| http://purl.uniprot.org/citations/16875859 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/16875859 | http://www.w3.org/2000/01/rdf-schema#comment | "Four structurally different protein phosphatases (PPs) inhibitors - fluoride, calyculin A, okadaic acid and cantharidin--were tested for their ability to modulate unidirectional Na(+) influx in rat red blood cells. Erythrocytes were incubated at 37 degrees C in isotonic and hypertonic media containing 1 mM ouabain and (22)Na in the absence or presence of PP inhibitors. Exposure of the cells to 20 mM fluoride or 50 nM calyculin A for 1 h under isosmotic conditions caused a significant stimulation of Na(+) influx, whereas addition of 200 microM cantharidin or 100 nM okadaic acid had no effect. After 2 h of treatment, however, all these PPs blockers significantly enhanced Na(+) transport in rat erythrocytes. Selective inhibitors of PP-1 and PP-2A types, calyculin A, cantharidin and okadaic acid, produced similar ( approximately 1.2-1.4-fold) stimulatory effects on Na(+) influx in the cells. Activation of Na(+) influx was unchanged with increasing calyculin A concentration from 50 to 200 nM. No additive stimulation of Na(+) influx was observed when the cells were treated with combination of 20 mM fluoride and 50 nM calyculin A. Na(+) influx induced by PPs blockers was inhibited by 1 mM amiloride and 200 muM bumetanide approximately in the equal extent, indicating the involvement of Na(+)/H(+) exchange and Na-K-2Cl cotransport in sodium transport through rat erythrocytes membrane. Activation of Na(+) transport in the cells induced by calyculin A and fluoride was associated with increase of intracellular Na(+) content. Shrinkage of the rat erythrocytes resulted in 2-fold activation of Na(+) influx. All tested PPs inhibitors additionally activated the Na(+) influx by 70-100% above basal shrinkage-induced level. Amiloride and bumetanide have diminished both the shrinkage-induced and PPs-inhibitors-induced Na(+) influxes. Thus, our observations clearly indicate that activities of Na(+)/H(+) exchanger and Na-K-2Cl cotransporter in rat erythrocytes are regulated by protein phosphatases and stimulated when protein dephosphorylation is inhibited."xsd:string |
| http://purl.uniprot.org/citations/16875859 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.cbpb.2006.06.005"xsd:string |
| http://purl.uniprot.org/citations/16875859 | http://purl.uniprot.org/core/author | "Agalakova N.I."xsd:string |
| http://purl.uniprot.org/citations/16875859 | http://purl.uniprot.org/core/author | "Gusev G.P."xsd:string |
| http://purl.uniprot.org/citations/16875859 | http://purl.uniprot.org/core/author | "Ivanova T.I."xsd:string |
| http://purl.uniprot.org/citations/16875859 | http://purl.uniprot.org/core/date | "2006"xsd:gYear |
| http://purl.uniprot.org/citations/16875859 | http://purl.uniprot.org/core/name | "Comp Biochem Physiol B Biochem Mol Biol"xsd:string |
| http://purl.uniprot.org/citations/16875859 | http://purl.uniprot.org/core/pages | "60-67"xsd:string |
| http://purl.uniprot.org/citations/16875859 | http://purl.uniprot.org/core/title | "Activation of sodium transport in rat erythrocytes by inhibition of protein phosphatases 1 and 2A."xsd:string |
| http://purl.uniprot.org/citations/16875859 | http://purl.uniprot.org/core/volume | "145"xsd:string |
| http://purl.uniprot.org/citations/16875859 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/16875859 |
| http://purl.uniprot.org/citations/16875859 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/16875859 |
| http://purl.uniprot.org/uniprot/#_A0A0G2JVX9-mappedCitation-16875859 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/16875859 |
| http://purl.uniprot.org/uniprot/#_D3ZQR3-mappedCitation-16875859 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/16875859 |
| http://purl.uniprot.org/uniprot/#_A0A8I5ZX87-mappedCitation-16875859 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/16875859 |
| http://purl.uniprot.org/uniprot/#_A6I3J8-mappedCitation-16875859 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/16875859 |
| http://purl.uniprot.org/uniprot/#_A6I3J9-mappedCitation-16875859 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/16875859 |
| http://purl.uniprot.org/uniprot/#_A6I3K1-mappedCitation-16875859 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/16875859 |
| http://purl.uniprot.org/uniprot/#_A6I3K3-mappedCitation-16875859 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/16875859 |
| http://purl.uniprot.org/uniprot/#_A6I3K4-mappedCitation-16875859 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/16875859 |
| http://purl.uniprot.org/uniprot/#_A6I3K8-mappedCitation-16875859 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/16875859 |
| http://purl.uniprot.org/uniprot/#_A0A8I6A885-mappedCitation-16875859 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/16875859 |
| http://purl.uniprot.org/uniprot/#_A6IVT2-mappedCitation-16875859 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/16875859 |
| http://purl.uniprot.org/uniprot/#_P62716-mappedCitation-16875859 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/16875859 |