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Current Topics in Bioenergetics, Volume 17: Molecular Basis by Author Unknown

By Author Unknown

The sphere of mitochondrial ailments is at present one of many swiftly transforming into fields of study in mobilephone and molecular biology. This quantity encompasses the newest improvement during this box of study. The chapters disguise subject matters in a variety of disciplines together with biophysics, biochemistry, mobilephone and molecular biology, molecular genetics, and medical drugs.

Summarizes starting to be facts of the position of mitochondria in a good number of pathological conditions
Brings jointly assorted methods towards figuring out mitochondria diseases
Molecular and mobile biology
Clinical body structure and medicine
Details the an important function this organelle performs in genetic law of varied organic features.

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Extra resources for Current Topics in Bioenergetics, Volume 17: Molecular Basis of Mitochondrial Pathology

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Biochem. Biophys. Res. Commun. 180, 894-899. Thomas, S. , Gebicki, J. , and Dean, R. T. (1989). Biochim. Biophys. Acta 1002, 189197. Thorsness, P. , and Fox, T. D. (1990). Nature (London) 346, 376-379. Tomkinson, A. , Bonk, R. T , and Linn, S. (1988). /. Biol. Chem. 263, 12532-12537. Tomkinson, A. , Bonk, R. , and Linn, S. (1990). Nucleic Acids Res. 18, 929-935. Traber, J. (1991). Diplomarbeit ΕΤΗ. , and Marzuki, S. (1989). Lancet 1, 637-639. Turrens, J. , Chavez, U. , and McCord, J. M. (1991).

1990). This mutation, a Τ to G substitution at nucleotide 8993, results in an arginine instead of a leucine at codon 156 in ATP synthase 6, a subunit of the F 0 portion. , 1992). , 1992) that the mutation occurs within F 0 , in a region postulated to be directly apposed to a glutamic acid residue of subunit 9 that is required for proton conducting activity. Thus, this mutation may result in altered proton translocation through F 0 , but this phenomenon or any other effect on ATP synthase activity remains to be proven.

Defects of Nuclear DNA (nDNA) B. Defects of Mitochondrial DNA (mtDNA) C. DNA/mtDNA Communication II. Mitochondrial Metabolism III. Mitochondrial Disorders A. Defects of substrate transport B. Defects of substrate utilization C. Defects of the Krebs cycle D. Defects of Oxidation-Phosphorylation Coupling E. Defects of the Respiratory Chain and ATP Synthase IV. Concluding Remarks References I. Introduction The concept of mitochondrial disease was introduced in 1962 when Luft et al. described "loose coupling" of muscle mitochondria in a patient with nonthyroidal hypermetabolism.

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