MitoP2: the mitochondrial proteome database--now including mouse data

The MitoP2 database (http://www.mitop.de) integrates information on mitochondrial proteins, their molecular functions and associated diseases. The central database features are manually annotated reference proteins localized or functionally associated with mitochondria supplied for yeast, human and...

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Bibliographic Details
Published in:Nucleic acids research 2006-01, Vol.34 (1), p.D705-D711
Main Authors: Prokisch, H, Andreoli, C, Ahting, U, Heiss, K, Ruepp, A, Scharfe, C, Meitinger, T
Format: Article
Language:English
Subjects:
Animals
Databases, Protein
Genes, Mitochondrial
Humans
Internet
Mice
Mitochondrial Diseases - genetics
Mitochondrial Proteins - analysis
Mitochondrial Proteins - genetics
Mitochondrial Proteins - physiology
Proteome - genetics
Proteome - physiology
Proteomics
Saccharomyces cerevisiae Proteins - analysis
Saccharomyces cerevisiae Proteins - genetics
Saccharomyces cerevisiae Proteins - physiology
User-Computer Interface
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Description
Summary:The MitoP2 database (http://www.mitop.de) integrates information on mitochondrial proteins, their molecular functions and associated diseases. The central database features are manually annotated reference proteins localized or functionally associated with mitochondria supplied for yeast, human and mouse. MitoP2 enables (i) the identification of putative orthologous proteins between these species to study evolutionarily conserved functions and pathways; (ii) the integration of data from systematic genome-wide studies such as proteomics and deletion phenotype screening; (iii) the prediction of novel mitochondrial proteins using data integration and the assignment of evidence scores; and (iv) systematic searches that aim to find the genes that underlie common and rare mitochondrial diseases. The data and analysis files are referenced to data sources in PubMed and other online databases and can be easily downloaded. MitoP2 users can explore the relationship between mitochondrial dysfunctions and disease and utilize this information to conduct systems biology approaches on mitochondria.
ISSN:0305-1048
1362-4962
DOI:10.1093/nar/gkj127