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)

Age-related sarcopenia is characterized by decreased muscle mass and muscle strength, and increased muscle fatigability. A decrease in synthesis rates of mixed muscle proteins (average of all muscle proteins), myosin heavy chain (responsible for adenosine triphosphatase action) and mitochondrial proteins (site of adenosine triphosphate production) have been described with aging. Most of these changes start by middle age, thus contributing to the progressive decline in muscle size and function. How closely these changes are related to lifestyle and the decline in several hormones, particularly growth hormone, insulin-like growth factor-I, testosterone and dehydroepiandrosterone, remains to be clearly defined. The ability to measure the specific effects of different types of exercise training on muscle protein metabolism has only recently become available. Thus, future investigations will continue to improve our understanding of protein metabolism in aging skeletal muscles. The development and assessment of successful countermeasures to age-related sarcopenia will hopefully follow these discoveries.
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PMID:Mechanisms of sarcopenia of aging. 1044 78

(Na(+)+K(+))-adenosine triphosphatase (NaK-ATPase), an ubiquitous membrane transport protein consisting of alpha and beta subunits, regulates Na(+)/K(+)fluxes and maintains many vital physiological functions, including cell growth. Results have indicated that platelet-derived growth factor (PDGF) and insulin-like growth factor-I (IGF-I) both enhance NaK-ATPase subunits. Genistein, an inhibitor of tyrosine phosphorylation, inhibits serum- and PDGF-BB-induced NaK-ATPase alpha(1)subunit protein levels without inhibiting IGF-I-induced NaK-ATPase alpha(1)subunit protein levels. These results indicate that PDGF-BB and IGF-I utilize separate signaling pathways to induce the synthesis of NaK-ATPase alpha(1)subunits. In addition, genistein failed to inhibit PDGF-BB-stimulated NaK-ATPase beta(1)subunit levels, suggesting that two separate pathways are involved to induce the synthesis of the NaK-ATPase alpha(1)and beta(1)subunits, respectively.
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PMID:PDGF-BB and IGF-I use different signaling pathways to induce NaK-ATPase subunits in cultured rat thoracic aortic smooth muscle cells. 1060 Feb 34