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Induction of Synthesis of Heat Shock Protein 72 in Tumor Necrosis Factor Gene‐transduced Cells
Heat shock protein (HSP) and endogenous tumor necrosis factor (enTNF) both act as resistance factors against the cytotoxicity of various cellular stresses. To clarify the relationship between these two stress response systems, we investigated whether or not enTNF is capable of inducing HSP72. Withou...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Blackwell Publishing Ltd
1994
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5919352/ https://www.ncbi.nlm.nih.gov/pubmed/7961110 http://dx.doi.org/10.1111/j.1349-7006.1994.tb02896.x |
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author | Watanabe, Naoki Akiyama, Shinichiro Tsuji, Naoki Sasaki, Hiroyoshi Yamauchi, Naofurai Okamoto, Tetsuro Kobayashi, Daisuke Niitsu, Yoshiro |
author_facet | Watanabe, Naoki Akiyama, Shinichiro Tsuji, Naoki Sasaki, Hiroyoshi Yamauchi, Naofurai Okamoto, Tetsuro Kobayashi, Daisuke Niitsu, Yoshiro |
author_sort | Watanabe, Naoki |
collection | PubMed |
description | Heat shock protein (HSP) and endogenous tumor necrosis factor (enTNF) both act as resistance factors against the cytotoxicity of various cellular stresses. To clarify the relationship between these two stress response systems, we investigated whether or not enTNF is capable of inducing HSP72. Without heating, no difference was found in HSP72 synthesis between enTNF‐nonexpressing L‐M cells and cells expressing L‐R or L‐M (pcDV‐TNF). After initiation of heat treatment, however, a remarkable increase in HSP72 synthesis was noted in enTNF‐expressing cells compared to enTNF‐nonexpressing L‐M cells. These findings indicated that enTNF augments heat‐inducihle HSP72 synthesis. |
format | Online Article Text |
id | pubmed-5919352 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1994 |
publisher | Blackwell Publishing Ltd |
record_format | MEDLINE/PubMed |
spelling | pubmed-59193522018-05-11 Induction of Synthesis of Heat Shock Protein 72 in Tumor Necrosis Factor Gene‐transduced Cells Watanabe, Naoki Akiyama, Shinichiro Tsuji, Naoki Sasaki, Hiroyoshi Yamauchi, Naofurai Okamoto, Tetsuro Kobayashi, Daisuke Niitsu, Yoshiro Jpn J Cancer Res Article Heat shock protein (HSP) and endogenous tumor necrosis factor (enTNF) both act as resistance factors against the cytotoxicity of various cellular stresses. To clarify the relationship between these two stress response systems, we investigated whether or not enTNF is capable of inducing HSP72. Without heating, no difference was found in HSP72 synthesis between enTNF‐nonexpressing L‐M cells and cells expressing L‐R or L‐M (pcDV‐TNF). After initiation of heat treatment, however, a remarkable increase in HSP72 synthesis was noted in enTNF‐expressing cells compared to enTNF‐nonexpressing L‐M cells. These findings indicated that enTNF augments heat‐inducihle HSP72 synthesis. Blackwell Publishing Ltd 1994-10 /pmc/articles/PMC5919352/ /pubmed/7961110 http://dx.doi.org/10.1111/j.1349-7006.1994.tb02896.x Text en |
spellingShingle | Article Watanabe, Naoki Akiyama, Shinichiro Tsuji, Naoki Sasaki, Hiroyoshi Yamauchi, Naofurai Okamoto, Tetsuro Kobayashi, Daisuke Niitsu, Yoshiro Induction of Synthesis of Heat Shock Protein 72 in Tumor Necrosis Factor Gene‐transduced Cells |
title | Induction of Synthesis of Heat Shock Protein 72 in Tumor Necrosis Factor Gene‐transduced Cells |
title_full | Induction of Synthesis of Heat Shock Protein 72 in Tumor Necrosis Factor Gene‐transduced Cells |
title_fullStr | Induction of Synthesis of Heat Shock Protein 72 in Tumor Necrosis Factor Gene‐transduced Cells |
title_full_unstemmed | Induction of Synthesis of Heat Shock Protein 72 in Tumor Necrosis Factor Gene‐transduced Cells |
title_short | Induction of Synthesis of Heat Shock Protein 72 in Tumor Necrosis Factor Gene‐transduced Cells |
title_sort | induction of synthesis of heat shock protein 72 in tumor necrosis factor gene‐transduced cells |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5919352/ https://www.ncbi.nlm.nih.gov/pubmed/7961110 http://dx.doi.org/10.1111/j.1349-7006.1994.tb02896.x |
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