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TNIP1 in Autoimmune Diseases: Regulation of Toll-like Receptor Signaling
TNIP1 protein is increasingly being recognized as a key repressor of inflammatory signaling and a potential factor in multiple autoimmune diseases. In addition to earlier foundational reports of TNIP1 SNPs in human autoimmune diseases and TNIP1 protein-protein interaction with receptor regulating pr...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6192141/ https://www.ncbi.nlm.nih.gov/pubmed/30402506 http://dx.doi.org/10.1155/2018/3491269 |
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author | Shamilov, Rambon Aneskievich, Brian J. |
author_facet | Shamilov, Rambon Aneskievich, Brian J. |
author_sort | Shamilov, Rambon |
collection | PubMed |
description | TNIP1 protein is increasingly being recognized as a key repressor of inflammatory signaling and a potential factor in multiple autoimmune diseases. In addition to earlier foundational reports of TNIP1 SNPs in human autoimmune diseases and TNIP1 protein-protein interaction with receptor regulating proteins, more recent studies have identified new potential interaction partners and signaling pathways likely modulated by TNIP1. Subdomains within the TNIP1 protein as well as how they interact with ubiquitin have not only been mapped but inflammatory cell- and tissue-specific consequences subsequent to their defective function are being recognized and related to human disease states such as lupus, scleroderma, and psoriasis. In this review, we emphasize receptor signaling complexes and regulation of cytoplasmic signaling steps downstream of TLR given their association with some of the same autoimmune diseases where TNIP1 has been implicated. TNIP1 dysfunction or deficiency may predispose healthy cells to the inflammatory response to otherwise innocuous TLR ligand exposure. The recognition of the anti-inflammatory roles of TNIP1 and improved integrated understanding of its physical and functional association with other signaling pathway proteins may position TNIP1 as a candidate target for the design and/or testing of next-generation anti-inflammatory therapeutics. |
format | Online Article Text |
id | pubmed-6192141 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Hindawi |
record_format | MEDLINE/PubMed |
spelling | pubmed-61921412018-11-06 TNIP1 in Autoimmune Diseases: Regulation of Toll-like Receptor Signaling Shamilov, Rambon Aneskievich, Brian J. J Immunol Res Review Article TNIP1 protein is increasingly being recognized as a key repressor of inflammatory signaling and a potential factor in multiple autoimmune diseases. In addition to earlier foundational reports of TNIP1 SNPs in human autoimmune diseases and TNIP1 protein-protein interaction with receptor regulating proteins, more recent studies have identified new potential interaction partners and signaling pathways likely modulated by TNIP1. Subdomains within the TNIP1 protein as well as how they interact with ubiquitin have not only been mapped but inflammatory cell- and tissue-specific consequences subsequent to their defective function are being recognized and related to human disease states such as lupus, scleroderma, and psoriasis. In this review, we emphasize receptor signaling complexes and regulation of cytoplasmic signaling steps downstream of TLR given their association with some of the same autoimmune diseases where TNIP1 has been implicated. TNIP1 dysfunction or deficiency may predispose healthy cells to the inflammatory response to otherwise innocuous TLR ligand exposure. The recognition of the anti-inflammatory roles of TNIP1 and improved integrated understanding of its physical and functional association with other signaling pathway proteins may position TNIP1 as a candidate target for the design and/or testing of next-generation anti-inflammatory therapeutics. Hindawi 2018-10-03 /pmc/articles/PMC6192141/ /pubmed/30402506 http://dx.doi.org/10.1155/2018/3491269 Text en Copyright © 2018 Rambon Shamilov and Brian J. Aneskievich. http://creativecommons.org/licenses/by/4.0/ 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 | Review Article Shamilov, Rambon Aneskievich, Brian J. TNIP1 in Autoimmune Diseases: Regulation of Toll-like Receptor Signaling |
title | TNIP1 in Autoimmune Diseases: Regulation of Toll-like Receptor Signaling |
title_full | TNIP1 in Autoimmune Diseases: Regulation of Toll-like Receptor Signaling |
title_fullStr | TNIP1 in Autoimmune Diseases: Regulation of Toll-like Receptor Signaling |
title_full_unstemmed | TNIP1 in Autoimmune Diseases: Regulation of Toll-like Receptor Signaling |
title_short | TNIP1 in Autoimmune Diseases: Regulation of Toll-like Receptor Signaling |
title_sort | tnip1 in autoimmune diseases: regulation of toll-like receptor signaling |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6192141/ https://www.ncbi.nlm.nih.gov/pubmed/30402506 http://dx.doi.org/10.1155/2018/3491269 |
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