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HUMAN MITOCHONDRIAL COMPLEX-I DYSFUNCTION

COOPER, JM; MANN, VM; KRIGE, D; SCHAPIRA, AHV; (1992) HUMAN MITOCHONDRIAL COMPLEX-I DYSFUNCTION. BIOCHIMICA ET BIOPHYSICA ACTA , 1101 (2) 198 - 203.

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Abstract

In humans, complex I dysfunction has been observed in a high percentage of patients with mitochondrial myopathy. Analysis of mitochondria from these patients suggests the function and assembly of complex I is particularly susceptible to abnormalities of mitochondrial DNA, involving either point mutations of tRNA genes or major deletions. The evidence for a complex I defect in Parkinson's disease is accumulating, although the cause of this deficiency or the role it plays in the events that culminate in dopaminergic cell death remains unresolved.

Type: Article
Title: HUMAN MITOCHONDRIAL COMPLEX-I DYSFUNCTION
Location: HELSINKI, FINLAND
Keywords: MITOCHONDRIAL MYOPATHY, PARKINSONS DISEASE, AGING, COMPLEX-I DYSFUNCTION, BOVINE HEART-MITOCHONDRIA, NADH-UBIQUINONE OXIDOREDUCTASE, ELECTRON-TRANSPORT CHAIN, IRON-SULFUR PROTEIN, PARKINSONS-DISEASE, MOLECULAR DEFECTS, CHLOROPLAST DNA, SUBUNIT, DEFICIENCY, DEHYDROGENASE
UCL classification: UCL > Provost and Vice Provost Offices
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Brain Sciences
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Brain Sciences > UCL Queen Square Institute of Neurology
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Brain Sciences > UCL Queen Square Institute of Neurology > Clinical and Movement Neurosciences
URI: http://discovery.ucl.ac.uk/id/eprint/192489
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