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KLF2 in Regulation of NF-κB-Mediated Immune Cell Function and Inflammation

KLF2 (Kruppel-like factor 2) is a member of the zinc finger transcription factor family, which critically regulates embryonic lung development, function of endothelial cells and maintenance of quiescence in T-cells and monocytes. It is expressed in naïve T-cells and monocytes, however its level of e...

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Detalles Bibliográficos
Autores principales: Jha, Prerana, Das, Hiranmoy
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5713352/
https://www.ncbi.nlm.nih.gov/pubmed/29125549
http://dx.doi.org/10.3390/ijms18112383
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author Jha, Prerana
Das, Hiranmoy
author_facet Jha, Prerana
Das, Hiranmoy
author_sort Jha, Prerana
collection PubMed
description KLF2 (Kruppel-like factor 2) is a member of the zinc finger transcription factor family, which critically regulates embryonic lung development, function of endothelial cells and maintenance of quiescence in T-cells and monocytes. It is expressed in naïve T-cells and monocytes, however its level of expression decreases during activation and differentiation. KLF2 also plays critical regulatory role in various inflammatory diseases and their pathogenesis. Nuclear factor-kappaB (NF-κB) is an important inducer of inflammation and the inflammation is mediated through the transcription of several proinflammatory cytokines, chemokines and adhesion molecules. So, both transcriptional factors KLF2 and NF-κB are being associated with the similar cellular functions and their maintenance. It was shown that KLF2 regulates most of the NF-κB-mediated activities. In this review, we focused on emphasizing the involvement of KLF2 in health and disease states and how they interact with transcriptional master regulator NF-κB.
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spelling pubmed-57133522017-12-07 KLF2 in Regulation of NF-κB-Mediated Immune Cell Function and Inflammation Jha, Prerana Das, Hiranmoy Int J Mol Sci Review KLF2 (Kruppel-like factor 2) is a member of the zinc finger transcription factor family, which critically regulates embryonic lung development, function of endothelial cells and maintenance of quiescence in T-cells and monocytes. It is expressed in naïve T-cells and monocytes, however its level of expression decreases during activation and differentiation. KLF2 also plays critical regulatory role in various inflammatory diseases and their pathogenesis. Nuclear factor-kappaB (NF-κB) is an important inducer of inflammation and the inflammation is mediated through the transcription of several proinflammatory cytokines, chemokines and adhesion molecules. So, both transcriptional factors KLF2 and NF-κB are being associated with the similar cellular functions and their maintenance. It was shown that KLF2 regulates most of the NF-κB-mediated activities. In this review, we focused on emphasizing the involvement of KLF2 in health and disease states and how they interact with transcriptional master regulator NF-κB. MDPI 2017-11-10 /pmc/articles/PMC5713352/ /pubmed/29125549 http://dx.doi.org/10.3390/ijms18112383 Text en © 2017 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Jha, Prerana
Das, Hiranmoy
KLF2 in Regulation of NF-κB-Mediated Immune Cell Function and Inflammation
title KLF2 in Regulation of NF-κB-Mediated Immune Cell Function and Inflammation
title_full KLF2 in Regulation of NF-κB-Mediated Immune Cell Function and Inflammation
title_fullStr KLF2 in Regulation of NF-κB-Mediated Immune Cell Function and Inflammation
title_full_unstemmed KLF2 in Regulation of NF-κB-Mediated Immune Cell Function and Inflammation
title_short KLF2 in Regulation of NF-κB-Mediated Immune Cell Function and Inflammation
title_sort klf2 in regulation of nf-κb-mediated immune cell function and inflammation
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5713352/
https://www.ncbi.nlm.nih.gov/pubmed/29125549
http://dx.doi.org/10.3390/ijms18112383
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