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Tropomyosin-receptor kinase fused gene (TFG) regulates lipid production in human sebocytes
The endoplasmic reticulum (ER) is an organelle in which important cellular events such as protein synthesis and lipid production occur. Although many lipid molecules are produced in the ER, the effect of ER-organizing proteins on lipid synthesis in sebocytes has not been completely elucidated. Tropo...
Autores principales: | , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6488642/ https://www.ncbi.nlm.nih.gov/pubmed/31036933 http://dx.doi.org/10.1038/s41598-019-43209-3 |
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author | Choi, So-Ra Hwang, Yul-Lye Kim, Soo Jung Sohn, Kyung-Cheol Choi, Chong Won Park, Kyung Duck Lee, Young Seo, Young-Joon Lee, Jeung-Hoon Hong, Seung-Phil Seo, Seong Jun Kim, Seong-Jin Kim, Chang Deok |
author_facet | Choi, So-Ra Hwang, Yul-Lye Kim, Soo Jung Sohn, Kyung-Cheol Choi, Chong Won Park, Kyung Duck Lee, Young Seo, Young-Joon Lee, Jeung-Hoon Hong, Seung-Phil Seo, Seong Jun Kim, Seong-Jin Kim, Chang Deok |
author_sort | Choi, So-Ra |
collection | PubMed |
description | The endoplasmic reticulum (ER) is an organelle in which important cellular events such as protein synthesis and lipid production occur. Although many lipid molecules are produced in the ER, the effect of ER-organizing proteins on lipid synthesis in sebocytes has not been completely elucidated. Tropomyosin-receptor kinase fused gene (TFG) is located in ER exit sites and participates in COPII-coated vesicle formation along with many scaffold proteins, such as Sec. 13 and Sec. 16. In this study, we investigated the putative role of TFG in lipid production in sebocytes using an immortalized human sebocyte line. During IGF-1-induced lipogenesis, the level of the TFG protein was increased in a time- and dose-dependent manner. When TFG was over-expressed using recombinant adenovirus, lipid production in sebocytes was increased along with an up-regulation of the expression of lipogenic regulators, such as PPAR-γ, SREBP-1 and SCD. Conversely, down-regulation of TFG using a microRNA (miR) decreased lipid production and the expression of lipogenic regulators. Based on these data, TFG is a novel regulator of lipid synthesis in sebocytes. |
format | Online Article Text |
id | pubmed-6488642 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-64886422019-05-16 Tropomyosin-receptor kinase fused gene (TFG) regulates lipid production in human sebocytes Choi, So-Ra Hwang, Yul-Lye Kim, Soo Jung Sohn, Kyung-Cheol Choi, Chong Won Park, Kyung Duck Lee, Young Seo, Young-Joon Lee, Jeung-Hoon Hong, Seung-Phil Seo, Seong Jun Kim, Seong-Jin Kim, Chang Deok Sci Rep Article The endoplasmic reticulum (ER) is an organelle in which important cellular events such as protein synthesis and lipid production occur. Although many lipid molecules are produced in the ER, the effect of ER-organizing proteins on lipid synthesis in sebocytes has not been completely elucidated. Tropomyosin-receptor kinase fused gene (TFG) is located in ER exit sites and participates in COPII-coated vesicle formation along with many scaffold proteins, such as Sec. 13 and Sec. 16. In this study, we investigated the putative role of TFG in lipid production in sebocytes using an immortalized human sebocyte line. During IGF-1-induced lipogenesis, the level of the TFG protein was increased in a time- and dose-dependent manner. When TFG was over-expressed using recombinant adenovirus, lipid production in sebocytes was increased along with an up-regulation of the expression of lipogenic regulators, such as PPAR-γ, SREBP-1 and SCD. Conversely, down-regulation of TFG using a microRNA (miR) decreased lipid production and the expression of lipogenic regulators. Based on these data, TFG is a novel regulator of lipid synthesis in sebocytes. Nature Publishing Group UK 2019-04-29 /pmc/articles/PMC6488642/ /pubmed/31036933 http://dx.doi.org/10.1038/s41598-019-43209-3 Text en © The Author(s) 2019 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Choi, So-Ra Hwang, Yul-Lye Kim, Soo Jung Sohn, Kyung-Cheol Choi, Chong Won Park, Kyung Duck Lee, Young Seo, Young-Joon Lee, Jeung-Hoon Hong, Seung-Phil Seo, Seong Jun Kim, Seong-Jin Kim, Chang Deok Tropomyosin-receptor kinase fused gene (TFG) regulates lipid production in human sebocytes |
title | Tropomyosin-receptor kinase fused gene (TFG) regulates lipid production in human sebocytes |
title_full | Tropomyosin-receptor kinase fused gene (TFG) regulates lipid production in human sebocytes |
title_fullStr | Tropomyosin-receptor kinase fused gene (TFG) regulates lipid production in human sebocytes |
title_full_unstemmed | Tropomyosin-receptor kinase fused gene (TFG) regulates lipid production in human sebocytes |
title_short | Tropomyosin-receptor kinase fused gene (TFG) regulates lipid production in human sebocytes |
title_sort | tropomyosin-receptor kinase fused gene (tfg) regulates lipid production in human sebocytes |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6488642/ https://www.ncbi.nlm.nih.gov/pubmed/31036933 http://dx.doi.org/10.1038/s41598-019-43209-3 |
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