| First Author | Enomoto K | Year | 1996 |
| Journal | Biol Signals | Volume | 5 |
| Issue | 1 | Pages | 9-21 |
| PubMed ID | 8739319 | Mgi Jnum | J:36938 |
| Mgi Id | MGI:84351 | Doi | 10.1159/000109169 |
| Citation | Enomoto K, et al. (1996) Expression cloning and signal transduction pathway of P2U receptor in mammary tumor cells. Biol Signals 5(1):9-21 |
| abstractText | Extracellularly applied ATP, UTP and UDP induce a transient increase in the intracellular Ca2+ concentration of mammary cells via a P2U receptor. The P2U receptor in the mammary tumor cell line MMT060562 was cloned and expressed in the human leukemia cell line K-562. The deduced amino acid sequence of the mammary tumor cell P2U receptor was 98% homologous with that of mouse NG108-15 cells. It was a member of the superfamily of GTP-binding-protein-coupled receptors. ATP and UTP induced the increase in the intracellular concentrations of Ca2+ and inositol-1,4,5-trisphosphate in both mammary tumor cells and P2U-receptor-expressed K562 cells. Dose-response curves on the production of inositol-1,4,5-trisphosphate and Ca2+ by ATP and UTP were consistently similar. Injection of GTP enhanced the ATP-induced outward current and injection of GTP gamma S induced a repetitive outward current. Both pertussis and cholera toxins did not affect ATP-induced calcium increase. It was suggested that the P2U receptor coupled with pertussis- and cholera-toxin-insensitive GTP-binding proteins and activated phosphoinositide turnover. |
