Volume 7 Supplement 1

Proceedings of the 2011 International Conference on Molecular Neurodegeneration

Open Access

Identifying an APP-binding protein in neuronal cell death

  • Yunwu Zhang1 and
  • Huaxi Xu2
Molecular Neurodegeneration20127(Suppl 1):L22

DOI: 10.1186/1750-1326-7-S1-L22

Published: 7 February 2012

Background

Apoptosis is an essential cellular process involved in multiple diseases and a major pathway for neuronal death in neurodegeneration. The detailed signaling events/pathways that lead to apoptosis, especially in neurons, require further elucidation.

Results

Here we find that a mitochondrial solute carrier family protein, appoptosin, induces reactive oxygen species release and intrinsic caspase-dependent apoptosis. The physiological function of appoptosin is to transport/exchange glycine/5-amino-levulinic acid across the mitochondrial membrane for heme synthesis. Alzheimer’s β-amyloid precursor protein interacts with appoptosin and modulates appoptosin-induced apoptosis. Levels of appoptosin are upregulated in brain samples from Alzheimer’s disease and infarct patients and in rodent stroke models, as well as in cells treated with β-amyloid (Aβ) and glutamate. Downregulation of appoptosin prevents the cell death and caspase activation caused by glutamate or Aβ insults.

Conclusion

Our study identifies appoptosin as a crucial player in apoptosis and a novel proapoptotic protein involved in neuronal cell death, providing a possible new therapeutic target for neurodegenerative disorders and cancers.

Authors’ Affiliations

(1)
Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, College of Medicine, Xiamen University
(2)
Neurodegenerative Disease Research Program, Sanford-Burnham Medical Research Institute

Copyright

© Zhang and Xu; licensee BioMed Central Ltd. 2012

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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