Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P20020 (adenosine triphosphatase)
 3,299 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Early atherosclerotic lesions in human aortas less than five hours postmortem were studied by light microscopy (20 cases) and electron microscopy (10 cases), to determine the morphological and cytochemical character of calcium deposition in the lesions. Routine and multiple special stains by light microscopy demonstrated atherosclerotic (intimal) calcium to be deposited as fine grains, ring-shaped droplets or small needle-shaped crystals, and medial calcium as fine grains or ring-shaped droplets. The calcium deposits were frequently associated with the PAS-positive basal lamina surrounding smooth muscle cells. In the intimal lesions the calcium deposits were often associated with fine granular lipid, while this association was much less frequent in the media. Calcium in atherosclerotic intima was generally not closely associated with elastic fibers but in the media was often deposited along or near elastic fibers. By electron microscopy the atherosclerotic lesions were composed of many smooth muscle cells (with or without lipid droplets), newly formed elastic fibers, amorphous ground substance, a few collagen fibrils and many membrane-limited matrix vesicle-like structures, 100-700 nm diameter. Many similar vesicles were present between the elastic laminae of the media. With the potassium pyroantimonate technique for demonstrating calcium, reaction products were most concentrated within these matrix vesicles but were also present in mitochondria of smooth muscle cells, within extracellular mitochondria-like structures, in pericellular basal lamina-like material and loosely dispersed in the interstitial ground substance. All elastic fibers were negative for calcium by this technique. The membrane of the matrix vesicle-like structures were cytochemically positive for alkaline phosphatase and adenosine triphosphatase. These studies suggest that calcification in human atherosclerosis and media is related to smooth muscle cell degeneration and that the major initial loci for calcium deposition are matrix vesicles from degraded cells, comparable to osteogenic calcification of cartilage.
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PMID:Calcification in atherosclerosis. I. Human studies. 294 18

To show adenylate cyclase (AC) activity in rat calvaria, it is necessary first to decalcify the specimen. In hard tissues, several enzymes (adenosine triphosphatase (ATPase), alkaline phosphatase (APase), adenylate cyclase (AC) and perhaps pyrophosphatase (PPiase) are able to degrade adenosine triphosphate (ATP). The presence of sodium fluoride (NaF) in the incubation medium reduces the quantity of precipitate formed, compared to that observed using a NaF-free incubation medium. Levamisole, used under the same conditions, gives similar results. Possibly NaF inhibits pyrophosphohydrolase and/or phosphatases which mask the AC activity. Adenylylimidophosphate (AMP-PNP), which is a specific AC substrate, confirms the results obtained with ATP. AC activity is demonstrated cytochemically in the osteoblast and preosteoblast membranes, at the junction between two osteoblasts and along the cytoplasmic processes of the osteoblast which penetrate into the osteoid matrix. The osteocytes never show a precipitate, except those which present some osteoblastic features and then only on the membrane facing the osteogenic layer. An intracellular reaction is also evident and is discussed. Parathyroid hormone (PTH) does not reveal new sites of AC activity but increases the quantity of precipitate observed.
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PMID:An attempt at localizing adenylate cyclase in rat calvaria. Influence of sodium fluoride and parathyroid hormone. 700 93