par Pouillon, Valérie 
;Hascakova-Bartova, Romana;Pajak, Bernard ;Adam, Emmanuelle ;Bex, Françoise ;Dewaste, Valérie ;Van Lint, Carine ;Leo, Oberdan ;Erneux, Christophe ;Schurmans, Stéphane
Référence Nature immunology, 4, 11, page (1136-1143)
Publication Publié, 2003
;Hascakova-Bartova, Romana;Pajak, Bernard ;Adam, Emmanuelle ;Bex, Françoise ;Dewaste, Valérie ;Van Lint, Carine ;Leo, Oberdan ;Erneux, Christophe ;Schurmans, Stéphane Référence Nature immunology, 4, 11, page (1136-1143)
Publication Publié, 2003
Article révisé par les pairs
| Résumé : | Inositol 1,4,5-trisphosphate (Ins(1,4,5)P(3)) is phosphorylated by Ins(1,4,5)P(3) 3-kinase, generating inositol 1,3,4,5-tetrakisphosphate (Ins(1,3,4,5)P(4)). The physiological function of Ins(1,3,4,5)P(4) is still unclear, but it has been reported to be a potential modulator of calcium mobilization. Disruption of the gene encoding the ubiquitously expressed Ins(1,4,5)P(3) 3-kinase isoform B (Itpkb) in mice caused a severe T cell deficiency due to major alterations in thymocyte responsiveness and selection. However, we were unable to detect substantial defects in Ins(1,4,5)P(3) amounts or calcium mobilization in Itpkb(-/-) thymocytes. These data indicate that Itpkb and Ins(1,3,4,5)P(4) define an essential signaling pathway for T cell precursor responsiveness and development. |
