Biomaterial Database

Proceedings: Precursors of cytochrome oxidase in cytochrome-oxidase deficient cells of Neurospora crassa. 1974

S Werner

UI	MeSH Term	Description	Entries
D008928	Mitochondria	Semiautonomous, self-reproducing organelles that occur in the cytoplasm of all cells of most, but not all, eukaryotes. Each mitochondrion is surrounded by a double limiting membrane. The inner membrane is highly invaginated, and its projections are called cristae. Mitochondria are the sites of the reactions of oxidative phosphorylation, which result in the formation of ATP. They contain distinctive RIBOSOMES, transfer RNAs (RNA, TRANSFER); AMINO ACYL T RNA SYNTHETASES; and elongation and termination factors. Mitochondria depend upon genes within the nucleus of the cells in which they reside for many essential messenger RNAs (RNA, MESSENGER). Mitochondria are believed to have arisen from aerobic bacteria that established a symbiotic relationship with primitive protoeukaryotes. (King & Stansfield, A Dictionary of Genetics, 4th ed)	Mitochondrial Contraction,Mitochondrion,Contraction, Mitochondrial,Contractions, Mitochondrial,Mitochondrial Contractions
D009154	Mutation	Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.	Mutations
D009491	Neurospora	A genus of ascomycetous fungi, family Sordariaceae, order SORDARIALES, comprising bread molds. They are capable of converting tryptophan to nicotinic acid and are used extensively in genetic and enzyme research. (Dorland, 27th ed)	Neurosporas
D009492	Neurospora crassa	A species of ascomycetous fungi of the family Sordariaceae, order SORDARIALES, much used in biochemical, genetic, and physiologic studies.	Chrysonilia crassa
D004792	Enzyme Precursors	Physiologically inactive substances that can be converted to active enzymes.	Enzyme Precursor,Proenzyme,Proenzymes,Zymogen,Zymogens,Precursor, Enzyme,Precursors, Enzyme
D030401	Cytochrome-c Oxidase Deficiency	A disease that results from a congenital defect in ELECTRON TRANSPORT COMPLEX IV. Defects in ELECTRON TRANSPORT COMPLEX IV can be caused by mutations in the SURF1, SCO2, COX10, or SCO1 genes. ELECTRON TRANSPORT COMPLEX IV deficiency caused by mutation in SURF1 manifests itself as LEIGH DISEASE; that caused by mutation in SCO2 as fatal infantile cardioencephalomyopathy; that caused by mutation in COX10 as tubulopathy and leukodystrophy; and that caused by mutation in SCO1 as early-onset hepatic failure and neurologic disorder. (from Online Mendelian Inheritance in Man, http://www.ncbi.nlm.nih.gov/Omim, MIM#220110, May 17, 2001)	Complex IV Deficiency,Cox Deficiency,Cytochrome C Oxidase Deficiency,Cytochrome Oxidase Deficiency,Deficiency, Cytochrome-c Oxidase,Mitochondrial Complex IV Deficiency,Complex IV Deficiencies,Cox Deficiencies,Cytochrome Oxidase Deficiencies,Cytochrome-c Oxidase Deficiencies,Deficiencies, Complex IV,Deficiencies, Cox,Deficiencies, Cytochrome Oxidase,Deficiencies, Cytochrome-c Oxidase,Deficiency, Complex IV,Deficiency, Cox,Deficiency, Cytochrome Oxidase,Deficiency, Cytochrome c Oxidase,Oxidase Deficiencies, Cytochrome,Oxidase Deficiencies, Cytochrome-c,Oxidase Deficiency, Cytochrome,Oxidase Deficiency, Cytochrome-c