The mitochondrial ADP/ATP carrier (SLC25 family): pathological implications of its dysfunction.

Clemençon, Benjamin; Babot, Marion; Trézéguet, Véronique (2013). The mitochondrial ADP/ATP carrier (SLC25 family): pathological implications of its dysfunction. Molecular aspects of medicine, 34(2-3), pp. 485-493. Elsevier 10.1016/j.mam.2012.05.006

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In aerobic eukaryotic cells, the high energy metabolite ATP is generated mainly within the mitochondria following the process of oxidative phosphorylation. The mitochondrial ATP is exported to the cytoplasm using a specialized transport protein, the ADP/ATP carrier, to provide energy to the cell. Any deficiency or dysfunction of this membrane protein leads to serious consequences on cell metabolism and can cause various diseases such as muscular dystrophy. Described as a decisive player in the programmed cell death, it was recently shown to play a role in cancer. The objective of this review is to summarize the current knowledge of the involvement of the ADP/ATP carrier, encoded by the SLC25A4, SLC25A5, SLC25A6 and SLC25A31 genes, in human diseases and of the efforts made at designing different model systems to study this carrier and the associated pathologies through biochemical, genetic, and structural approaches.

Item Type:

Journal Article (Original Article)

Division/Institute:

04 Faculty of Medicine > Pre-clinic Human Medicine > Institute of Biochemistry and Molecular Medicine

Graduate School:

Graduate School for Cellular and Biomedical Sciences (GCB)

UniBE Contributor:

Clemençon, Benjamin

Subjects:

500 Science > 570 Life sciences; biology
600 Technology > 610 Medicine & health

ISSN:

0098-2997

Publisher:

Elsevier

Language:

English

Submitter:

Kevin Marc Rupp

Date Deposited:

18 May 2015 17:15

Last Modified:

16 Oct 2015 09:52

Publisher DOI:

10.1016/j.mam.2012.05.006

PubMed ID:

23506884

BORIS DOI:

10.7892/boris.68796

URI:

https://boris.unibe.ch/id/eprint/68796

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