Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.6.3.14 (ATP synthase)
 7,042 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diverse oxidative pathways, such as direct oxidation of amino acids, glycoxidation, and lipoxidation could contribute to Alzheimer disease pathogenesis. A global survey for the amount of structurally characterized probes for these reactions is lacking and could overcome the lack of specificity derived from measurement of 2,4-dinitrophenylhydrazine reactive carbonyls. Consequently we analyzed (i) the presence and concentrations of glutamic and aminoadipic semialdehydes, N(epsilon)-(carboxymethyl)-lysine, N(epsilon)-(carboxyethyl)-lysine, and N(epsilon)-(malondialdehyde)-lysine by means of gas chromatography/mass spectrometry, (ii) the biological response through expression of the receptor for advanced glycation end products, (iii) the fatty acid composition in brain samples from Alzheimer disease patients and age-matched controls, and (iv) the targets of N(epsilon)-(malondialdehyde)-lysine formation in brain cortex by proteomic techniques. Alzheimer disease was associated with significant, although heterogeneous, increases in the concentrations of all evaluated markers. Alzheimer disease samples presented increases in expression of the receptor for advanced glycation end products with high molecular heterogeneity. Samples from Alzheimer disease patients also showed content of docosahexaenoic acid, which increased lipid peroxidizability. In accordance, N(epsilon)-(malondialdehyde)-lysine formation targeted important proteins for both glial and neuronal homeostasis such as neurofilament L, alpha-tubulin, glial fibrillary acidic protein, ubiquinol-cytochrome c reductase complex protein I, and the beta chain of ATP synthase. These data support an important role for lipid peroxidation-derived protein modifications in Alzheimer disease pathogenesis.
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PMID:Proteins in human brain cortex are modified by oxidation, glycoxidation, and lipoxidation. Effects of Alzheimer disease and identification of lipoxidation targets. 1579 62

Autoantibody response to tumor antigens has been widely used to identify novel tumor markers for different cancers, including that of the head and neck. The oral cavity, which is in the head and neck region, comprises of many sub sites with distinct biologies and incidence of cancer of each sub site of the oral cavity is different. It is anticipated therefore that each sub site of the oral cavity may elicit a differential autoantibody response. This report evaluates the autoantibody response in 15 patients with cancer of gingivo-buccal complex and in 15 patients with cancer of tongue using Immunoproteomics, and shows that the autoantibody response to alpha-enolase, HSP 70, peroxiredoxin-VI, annexin II, pyruvate kinase, alpha-tubulin, beta-tubulin, ATP synthase, triose phosphate isomerase and aldose reductase seen in patients with cancer of gingivo-buccal complex is absent in patients with cancer of tongue. This suggests that cancer of these sub sites should be studied separately because of their different biology and emerging site specific molecular signatures including autoantibody responses to ensure unambiguous clinical interpretations.
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PMID:Immunoproteomics reveals that cancer of the tongue and the gingivobuccal complex exhibit differential autoantibody response. 1940 67