alexa Repression of FasL expression by retinoic acid involves a novel mechanism of inhibition of transactivation function of the nuclear factors of activated T-cells.
Molecular Biology

Molecular Biology

Journal of Cytology & Histology

Author(s): Lee MO, Kang HJ, Kim YM, Oum JH, Park J

Abstract Share this page

Abstract Retinoids are potent immune modulators that inhibit Fas ligand (FasL) expression and thereby repress the activation-induced apoptosis of immature thymocytes and T-cell hybridomas. In this study, we demonstrate that all-trans-retinoic acid (all-trans-RA) directly represses the transcriptional activity of the nuclear factors of activated T-cells (NFAT), which is an important transactivator of the FasL promoter. The analysis of reporter constructs containing the FasL promoter and wild-type or mutant NFAT binding-sites indicated that all-trans-RA repression was mediated via an NFAT binding element located in the promoter. A reporter construct comprising the NFAT binding sequence linked to a heterologous SV-40 promoter showed that NFAT transcriptional activity was significantly inhibited by all-trans-RA. Furthermore, all-trans-RA inhibited activation of the distal NFAT binding motif present in the interleukin (IL)-2 promoter, suggesting that the inhibition of NFAT function by all-trans-RA was not specific to the FasL promoter. Gel shift assays corroborated the results of the gene reporter studies by showing that all-trans-RA decreased the NFAT binding to DNA. All-trans-RA blocked translocation of NFATp from the cytosol into the nucleus, which was induced by PMA/ionomycin treatment in HeLa cells transfected with a Flag-tagged NFATp. Taken together, our results indicate that FasL inhibition by all-trans-RA involves a novel mechanism whereby the transcriptional function of NFAT is blocked.
This article was published in Eur J Biochem and referenced in Journal of Cytology & Histology

Relevant Expert PPTs

Relevant Speaker PPTs

Peer Reviewed Journals
 
Make the best use of Scientific Research and information from our 700 + peer reviewed, Open Access Journals
International Conferences 2017-18
 
Meet Inspiring Speakers and Experts at our 3000+ Global Annual Meetings

Contact Us

Agri, Food, Aqua and Veterinary Science Journals

Dr. Krish

[email protected]

1-702-714-7001 Extn: 9040

Clinical and Biochemistry Journals

Datta A

[email protected]

1-702-714-7001Extn: 9037

Business & Management Journals

Ronald

[email protected]

1-702-714-7001Extn: 9042

Chemical Engineering and Chemistry Journals

Gabriel Shaw

[email protected]

1-702-714-7001 Extn: 9040

Earth & Environmental Sciences

Katie Wilson

[email protected]

1-702-714-7001Extn: 9042

Engineering Journals

James Franklin

[email protected]

1-702-714-7001Extn: 9042

General Science and Health care Journals

Andrea Jason

[email protected]

1-702-714-7001Extn: 9043

Genetics and Molecular Biology Journals

Anna Melissa

[email protected]

1-702-714-7001 Extn: 9006

Immunology & Microbiology Journals

David Gorantl

[email protected]

1-702-714-7001Extn: 9014

Informatics Journals

Stephanie Skinner

[email protected]online.com

1-702-714-7001Extn: 9039

Material Sciences Journals

Rachle Green

[email protected]

1-702-714-7001Extn: 9039

Mathematics and Physics Journals

Jim Willison

[email protected]

1-702-714-7001 Extn: 9042

Medical Journals

Nimmi Anna

[email protected]

1-702-714-7001 Extn: 9038

Neuroscience & Psychology Journals

Nathan T

[email protected]

1-702-714-7001Extn: 9041

Pharmaceutical Sciences Journals

John Behannon

[email protected]

1-702-714-7001Extn: 9007

Social & Political Science Journals

Steve Harry

[email protected]

1-702-714-7001 Extn: 9042

 
© 2008-2017 OMICS International - Open Access Publisher. Best viewed in Mozilla Firefox | Google Chrome | Above IE 7.0 version
adwords