Inducible nitric oxide synthase in human diseases - PubMed (original) (raw)
Review
Inducible nitric oxide synthase in human diseases
K D Kröncke et al. Clin Exp Immunol. 1998 Aug.
No abstract available
Figures
Fig. 1
Schematic structure of the human inducible nitric oxide synthase (iNOS) 5′ flanking region (a), the upstream enhancer region (b), and the human iNOS mRNA (c). (a) The main transcriptional start site is denoted at position + 1. Several potential transcription factor binding sites are indicated. The TATA box begins at −30. TATA-independent iNOS transcripts have alternative splice sites at positions −221, −36 and +191 in the 5′ UTR of the gene. Possible start codons (▪) of open reading frames are located at −256, −65, −45, −40 and +187. (b) Structure of the distal part of the human iNOS promoter which seems to be a cytokine-responsive enhancer element. This promoter region (−10.9 to −8.7 kb) increases iNOS transcription orientation independently by a factor of 2. It contains multiple binding sites for transcription factors, which are activated in response to either IFN-γ (IRF-1, STAT1) or IL-1β (AP-1, IRF-1). (c) Alternative splicing of human iNOS mRNA. The ratios of alternatively to constitutively spliced mRNA differ among tissues and depend on activation by cytokines. *Truncated iNOS with exon 5 deletion abundant in human cerebellum [29]. γIRE, IFN-γ-responsive element; NF, nuclear factor; AABS, activator binding site; SSRE, shear stress responsive element; E, exon; I, intron; IRF, interferon regulatory factor; STAT, signal transducer and activator transcription.
Fig. 2
Current data suggest that inducible nitric oxide synthase (iNOS) expression and NO production in humans are much more tightly regulated than in rodents. In addition, human cells appear to be less susceptible to NO than rodent cells. Thus, in humans NO-mediated gene regulatory effects may be of more relevance than cytotoxic effects.
Similar articles
- Lethal autoimmune myocarditis in interferon-gamma receptor-deficient mice: enhanced disease severity by impaired inducible nitric oxide synthase induction.
Eriksson U, Kurrer MO, Bingisser R, Eugster HP, Saremaslani P, Follath F, Marsch S, Widmer U. Eriksson U, et al. Circulation. 2001 Jan 2;103(1):18-21. doi: 10.1161/01.cir.103.1.18. Circulation. 2001. PMID: 11136679 - Inducible nitric oxide synthase and inflammatory diseases.
Zamora R, Vodovotz Y, Billiar TR. Zamora R, et al. Mol Med. 2000 May;6(5):347-73. Mol Med. 2000. PMID: 10952018 Free PMC article. Review. No abstract available. - Inhibition of inducible nitric oxide synthase intensifies injury and functional deterioration in autoimmune interstitial nephritis.
Gabbai FB, Boggiano C, Peter T, Khang S, Archer C, Gold DP, Kelly CJ. Gabbai FB, et al. J Immunol. 1997 Dec 15;159(12):6266-75. J Immunol. 1997. PMID: 9550431 - Expression of nitric oxide synthase-2 in glia associated with CNS pathology.
Loihl AK, Murphy S. Loihl AK, et al. Prog Brain Res. 1998;118:253-67. doi: 10.1016/s0079-6123(08)63213-6. Prog Brain Res. 1998. PMID: 9932447 Free PMC article. Review. - Induction of neuronal and inducible nitric oxide synthase in the motoneurons of spinal cord following transient abdominal aorta occlusion in rats.
Zhou Y, Zhao YN, Yang EB, Ling EA, Wang Y, Hassouna MM, Mack P. Zhou Y, et al. J Surg Res. 1999 Dec;87(2):185-93. doi: 10.1006/jsre.1999.5754. J Surg Res. 1999. PMID: 10600348
Cited by
- Sulfate-Reducing Bacteria Induce Pro-Inflammatory TNF-α and iNOS via PI3K/Akt Pathway in a TLR 2-Dependent Manner.
Singh SB, Braun CA, Carroll-Portillo A, Coffman CN, Lin HC. Singh SB, et al. Microorganisms. 2024 Sep 5;12(9):1833. doi: 10.3390/microorganisms12091833. Microorganisms. 2024. PMID: 39338507 Free PMC article. - Focus on Achalasia in the Omics Era.
Di Brina ALP, Palmieri O, Cannarozzi AL, Tavano F, Guerra M, Bossa F, Gentile M, Merla A, Biscaglia G, Cuttitta A, Perri F, Latiano A. Di Brina ALP, et al. Int J Mol Sci. 2024 Sep 21;25(18):10148. doi: 10.3390/ijms251810148. Int J Mol Sci. 2024. PMID: 39337632 Free PMC article. Review. - Clinical characteristics and molecular mechanisms underlying bladder cancer in individuals with spinal cord injury: a systematic review.
Wang XL, Wang YX, Chen JZ, Liu XY, Liu X, Zhong QK, Zhao ZL, Shi ZD, Han CH. Wang XL, et al. BMC Urol. 2024 May 22;24(1):111. doi: 10.1186/s12894-024-01457-0. BMC Urol. 2024. PMID: 38778291 Free PMC article. - Uncovering Novel Protein Partners of Inducible Nitric Oxide Synthase in Human Testis.
Prabhakara KS, Ganapathy K, Islam KN, Thyagarajan HM, Tiwari KK, Parimi RL, Rashid MB. Prabhakara KS, et al. Biomolecules. 2024 Mar 24;14(4):388. doi: 10.3390/biom14040388. Biomolecules. 2024. PMID: 38672406 Free PMC article. - Laminin-derived peptide, IKVAV, modulates macrophage phenotype through integrin mediation.
Jha A, Moore E. Jha A, et al. Matrix Biol Plus. 2024 Feb 15;22:100143. doi: 10.1016/j.mbplus.2024.100143. eCollection 2024 Jun. Matrix Biol Plus. 2024. PMID: 38405086 Free PMC article.
References
- Kröncke KD, Fehsel K, Kolb-Bachofen V. Nitric oxide: cytotoxicity versus cytoprotection. How, why, when where? NO Biol Chem. 1997;1:107–20. - PubMed
- Kröncke KD, Fehsel K, Kolb-Bachofen V. Inducible nitric oxide synthase and its product nitric oxide, a small molecule with complex biological activities. Biol Chem. 1995;376:327–43. - PubMed
- Sherman PA, Laubach VE, Reep BR, Wood ER. Purification and cDNA sequence of an inducible nitric oxide synthase from a human tumor cell line. Biochemistry. 1993;32:11600–5. - PubMed
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources