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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...

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Detalles Bibliográficos
Autores principales: Watanabe, Naoki, Akiyama, Shinichiro, Tsuji, Naoki, Sasaki, Hiroyoshi, Yamauchi, Naofurai, Okamoto, Tetsuro, Kobayashi, Daisuke, Niitsu, Yoshiro
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Blackwell Publishing Ltd 1994
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
Descripción
Sumario: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.