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SerpinB2 is involved in cellular response upon UV irradiation
Ultraviolet light induced pyrimidine dimer is a helix distortion DNA damage type, which recruits repair complexes. However, proteins of these complexes that take part in both DNA damage recognition and repair have been well-described, the regulation of the downstream steps of nucleotide excision rep...
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/PMC6391458/ https://www.ncbi.nlm.nih.gov/pubmed/30808882 http://dx.doi.org/10.1038/s41598-019-39073-w |
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author | Majoros, Hajnalka Ujfaludi, Zsuzsanna Borsos, Barbara Nikolett Hudacsek, Viktória Vivien Nagy, Zita Coin, Frederic Buzas, Krisztina Kovács, Ilona Bíró, Tamás Boros, Imre Miklós Pankotai, Tibor |
author_facet | Majoros, Hajnalka Ujfaludi, Zsuzsanna Borsos, Barbara Nikolett Hudacsek, Viktória Vivien Nagy, Zita Coin, Frederic Buzas, Krisztina Kovács, Ilona Bíró, Tamás Boros, Imre Miklós Pankotai, Tibor |
author_sort | Majoros, Hajnalka |
collection | PubMed |
description | Ultraviolet light induced pyrimidine dimer is a helix distortion DNA damage type, which recruits repair complexes. However, proteins of these complexes that take part in both DNA damage recognition and repair have been well-described, the regulation of the downstream steps of nucleotide excision repair (NER) have not been clearly clarified yet. In a high-throughput screen, we identified SerpinB2 (SPB2) as one of the most dramatically upregulated gene in keratinocytes following UV irradiation. We found that both the mRNA and the protein levels of SPB2 were increased upon UV irradiation in various cell lines. Additionally, UV damage induced translocation of SPB2 from the cytoplasm to the nucleus as well as the damage induced foci formation of it. Here we show that SPB2 co-localizes with XPB involved in the NER pathway at UV-induced repair foci. Finally, we demonstrated that UV irradiation promoted the association of SPB2 with ubiquitylated proteins. In basal cell carcinoma tumour cells, we identified changes in the subcellular localization of SPB2. Based on our results, we conclude that SPB2 protein has a novel role in UV-induced NER pathway, since it regulates the removal of the repair complex from the damaged site leading to cancerous malformation. |
format | Online Article Text |
id | pubmed-6391458 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-63914582019-03-01 SerpinB2 is involved in cellular response upon UV irradiation Majoros, Hajnalka Ujfaludi, Zsuzsanna Borsos, Barbara Nikolett Hudacsek, Viktória Vivien Nagy, Zita Coin, Frederic Buzas, Krisztina Kovács, Ilona Bíró, Tamás Boros, Imre Miklós Pankotai, Tibor Sci Rep Article Ultraviolet light induced pyrimidine dimer is a helix distortion DNA damage type, which recruits repair complexes. However, proteins of these complexes that take part in both DNA damage recognition and repair have been well-described, the regulation of the downstream steps of nucleotide excision repair (NER) have not been clearly clarified yet. In a high-throughput screen, we identified SerpinB2 (SPB2) as one of the most dramatically upregulated gene in keratinocytes following UV irradiation. We found that both the mRNA and the protein levels of SPB2 were increased upon UV irradiation in various cell lines. Additionally, UV damage induced translocation of SPB2 from the cytoplasm to the nucleus as well as the damage induced foci formation of it. Here we show that SPB2 co-localizes with XPB involved in the NER pathway at UV-induced repair foci. Finally, we demonstrated that UV irradiation promoted the association of SPB2 with ubiquitylated proteins. In basal cell carcinoma tumour cells, we identified changes in the subcellular localization of SPB2. Based on our results, we conclude that SPB2 protein has a novel role in UV-induced NER pathway, since it regulates the removal of the repair complex from the damaged site leading to cancerous malformation. Nature Publishing Group UK 2019-02-26 /pmc/articles/PMC6391458/ /pubmed/30808882 http://dx.doi.org/10.1038/s41598-019-39073-w 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 Majoros, Hajnalka Ujfaludi, Zsuzsanna Borsos, Barbara Nikolett Hudacsek, Viktória Vivien Nagy, Zita Coin, Frederic Buzas, Krisztina Kovács, Ilona Bíró, Tamás Boros, Imre Miklós Pankotai, Tibor SerpinB2 is involved in cellular response upon UV irradiation |
title | SerpinB2 is involved in cellular response upon UV irradiation |
title_full | SerpinB2 is involved in cellular response upon UV irradiation |
title_fullStr | SerpinB2 is involved in cellular response upon UV irradiation |
title_full_unstemmed | SerpinB2 is involved in cellular response upon UV irradiation |
title_short | SerpinB2 is involved in cellular response upon UV irradiation |
title_sort | serpinb2 is involved in cellular response upon uv irradiation |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6391458/ https://www.ncbi.nlm.nih.gov/pubmed/30808882 http://dx.doi.org/10.1038/s41598-019-39073-w |
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