Sumbayev, Vadim V., Yasinska, Inna M. (2007) Mechanisms of hypoxic signal transduction regulated by reactive nitrogen species. Scandinavian Journal of Immunology, 65 (5). pp. 399-406. ISSN 0300-9475. (doi:10.1111/j.1365-3083.2007.01919.x) (The full text of this publication is not currently available from this repository. You may be able to access a copy if URLs are provided) (KAR id:1418)
The full text of this publication is not currently available from this repository. You may be able to access a copy if URLs are provided. | |
Official URL: http://dx.doi.org/doi:10.1111/j.1365-3083.2007.019... |
Abstract
Recent reports devoted to the field of oxygen sensing outline that signalling molecules such as nitric oxide/nitric oxide derived species as well as cytokines and other inflammatory mediators participate in hypoxic signal transduction. In the present review, we summarize the current knowledge about the role of nitric oxide and reactive nitrogen species (RNS) derived from it in hypoxic signal transduction and particularly in accumulation/de-accumulation of hypoxia inducible factor I alpha (HIF-1 alpha) protein, which is critical not only for cellular adaptation to low oxygen availability but also for generation of inflammatory and innate immune responses. After brief description of nitric oxide and other RNS as multifunctional messengers we analyse and discuss the RNS-dependent accumulation of HIF-1 alpha protein under normoxia followed by discussion of the mechanisms of nitric oxide (NO)-dependent enzyme-regulared degradation of HIF-1 alpha protein under low oxygen availability.
Item Type: | Article |
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DOI/Identification number: | 10.1111/j.1365-3083.2007.01919.x |
Uncontrolled keywords: | Immunology |
Subjects: | R Medicine > RC Internal medicine |
Divisions: | Divisions > Division of Natural Sciences > Medway School of Pharmacy |
Depositing User: | Stephen Holland |
Date Deposited: | 19 Dec 2007 18:55 UTC |
Last Modified: | 16 Nov 2021 09:40 UTC |
Resource URI: | https://kar.kent.ac.uk/id/eprint/1418 (The current URI for this page, for reference purposes) |
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