| DOI | Resolve DOI: https://doi.org/10.1038/sj.cdd.4402012 |
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| Author | Search for: Delom, F.; Search for: Emadali, A.; Search for: Cocolakis, E.; Search for: Lebrun, J.-J.; Search for: Nantel, A.1; Search for: Chevet, E. |
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| Affiliation | - National Research Council Canada. NRC Biotechnology Research Institute
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| Format | Text, Article |
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| Subject | amino acid sequence; apoptosis; bap31; breast neoplasms; calnexin; carcinoma; caspase 3; cell line, tumor; clone cells; drug resistance, neoplasm; endoplasmic reticulum; enzyme activation; ER stress; gene expression regulation, neoplastic; molecular sequence data; tunic amycin |
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| Abstract | The endoplasmic reticulum (ER) has evolved specific mechanisms to ensure protein folding as well as the maintenance of its own homeostasis. When these functions are not achieved, specific ER stress signals are triggered to activate either adaptive or apoptotic responses. Here, we demonstrate that MCF-7 cells are resistant to tunicamycin-induced apoptosis. We show that the expression level of the ER chaperone calnexin can directly influence tunicamycin sensitivity in this cell line. Interestingly, the expression of a calnexin lacking the chaperone domain (DeltaE) partially restores their sensitivity to tunicamycin-induced apoptosis. Indeed, we show that DeltaE acts as a scaffold molecule to allow the cleavage of Bap31 and thus generate the proapoptotic p20 fragment. Utilizing the ability of MCF-7 cells to resist tunicamycin-induced apoptosis, we have characterized a molecular mechanism by which calnexin regulates ER-stress-mediated apoptosis in a manner independent of its chaperone functions but dependent of its binding to Bap31. |
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| Publication date | 2006-07-21 |
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| Publisher | Springer Nature |
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| In | |
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| Language | English |
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| Peer reviewed | Yes |
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| NRC number | NRC-IRN-1053054x |
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| NPARC number | 12330241 |
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| Export citation | Export as RIS |
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| Report a correction | Report a correction (opens in a new tab) |
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| Record identifier | 9aaa67b4-6a94-4b35-9d41-ad97d9c33a9c |
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| Record created | 2009-09-10 |
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| Record modified | 2020-04-22 |
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