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pro vyhledávání: '"Kate Duberley"'
Publikováno v:
Methods in molecular biology (Clifton, N.J.). 2138
Coenzyme Q
Autor:
Simon Heales, Kate Duberley, A. Chalasani, Iain P. Hargreaves, J.M. Land, Shamima Rahman, Andrey Y. Abramov
Publikováno v:
The International Journal of Biochemistry & Cell Biology. 50:60-63
Primary Coenzyme Q10 (CoQ10) deficiency is an autosomal recessive disorder with a heterogeneous clinical presentation. Common presenting features include both muscle and neurological dysfunction. Muscle abnormalities can improve, both clinically and
Autor:
Antony Briddon, Iain P. Hargreaves, Berna Demiray, John M. Land, Elaine Murphy, Kate Duberley, Fiona Turkes
Publikováno v:
Toxicology Mechanisms and Methods. 23:459-463
Elevated plasma homocysteine (Hcy) has been detected in patients with various neurodegenerative conditions. Studies on neurones and cerebral tissue have revealed that hyperhomocystinaemia may inhibit mitochondrial electron transport chain (ETC) enzym
Autor:
John M. Land, Kevin Mills, Iain P. Hargreaves, Shamima Rahman, Simon Eaton, Korn-Anong Chaiwatanasirikul, Simon Heales, Kate Duberley
Publikováno v:
Rapid Communications in Mass Spectrometry. 27:924-930
RATIONALE Neurological dysfunction is common in primary coenzyme Q10 (2,3-dimethoxy, 5-methyl, 6-polyisoprene parabenzoquinone; CoQ10; ubiquinone) deficiencies, the most readily treatable subgroup of mitochondrial disorders. Therapeutic benefit from
Autor:
Shamima Rahman, Annapurna Chalasani, Kate Duberley, Andrey Y. Abramov, Simon Heales, Iain P. Hargreaves
Publikováno v:
Journal of Inherited Metabolic Disease. 36:63-73
Disorders of coenzyme Q(10) (CoQ(10)) biosynthesis represent the most treatable subgroup of mitochondrial diseases. Neurological involvement is frequently observed in CoQ(10) deficiency, typically presenting as cerebellar ataxia and/or seizures. The
Publikováno v:
Alzheimer's & Dementia. 7
Publikováno v:
Alzheimer's & Dementia. 6
Publikováno v:
Methods in Molecular Biology ISBN: 9781071604700
Coenzyme Q10 (CoQ10) plays a key role as an electron carrier in the mitochondrial respiratory chain and as a cellular antioxidant molecule. A deficit in CoQ10 status may contribute to disease pathophysiology by causing a failure mitochondrial energy
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::e3179afe76e186b67159b3942fe0bfd6