has been recognized as one of the most versatile players in the immune system. Cells of the innate immune system--macrophages, neutrophils and natural killer cells--use pattern recognition receptors to recognize the molecular patterns associated with pathogens. Activated macrophages then inhibit pathogen replication by releasing a variety of effector molecules, including NO. In addition to macrophages, a large number of other immune-system cells produce and respond to NO. Thus, NO is important as a toxic defense molecule against infectious organisms. It also regulates the functional activity, growth and death of many immune and inflammatory cell types including macrophages, T lymphocytes, antigen-presenting cells, mast cells, neutrophils and natural killer cells. However, the role of NO in nonspecific and specific immunity in vivo and in immunologically mediated diseases and inflammation is poorly understood. This Minireview will discuss the role of NO in immune response and inflammation, and its mechanisms of action in these processes.

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Section: Generation and Regulation Of No In Immune Systemmentioning

confidence: 99%

The role of nitric oxide in inflammatory reactions

Tripathi

Kashyap

et al. 2007

FEMS Immunology &Amp; Medical Microbiology

416

274

View full text Add to dashboard Cite

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“…Southern blot analysis revealed single bands for nNOS and eNOS but multiple bands for iNOS exons 22–26 in humans and apes [ 13, 14] when using the 3′ end of an iNOS cDNA probe. An unprocessed, highly mutated pseudogene has been localized on the same chromosomal region as the functional iNOS gene by fluorescence in situ hybridization (FISH) analysis [ 15]. Three minor allelic variants have been described [ 16–18], one bearing pathophysiological significance in resistance against malaria infection [ 18].…”

Section: Molecular Biology Of Human Inosmentioning

confidence: 99%

Inducible nitric oxide synthase in human diseases

Kröncke

Fehsel

Kolb‐Bachofen

1998

Clinical and Experimental Immunology

513

353

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“…The genes for the different NOS isoforms are located on different chromosomes in both humans and mice (7,20). The human genome contains at least two loci for the iNOS gene (21), whereas only one locus has been recognized for the murine iNOS gene. Although nNOS and eNOS genes show a single chromosomal localization, multiple copies of iNOS gene‐like sequences have been found (7,8,20).…”

Section: Introductionmentioning

confidence: 99%

Expression of inducible nitric oxide synthase (iNOS) mRNA in target organs of lethal and non‐lethal strains of murine malaria

Nahrevanian

Dascombe

2002

Parasite Immunology

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Nitric oxide (NO) is a putative mediator of the immunological and/or pathological responses to malaria, consequently it is a potential target for novel drug therapy. Numerous cell types increase expression of inducible nitric oxide synthase (iNOS) under inflammatory conditions, the most relevant stimuli being cytokines and endotoxins. In this study the expression of iNOS mRNA in several target organs (brain, liver, spleen) of malaria have been investigated in MF1 mice during lethal Plasmodium (P.) berghei and non-lethal P. c. chabaudi infection. In P. berghei malaria, iNOS mRNA decreased in liver and was unchanged in spleen during the period of rising parasitaemia, but increased in both organs late in the infection, when parasitaemia was high and death imminent. In mice infected with P. c. chabaudi, spleen iNOS mRNA increased progressively throughout the early, peak and recovery periods of parasitaemia, but decreased in liver. Brain iNOS mRNA decreased in samples collected throughout the time courses of both infections. Hence it is evident that changes in iNOS mRNA in murine malaria depend upon the tissue, day of infection, degree of parasitaemia and strain of Plasmodium. These data indicate induction of iNOS mRNA in the spleen has a role in combating these strains of Plasmodium in MF1 mice. Failure to clear lethal P. berghei parasitaemia was associated with increased iNOS mRNA expression in the liver, which may contribute to the pathology of this malaria.

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An Unprocessed Pseudogene of Inducible Nitric Oxide Synthase Gene in Human

Cited by 10 publications

References 25 publications

The role of nitric oxide in inflammatory reactions

The role of nitric oxide in inflammatory reactions

Inducible nitric oxide synthase in human diseases

Expression of inducible nitric oxide synthase (iNOS) mRNA in target organs of lethal and non‐lethal strains of murine malaria

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