| pubmed-article:7971730 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:7971730 | lifeskim:mentions | umls-concept:C0001480 | lld:lifeskim |
| pubmed-article:7971730 | lifeskim:mentions | umls-concept:C0023175 | lld:lifeskim |
| pubmed-article:7971730 | lifeskim:mentions | umls-concept:C1545588 | lld:lifeskim |
| pubmed-article:7971730 | lifeskim:mentions | umls-concept:C1152633 | lld:lifeskim |
| pubmed-article:7971730 | lifeskim:mentions | umls-concept:C0123610 | lld:lifeskim |
| pubmed-article:7971730 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:7971730 | pubmed:dateCreated | 1994-11-28 | lld:pubmed |
| pubmed-article:7971730 | pubmed:abstractText | Receptor-mediated phosphoinositide signaling pathway which generates a variety of second messengers is regulated by intracellular free Ca2+ concentrations. Since toxic metal cations like Pb2+ are known to alter Ca(2+)-dependent processes, the present study was initiated to study the effects of Pb2+ on inositol 1,4,5-trisphosphate (InsP3) and inositol 1,3,4,5-tetrakisphosphate (InsP4) receptor binding and InsP3-mediated Ca(2+)-release. Rat cerebellar membrane and microsomal fractions were incubated with various concentrations of Pb2+ (0.01-100 microM). Pb2+ significantly stimulated [3H]-InsP3 and [3H]-InsP4 receptor binding (EC50 22.7 and 13.5 microM respectively) as a function of metal concentrations. However, InsP3-mediated Ca2+ release, determined by measuring the changes in fluorescence intensity of Fura-2, was significantly inhibited by varying concentrations of Pb2+. Re-uptake of Ca2+ into the microsomes was also inhibited by Pb2+. A significant inhibition of microsomal Ca(2+)-pump by micromolar concentration of Pb2+ was also observed. ATP at 5-1000 microM concentration range inhibited [3H]-InsP3 and [3H]-InsP4 binding to the specific receptors. [3H]-InsP4 receptor binding was more sensitive to ATP inhibition as compared to [3H]-InsP3 receptor binding. Furthermore, varying concentrations of ATP also inhibited Pb(2+)-mediated increase in [3H]-InsP3 and [3H]-InsP4 receptor binding. The kinetic analysis of ATP effect on Pb(2+)-stimulated [3H]-InsP4 receptor binding revealed non-competitive type of interaction. The results of the present study suggest that Pb2+ may be increasing the binding of [3H]-InsP3 and [3H]-InsP4 to the specific receptors by modulating the conformation of the receptor sites. ATP may be playing a protective role in Pb2+ induced alteration of the receptor sites. | lld:pubmed |
| pubmed-article:7971730 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7971730 | pubmed:language | eng | lld:pubmed |
| pubmed-article:7971730 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7971730 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:7971730 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7971730 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7971730 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7971730 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7971730 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7971730 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7971730 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7971730 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7971730 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7971730 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:7971730 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:7971730 | pubmed:issn | 0901-9928 | lld:pubmed |
| pubmed-article:7971730 | pubmed:author | pubmed-author:DesaiahDD | lld:pubmed |
| pubmed-article:7971730 | pubmed:author | pubmed-author:RajannaBB | lld:pubmed |
| pubmed-article:7971730 | pubmed:author | pubmed-author:PentyalaS NSN | lld:pubmed |
| pubmed-article:7971730 | pubmed:author | pubmed-author:ChettyC SCS | lld:pubmed |
| pubmed-article:7971730 | pubmed:author | pubmed-author:RayT PTP | lld:pubmed |
| pubmed-article:7971730 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:7971730 | pubmed:volume | 75 | lld:pubmed |
| pubmed-article:7971730 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:7971730 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:7971730 | pubmed:pagination | 17-22 | lld:pubmed |
| pubmed-article:7971730 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
| pubmed-article:7971730 | pubmed:meshHeading | pubmed-meshheading:7971730-... | lld:pubmed |
| pubmed-article:7971730 | pubmed:meshHeading | pubmed-meshheading:7971730-... | lld:pubmed |
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| pubmed-article:7971730 | pubmed:meshHeading | pubmed-meshheading:7971730-... | lld:pubmed |
| pubmed-article:7971730 | pubmed:meshHeading | pubmed-meshheading:7971730-... | lld:pubmed |
| pubmed-article:7971730 | pubmed:meshHeading | pubmed-meshheading:7971730-... | lld:pubmed |
| pubmed-article:7971730 | pubmed:meshHeading | pubmed-meshheading:7971730-... | lld:pubmed |
| pubmed-article:7971730 | pubmed:meshHeading | pubmed-meshheading:7971730-... | lld:pubmed |
| pubmed-article:7971730 | pubmed:meshHeading | pubmed-meshheading:7971730-... | lld:pubmed |
| pubmed-article:7971730 | pubmed:meshHeading | pubmed-meshheading:7971730-... | lld:pubmed |
| pubmed-article:7971730 | pubmed:meshHeading | pubmed-meshheading:7971730-... | lld:pubmed |
| pubmed-article:7971730 | pubmed:meshHeading | pubmed-meshheading:7971730-... | lld:pubmed |
| pubmed-article:7971730 | pubmed:year | 1994 | lld:pubmed |
| pubmed-article:7971730 | pubmed:articleTitle | Lead alters inositol polyphosphate receptor activities: protection by ATP. | lld:pubmed |
| pubmed-article:7971730 | pubmed:affiliation | Department of Neurology, University of Mississippi Medical Center, Jackson 39216. | lld:pubmed |
| pubmed-article:7971730 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:7971730 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
