Bax inhibitor-1 protects neurons from oxygen-glucose deprivation

2006 | journal article; research paper. A publication with affiliation to the University of Göttingen.

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​Bax inhibitor-1 protects neurons from oxygen-glucose deprivation​
Dohm, C. P. ; Siedenberg, S. ; Liman, J. ; Esposito, A.; Wouters, F. S. ; Reed, J. C. & Bähr, M.  et al.​ (2006) 
Journal of Molecular Neuroscience29(1) pp. 1​-8​.​ DOI: 

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Dohm, Christoph P. ; Siedenberg, Sandra ; Liman, Jan ; Esposito, Alessandro; Wouters, Fred S. ; Reed, John C.; Bähr, Mathias ; Kermer, Pawel 
Bax ihibitor-1 (BI-1) has been characterized as an inhibitor of Bax-induced cell death in plants and various mammalian cell systems. To explore the function of BI-1 in neurons, we overexpressed BI-1 tagged to HA or GFP in rat nigral CSM14.1 and human SH-SY5Y neuroblastoma cells. Stable BI-1 expression proved marked protection from cell death induced by thapsigargine, a stress agent blocking the Call-ATPase of the endoplasmic reticulum (ER) but failed to inhibit cell death induced by staurosporine, a kinase inhibitor initiating mitochondria-dependent apoptosis. Moreover, BI-1 was neuroprotective in a paradigm mimicking ischemia, namely oxygen-glucose as well as serum deprivation. Examination of the subcellular distribution revealed that BI-1 predominantly locates to the ER and nuclear envelope but not mitochondria. Taken together, BI-1 overexpression in the ER is protective in neurons, making BI-1 an interesting target for future studies aiming at the inhibition of neuronal cell death during neurodegenerative diseases and stroke.
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Journal of Molecular Neuroscience 



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