| pubmed-article:6594338 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:6594338 | lifeskim:mentions | umls-concept:C0079382 | lld:lifeskim |
| pubmed-article:6594338 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
| pubmed-article:6594338 | lifeskim:mentions | umls-concept:C0023440 | lld:lifeskim |
| pubmed-article:6594338 | lifeskim:mentions | umls-concept:C0521119 | lld:lifeskim |
| pubmed-article:6594338 | lifeskim:mentions | umls-concept:C0001480 | lld:lifeskim |
| pubmed-article:6594338 | lifeskim:mentions | umls-concept:C0022023 | lld:lifeskim |
| pubmed-article:6594338 | lifeskim:mentions | umls-concept:C0018270 | lld:lifeskim |
| pubmed-article:6594338 | lifeskim:mentions | umls-concept:C2348693 | lld:lifeskim |
| pubmed-article:6594338 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:6594338 | pubmed:issue | 22 | lld:pubmed |
| pubmed-article:6594338 | pubmed:dateCreated | 1984-12-27 | lld:pubmed |
| pubmed-article:6594338 | pubmed:abstractText | Extracellular ATP (1 mM) inhibited the growth of Friend virus-infected murine erythroleukemia cells (MEL cells) but had no effect on dimethyl sulfoxide-induced differentiation. ATP (1 mM) also caused changes in the permeability of MEL cells to ions. There was an increased influx of 45Ca2+ from a basal level of 5 pmol/min to 18 pmol/min/10(6) cells to achieve a 2-fold increase in steady-state Ca2+ as measured at isotopic equilibration. Ca2+ influx was blocked by diisothiocyanostilbene disulfonate (DIDS), an inhibitor of anion transport. ATP also stimulated Cl- uptake, and this flux was inhibited by DIDS. The ratio of ATP stimulated Cl- to Ca2+ uptake was 1.6:1. K+ and Na+ influx were also stimulated by ATP, but phosphate uptake was inhibited; the Na+ influx dissipated the Na+ gradient and thus inhibited nutrient uptake. ATP-stimulated K+ influx was ouabain inhibitable; however, the total cellular K+ decreased due to an ATP-stimulated ouabain-resistant K+ efflux. Na+ influx and Ca2+ influx occurred by separate independent routes, since Na+ influx was not inhibited by DIDS. The effects observed were specific for ATP *K1/2 MgATP = 0.7 mM) since AMP, GTP, adenosine, and the slowly hydrolyzable ATP analogue adenyl-5'-yl imidodiphosphate were without effect. The major ionic changes in the cell were a decrease in K+ and increase in Na+; cytoplasmic pH and free Ca2+ did not change appreciably. These ATP-induced changes in ion flux are considered to be responsible for growth inhibition. | lld:pubmed |
| pubmed-article:6594338 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:6594338 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:6594338 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:6594338 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:6594338 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:6594338 | pubmed:issn | 0021-9258 | lld:pubmed |
| pubmed-article:6594338 | pubmed:author | pubmed-author:ChahwalaS BSB | lld:pubmed |
| pubmed-article:6594338 | pubmed:author | pubmed-author:CantleyL CLC | lld:pubmed |
| pubmed-article:6594338 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:6594338 | pubmed:day | 25 | lld:pubmed |
| pubmed-article:6594338 | pubmed:volume | 259 | lld:pubmed |
| pubmed-article:6594338 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:6594338 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:6594338 | pubmed:pagination | 13717-22 | lld:pubmed |
| pubmed-article:6594338 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:6594338 | pubmed:year | 1984 | lld:pubmed |
| pubmed-article:6594338 | pubmed:articleTitle | Extracellular ATP induces ion fluxes and inhibits growth of Friend erythroleukemia cells. | lld:pubmed |
| pubmed-article:6594338 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:6594338 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:6594338 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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