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NFATc1 regulates the transcription of DNA damage-induced apoptosis suppressor

DNA damage induced apoptosis suppressor (DDIAS), or human Noxin (hNoxin), is strongly expressed in lung cancers. DDIAS knockdown induced apoptosis in non-small cell lung carcinoma A549 cells in response to DNA damage, indicating DDIAS as a potential therapeutic target in lung cancer. To understand t...

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Autores principales: Im, Joo-Young, Lee, Kang-Woo, Won, Kyoung-Jae, Kim, Bo-Kyung, Ban, Hyun Seung, Yoon, Sung-Hoon, Lee, Young-Ju, Kim, Young-Joo, Song, Kyung-Bin, Won, Misun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4675896/
https://www.ncbi.nlm.nih.gov/pubmed/26740967
http://dx.doi.org/10.1016/j.dib.2015.11.011
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author Im, Joo-Young
Lee, Kang-Woo
Won, Kyoung-Jae
Kim, Bo-Kyung
Ban, Hyun Seung
Yoon, Sung-Hoon
Lee, Young-Ju
Kim, Young-Joo
Song, Kyung-Bin
Won, Misun
author_facet Im, Joo-Young
Lee, Kang-Woo
Won, Kyoung-Jae
Kim, Bo-Kyung
Ban, Hyun Seung
Yoon, Sung-Hoon
Lee, Young-Ju
Kim, Young-Joo
Song, Kyung-Bin
Won, Misun
author_sort Im, Joo-Young
collection PubMed
description DNA damage induced apoptosis suppressor (DDIAS), or human Noxin (hNoxin), is strongly expressed in lung cancers. DDIAS knockdown induced apoptosis in non-small cell lung carcinoma A549 cells in response to DNA damage, indicating DDIAS as a potential therapeutic target in lung cancer. To understand the transcriptional regulation of DDIAS, we determined the transcription start site, promoter region, and transcription factor. We found that DDIAS transcription begins at nucleotide 212 upstream of the DDIAS translation start site. We cloned the DDIAS promoter region and identified NFAT2 as a major transcription factor (Im et al., 2016 [1]). We demonstrated that NFATc1 regulates DDIAS expression in both pancreatic cancer Panc-1 cells and lung cancer cells.
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spelling pubmed-46758962016-01-06 NFATc1 regulates the transcription of DNA damage-induced apoptosis suppressor Im, Joo-Young Lee, Kang-Woo Won, Kyoung-Jae Kim, Bo-Kyung Ban, Hyun Seung Yoon, Sung-Hoon Lee, Young-Ju Kim, Young-Joo Song, Kyung-Bin Won, Misun Data Brief Data Article DNA damage induced apoptosis suppressor (DDIAS), or human Noxin (hNoxin), is strongly expressed in lung cancers. DDIAS knockdown induced apoptosis in non-small cell lung carcinoma A549 cells in response to DNA damage, indicating DDIAS as a potential therapeutic target in lung cancer. To understand the transcriptional regulation of DDIAS, we determined the transcription start site, promoter region, and transcription factor. We found that DDIAS transcription begins at nucleotide 212 upstream of the DDIAS translation start site. We cloned the DDIAS promoter region and identified NFAT2 as a major transcription factor (Im et al., 2016 [1]). We demonstrated that NFATc1 regulates DDIAS expression in both pancreatic cancer Panc-1 cells and lung cancer cells. Elsevier 2015-11-17 /pmc/articles/PMC4675896/ /pubmed/26740967 http://dx.doi.org/10.1016/j.dib.2015.11.011 Text en © 2015 Published by Elsevier Inc. http://creativecommons.org/licenses/by/4.0/ This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Data Article
Im, Joo-Young
Lee, Kang-Woo
Won, Kyoung-Jae
Kim, Bo-Kyung
Ban, Hyun Seung
Yoon, Sung-Hoon
Lee, Young-Ju
Kim, Young-Joo
Song, Kyung-Bin
Won, Misun
NFATc1 regulates the transcription of DNA damage-induced apoptosis suppressor
title NFATc1 regulates the transcription of DNA damage-induced apoptosis suppressor
title_full NFATc1 regulates the transcription of DNA damage-induced apoptosis suppressor
title_fullStr NFATc1 regulates the transcription of DNA damage-induced apoptosis suppressor
title_full_unstemmed NFATc1 regulates the transcription of DNA damage-induced apoptosis suppressor
title_short NFATc1 regulates the transcription of DNA damage-induced apoptosis suppressor
title_sort nfatc1 regulates the transcription of dna damage-induced apoptosis suppressor
topic Data Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4675896/
https://www.ncbi.nlm.nih.gov/pubmed/26740967
http://dx.doi.org/10.1016/j.dib.2015.11.011
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