Literature DB >> 2165819

Apocytochrome c: an exceptional mitochondrial precursor protein using an exceptional import pathway.

R A Stuart1, W Neupert.   

Abstract

The cytochrome c import pathway differs markedly from the general route taken by the majority of other imported proteins, which is characterized by the import involvement of namely, surface receptors, the general insertion protein (GIP), contact sites and by the requirement of a membrane potential (delta psi). Unique features of both the cytochrome c precursor (apocytochrome c) and of the mechanism that transports it into mitochondria, have contributed to the evolution of a distinct import pathway that is not shared by any other mitochondrial protein analysed thus far. The cytochrome c pathway is particularly unique because i) apocytochrome c appears to have spontaneous membrane insertion-activity; ii) cytochrome c heme lyase seems to act as a specific binding site in lieu of a surface receptor and; iii) covalent heme addition and the associated refolding of the polypeptide appears to provide the free energy for the translocation of the cytochrome c polypeptide across the outer mitochondrial membrane.

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Year:  1990        PMID: 2165819     DOI: 10.1016/0300-9084(90)90136-5

Source DB:  PubMed          Journal:  Biochimie        ISSN: 0300-9084            Impact factor:   4.079


  21 in total

1.  Apocytochrome c requires the TOM complex for translocation across the mitochondrial outer membrane.

Authors:  K Diekert; A I de Kroon; U Ahting; B Niggemeyer; W Neupert; B de Kruijff; R Lill
Journal:  EMBO J       Date:  2001-10-15       Impact factor: 11.598

2.  Folding of apocytochrome c induced by the interaction with negatively charged lipid micelles proceeds via a collapsed intermediate state.

Authors:  S E Rankin; A Watts; H Roder; T J Pinheiro
Journal:  Protein Sci       Date:  1999-02       Impact factor: 6.725

Review 3.  Mitochondrial protein import.

Authors:  V Geli; B Glick
Journal:  J Bioenerg Biomembr       Date:  1990-12       Impact factor: 2.945

4.  Protective effect of zinc on amyloid-beta 25-35 and 1-40 mediated toxicity.

Authors:  S M Cardoso; A C Rego; C Pereira; C R Oliveira
Journal:  Neurotox Res       Date:  2005       Impact factor: 3.911

5.  Caspase-independent mitochondrial cell death results from loss of respiration, not cytotoxic protein release.

Authors:  Lydia Lartigue; Yulia Kushnareva; Youngmo Seong; Helen Lin; Benjamin Faustin; Donald D Newmeyer
Journal:  Mol Biol Cell       Date:  2009-09-30       Impact factor: 4.138

6.  Mitochondrial cytochrome c release in apoptosis occurs upstream of DEVD-specific caspase activation and independently of mitochondrial transmembrane depolarization.

Authors:  E Bossy-Wetzel; D D Newmeyer; D R Green
Journal:  EMBO J       Date:  1998-01-02       Impact factor: 11.598

Review 7.  The first steps of protein import into mitochondria.

Authors:  V Haucke; T Lithgow
Journal:  J Bioenerg Biomembr       Date:  1997-02       Impact factor: 2.945

8.  Apoptosis-associated release of Smac/DIABLO from mitochondria requires active caspases and is blocked by Bcl-2.

Authors:  C Adrain; E M Creagh; S J Martin
Journal:  EMBO J       Date:  2001-12-03       Impact factor: 11.598

9.  The Rhodobacter sphaeroides cytochrome c2 signal peptide is not necessary for export and heme attachment.

Authors:  J P Brandner; T J Donohue
Journal:  J Bacteriol       Date:  1994-02       Impact factor: 3.490

10.  Increased expression but not sensitivity to Fas/CD95 in glioblastoma cells depleted of mitochondrial DNA.

Authors:  Bertrand C Liang
Journal:  Exp Ther Med       Date:  2010-09-29       Impact factor: 2.447

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