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Upregulation of Endogenous HMOX1 Expression by a Computer-Designed Artificial Transcription Factor

Heme oxygenase-1 (HO-1) is well known as a cytoprotective factor. Research has revealed that it is a promising therapeutic target for cardiovascular diseases. In the current study, an HMOX1 (HO-1 gene) enhancer-specific artificial zinc-finger protein (AZP) was designed using bioinformatical methods....

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Detalles Bibliográficos
Autores principales: Guo, Hongfeng, Tian, Yi, Lu, Hai, Wei, Yong, Ying, Dajun
Formato: Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2010
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2913762/
https://www.ncbi.nlm.nih.gov/pubmed/20706680
http://dx.doi.org/10.1155/2010/168689
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author Guo, Hongfeng
Tian, Yi
Lu, Hai
Wei, Yong
Ying, Dajun
author_facet Guo, Hongfeng
Tian, Yi
Lu, Hai
Wei, Yong
Ying, Dajun
author_sort Guo, Hongfeng
collection PubMed
description Heme oxygenase-1 (HO-1) is well known as a cytoprotective factor. Research has revealed that it is a promising therapeutic target for cardiovascular diseases. In the current study, an HMOX1 (HO-1 gene) enhancer-specific artificial zinc-finger protein (AZP) was designed using bioinformatical methods. Then, an artificial transcription factor (ATF) was constructed based on the AZP. In the ATF, the p65 functional domain was used as the effector domain (ED), and a nuclear localization sequence (NLS) was also included. We next analyzed the affinity of the ATF to the HMOX1 enhancer and the effect of the ATF on endogenous HMOX1 expression. The results suggest that the ATF could effectively upregulate endogenous HMOX1 expression in ECV304 cells. With further research, the ATF could be developed as a potential drug for cardiovascular diseases.
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spelling pubmed-29137622010-08-12 Upregulation of Endogenous HMOX1 Expression by a Computer-Designed Artificial Transcription Factor Guo, Hongfeng Tian, Yi Lu, Hai Wei, Yong Ying, Dajun J Biomed Biotechnol Research Article Heme oxygenase-1 (HO-1) is well known as a cytoprotective factor. Research has revealed that it is a promising therapeutic target for cardiovascular diseases. In the current study, an HMOX1 (HO-1 gene) enhancer-specific artificial zinc-finger protein (AZP) was designed using bioinformatical methods. Then, an artificial transcription factor (ATF) was constructed based on the AZP. In the ATF, the p65 functional domain was used as the effector domain (ED), and a nuclear localization sequence (NLS) was also included. We next analyzed the affinity of the ATF to the HMOX1 enhancer and the effect of the ATF on endogenous HMOX1 expression. The results suggest that the ATF could effectively upregulate endogenous HMOX1 expression in ECV304 cells. With further research, the ATF could be developed as a potential drug for cardiovascular diseases. Hindawi Publishing Corporation 2010 2010-07-14 /pmc/articles/PMC2913762/ /pubmed/20706680 http://dx.doi.org/10.1155/2010/168689 Text en Copyright © 2010 Hongfeng Guo et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Guo, Hongfeng
Tian, Yi
Lu, Hai
Wei, Yong
Ying, Dajun
Upregulation of Endogenous HMOX1 Expression by a Computer-Designed Artificial Transcription Factor
title Upregulation of Endogenous HMOX1 Expression by a Computer-Designed Artificial Transcription Factor
title_full Upregulation of Endogenous HMOX1 Expression by a Computer-Designed Artificial Transcription Factor
title_fullStr Upregulation of Endogenous HMOX1 Expression by a Computer-Designed Artificial Transcription Factor
title_full_unstemmed Upregulation of Endogenous HMOX1 Expression by a Computer-Designed Artificial Transcription Factor
title_short Upregulation of Endogenous HMOX1 Expression by a Computer-Designed Artificial Transcription Factor
title_sort upregulation of endogenous hmox1 expression by a computer-designed artificial transcription factor
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2913762/
https://www.ncbi.nlm.nih.gov/pubmed/20706680
http://dx.doi.org/10.1155/2010/168689
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