Mouse models of oxidative phosphorylation defects: powerful tools to study the pathobiology of mitochondrial diseases. - Wikidata - awgldk - TriplyDB

Mouse models of oxidative phosphorylation defects: powerful tools to study the pathobiology of mitochondrial diseases.

Mouse models of oxidative phosphorylation defects: powerful tools to study the pathobiology of mitochondrial diseases.

http://www.wikidata.org/entity/Q37120797

about

Cisd2 deficiency drives premature aging and causes mitochondria-mediated defects in mice A defect in the mitochondrial complex III, but not complex IV, triggers early ROS-dependent damage in defined brain regions.A Drosophila model of mitochondrial disease caused by a complex I mutation that uncouples proton pumping from electron transfer.Metabolic control of mitochondrial biogenesis through the PGC-1 family regulatory network Andropause and the development of cardiovascular disease presentation-more than an epi-phenomenon.A Metabolic Signature of Mitochondrial Dysfunction Revealed through a Monogenic Form of Leigh Syndrome Mouse models of mitochondrial complex I dysfunction Mitochondrial biogenesis: a therapeutic target for neurodevelopmental disorders and neurodegenerative diseases The mitochondrial brain: From mitochondrial genome to neurodegeneration Turn up the power - pharmacological activation of mitochondrial biogenesis in mouse models.Functional and Molecular Insights of Hydrogen Sulfide Signaling and Protein Sulfhydration.Region-specific expression of mitochondrial complex I genes during murine brain development.Nutritional Interventions for Mitochondrial OXPHOS Deficiencies: Mechanisms and Model Systems.

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Mouse models of oxidative phosphorylation defects: powerful tools to study the pathobiology of mitochondrial diseases.

http://www.wikidata.org/entity/Q37120797

description

article científic

@ca

article scientifique

@fr

articolo scientifico

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artigo científico

@pt

bilimsel makale

@tr

scientific article published on 13 June 2008

@en

vedecký článok

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vetenskaplig artikel

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videnskabelig artikel

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vědecký článek

@cs

name

Mouse models of oxidative phos ...... ogy of mitochondrial diseases.

@en

Mouse models of oxidative phos ...... ogy of mitochondrial diseases.

@nl

type

label

Mouse models of oxidative phos ...... ogy of mitochondrial diseases.

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Mouse models of oxidative phos ...... ogy of mitochondrial diseases.

@nl

prefLabel

Mouse models of oxidative phos ...... ogy of mitochondrial diseases.

@en

Mouse models of oxidative phos ...... ogy of mitochondrial diseases.

@nl

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J.BBAMCR.2008.06.003

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Biochimica et Biophysica Acta

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Mouse models of oxidative phos ...... ogy of mitochondrial diseases.

@en

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Alessandra Torraco

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Carlos T Moraes

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Francisca Diaz

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Uma D Vempati

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SURF1, encoding a factor involved in the biogenesis of cytochrome c oxidase, is mutated in Leigh syndrome

Thymidine phosphorylase gene mutations in MNGIE, a human mitochondrial disorder

Fatal infantile cardioencephalomyopathy with COX deficiency and mutations in SCO2, a COX assembly gene

The mitochondrial p55 accessory subunit of human DNA polymerase gamma enhances DNA binding, promotes processive DNA synthesis, and confers N-ethylmaleimide resistance

A mutation in the human heme A:farnesyltransferase gene (COX10 ) causes cytochrome c oxidase deficiency

Role of adenine nucleotide translocator 1 in mtDNA maintenance

Premature ageing in mice expressing defective mitochondrial DNA polymerase

Mitochondrial transcription factors B1 and B2 activate transcription of human mtDNA

OPA1 mutations induce mitochondrial DNA instability and optic atrophy 'plus' phenotypes

Mutations in COX10 result in a defect in mitochondrial heme A biosynthesis and account for multiple, early-onset clinical phenotypes associated with isolated COX deficiency

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171-180

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scholarly article

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10.1016/J.BBAMCR.2008.06.003

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1

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2008-06-13T00:00:00Z

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223469122

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18601959

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phosphorylation

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2652735

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