The mitochondrial TIM22 preprotein translocase is highly conserved throughout the eukaryotic kingdom

Matthias F Bauer; Uli Rothbauer; Nicole Mühlenbein; Richard J.H Smith; Klaus-Dieter Gerbitz; Walter Neupert; Michael Brunner; Sabine Hofmann

doi:10.1016/S0014-5793(99)01665-8

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The mitochondrial TIM22 preprotein translocase is highly conserved throughout the eukaryotic kingdom

Journal article

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The mitochondrial TIM22 preprotein translocase is highly conserved throughout the eukaryotic kingdom

Matthias F Bauer, Uli Rothbauer, Nicole Mühlenbein, Richard J.H Smith, Klaus-Dieter Gerbitz, Walter Neupert, Michael Brunner and Sabine Hofmann

FEBS letters, Vol.464(1), pp.41-47

1999

DOI: 10.1016/S0014-5793(99)01665-8

PMID: 10611480

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Abstract

The Mohr–Tranebjaerg syndrome (MTS), a neurodegenerative syndrome characterized by progressive sensorineural hearing loss, dystonia, mental retardation and blindness, is a mitochondrial disease caused by mutations in the deafness/dystonia peptide 1 (DDP1) gene. DDP1 shows similarity to the yeast proteins Tim9, Tim10 and Tim12, components of the mitochondrial import machinery for carrier proteins. Here, we show that DDP1 belongs to a large family of evolutionarily conserved proteins. We report the identification, chromosomal localization and expressional analysis of six human family members which represent further candidate genes for neurodegenerative diseases.

Mitochondrial inner membrane translocase TIM22

Deafness/dystonia peptide 1/Tim10 protein family

Mohr–Tranebjaerg syndrome

Details

Title: Subtitle: The mitochondrial TIM22 preprotein translocase is highly conserved throughout the eukaryotic kingdom
Creators: Matthias F Bauer - Institut für Klinische Chemie, Molekular Diagnostik und Mitochondriale Genetik und Institut für Diabetesforschung, Akad. Krankenhaus München-Schwabing, Kölner Platz 1, D-80804 Munich, Germany
Uli Rothbauer - Institut für Klinische Chemie, Molekular Diagnostik und Mitochondriale Genetik und Institut für Diabetesforschung, Akad. Krankenhaus München-Schwabing, Kölner Platz 1, D-80804 Munich, Germany
Nicole Mühlenbein - Institut für Klinische Chemie, Molekular Diagnostik und Mitochondriale Genetik und Institut für Diabetesforschung, Akad. Krankenhaus München-Schwabing, Kölner Platz 1, D-80804 Munich, Germany
Richard J.H Smith - Department of Otolaryngology, University of Iowa Hospitals and Clinics, Iowa City, IA 52242-0001, USA
Klaus-Dieter Gerbitz - Institut für Klinische Chemie, Molekular Diagnostik und Mitochondriale Genetik und Institut für Diabetesforschung, Akad. Krankenhaus München-Schwabing, Kölner Platz 1, D-80804 Munich, Germany
Walter Neupert - Institut für Physiologische Chemie der Universität München, Goethestraße 33, 80336 Munich, Germany
Michael Brunner - Institut für Physiologische Chemie der Universität München, Goethestraße 33, 80336 Munich, Germany
Sabine Hofmann - Institut für Klinische Chemie, Molekular Diagnostik und Mitochondriale Genetik und Institut für Diabetesforschung, Akad. Krankenhaus München-Schwabing, Kölner Platz 1, D-80804 Munich, Germany
Resource Type: Journal article
Publication Details: FEBS letters, Vol.464(1), pp.41-47
DOI: 10.1016/S0014-5793(99)01665-8
PMID: 10611480
NLM abbreviation: FEBS Lett
ISSN: 0014-5793
eISSN: 1873-3468
Publisher: Elsevier B.V
Language: English
Date published: 1999
Academic Unit: Roy J. Carver Department of Biomedical Engineering; Molecular Physiology and Biophysics; Anatomy and Cell Biology; Stead Family Department of Pediatrics; Iowa Neuroscience Institute; Otolaryngology; Internal Medicine
Record Identifier: 9984006321302771

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