Other names published for YTA12: RCA1, m-AAA protease subunit YTA12, YMR089C
YTA12 LITERATURE TOPICS
- Curated Literature
- Genetics/Cell Biology
- Nucleic Acid Information
- Gene Product Information
- Protein Physical Properties
- Protein Sequence Features
- Protein-protein Interactions
- Substrates/Ligands/Cofactors
- Related Genes/Proteins
- Research Aids
- Genome-wide Analysis
- Proteome-wide Analysis
- Other Topics
- Additional Information
YTA12 - Substrates/Ligands/Cofactors (10)
| Reference | Other Genes Addressed |
|---|---|
| Claypool SM, et al. (2011) Barth syndrome mutations that cause tafazzin complex lability. J Cell Biol 192(3):447-62 | |
| Lee S, et al. (2011) Electron Cryomicroscopy Structure of a Membrane-anchored Mitochondrial AAA Protease. J Biol Chem 286(6):4404-11 | |
| Di Bella D, et al. (2010) Mutations in the mitochondrial protease gene AFG3L2 cause dominant hereditary ataxia SCA28. Nat Genet 42(4):313-21 | |
| Augustin S, et al. (2009) An intersubunit signaling network coordinates ATP hydrolysis by m-AAA proteases. Mol Cell 35(5):574-85 | |
| Suppanz IE, et al. (2009) The m-AAA protease processes cytochrome c peroxidase preferentially at the inner boundary membrane of mitochondria. Mol Biol Cell 20(2):572-80 | |
| Tatsuta T, et al. (2007) m-AAA protease-driven membrane dislocation allows intramembrane cleavage by rhomboid in mitochondria. EMBO J 26(2):325-35 | |
| Ishihara N, et al. (2006) Regulation of mitochondrial morphology through proteolytic cleavage of OPA1. EMBO J 25(13):2966-77 | |
| Korbel D, et al. (2004) Membrane protein turnover by the m-AAA protease in mitochondria depends on the transmembrane domains of its subunits. EMBO Rep 5(7):698-703 | |
| Esser K, et al. (2002) A novel two-step mechanism for removal of a mitochondrial signal sequence involves the mAAA complex and the putative rhomboid protease Pcp1. J Mol Biol 323(5):835-43 | |
| Leonhard K, et al. (2000) Membrane protein degradation by AAA proteases in mitochondria: extraction of substrates from either membrane surface. Mol Cell 5(4):629-38 |




