Aconitase and mitochondrial iron-sulphur protein deficiency in Friedreich ataxia (Q28250989)

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P de Lonlay

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D Chretien

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F Foury

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M Koenig

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D Sidi

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P Rustin

Regulation of mitochondrial iron accumulation by Yfh1p, a putative homolog of frataxin

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language of work or name

English

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publication date

October 1997

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published in

Nature Genetics

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volume

17

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issue

2

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page(s)

215-7

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cites work

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Studies of human, mouse and yeast homologues indicate a mitochondrial function for frataxin

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Molecular control of vertebrate iron metabolism: mRNA-based regulatory circuits operated by iron, nitric oxide, and oxidative stress

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Deletion of the yeast homologue of the human gene associated with Friedreich's ataxia elicits iron accumulation in mitochondria

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Assessment of the mitochondrial respiratory chain

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Clinical Description and Roentgenologic Evaluation of Patients with Friedreich's Ataxia

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Friedreich's ataxia: a clinical and genetic study of 90 families with an analysis of early diagnostic criteria and intrafamilial clustering of clinical features

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Friedreich's ataxia: autosomal recessive disease caused by an intronic GAA triplet repeat expansion

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Pathology of the Heart in Friedreich's Ataxia: Review of the Literature and Report of One Case

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Superoxide radical and superoxide dismutases

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Mitochondrial dysfunction and spinocerebellar degenerations

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Endomyocardial biopsies for early detection of mitochondrial disorders in hypertrophic cardiomyopathies

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A regulated RNA binding protein also possesses aconitase activity

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Dilated cardiomyopathy and neonatal lethality in mutant mice lacking manganese superoxide dismutase

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Biochemical and molecular investigations in respiratory chain deficiencies

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