Although interleukin 1 (IL-1) functions have been extensively characterized, the mechanisms by which IL-l signals are transduced from the plasma membrane to the nucleus are less known. Recent evidence indicates that phosphatidylinositol 3-kinase (PI3-kinase) could be activated by a direct association with the activated IL-1 receptor. In this study we analyzed the effects of IL-1 on the intracellular distribution of PI3-kinase in wild-type Saos-2 human osteosarcoma cells, and in cell clones overexpressing type I IL-I receptor (IL-1RI), PI3-kinase intracellular distribution displays two distinct patterns, In quiescent cells, PI3-kinase is distributed through the cytoplasm, although a portion is present in the nucleus; following stimulation with IL-1, PI3-kinase is redistributed, increasing in the nuclear compartment. Both immunoblotting and immunofluorescence data indicate that IL-1 causes a rapid and transient translocation of PIS-kinase from the cytoplasm to the nucleus, This phenomenon is prevented by PI3-kinase inhibitors, suggesting that the maintenance of PI3-kinase activity is essential for IL-l-induced translocation, Indeed, in cell clones stably transfected with Y479F receptor mutant, in which the binding of the enzyme to the activated receptor is blocked, IL-l-induced PI3-kinase translocation to the nucleus is completely prevented, These data suggest that PI3-kinase translocation to the nucleus upon IL-1R activation is an early event in IL-l signaling mechanism, and may be involved in transcriptional activation.

Phosphatidylinositol 3-kinase translocation to the nucleus is induced by interleukin 1 and prevented by mutation of interleukin 1 receptor in human osteosarcoma Saos-2 cells / A., Bavelloni; S., Santi; A., Sirri; Riccio, Massimo; I., Faenza; N., Zini; S., Cecchi; A., Ferri; P., Auron; N. M., Maraldi; Marmiroli, Sandra. - In: JOURNAL OF CELL SCIENCE. - ISSN 0021-9533. - STAMPA. - 112:(1999), pp. 631-640.

Phosphatidylinositol 3-kinase translocation to the nucleus is induced by interleukin 1 and prevented by mutation of interleukin 1 receptor in human osteosarcoma Saos-2 cells

RICCIO, Massimo;MARMIROLI, Sandra
1999-01-01

Abstract

Although interleukin 1 (IL-1) functions have been extensively characterized, the mechanisms by which IL-l signals are transduced from the plasma membrane to the nucleus are less known. Recent evidence indicates that phosphatidylinositol 3-kinase (PI3-kinase) could be activated by a direct association with the activated IL-1 receptor. In this study we analyzed the effects of IL-1 on the intracellular distribution of PI3-kinase in wild-type Saos-2 human osteosarcoma cells, and in cell clones overexpressing type I IL-I receptor (IL-1RI), PI3-kinase intracellular distribution displays two distinct patterns, In quiescent cells, PI3-kinase is distributed through the cytoplasm, although a portion is present in the nucleus; following stimulation with IL-1, PI3-kinase is redistributed, increasing in the nuclear compartment. Both immunoblotting and immunofluorescence data indicate that IL-1 causes a rapid and transient translocation of PIS-kinase from the cytoplasm to the nucleus, This phenomenon is prevented by PI3-kinase inhibitors, suggesting that the maintenance of PI3-kinase activity is essential for IL-l-induced translocation, Indeed, in cell clones stably transfected with Y479F receptor mutant, in which the binding of the enzyme to the activated receptor is blocked, IL-l-induced PI3-kinase translocation to the nucleus is completely prevented, These data suggest that PI3-kinase translocation to the nucleus upon IL-1R activation is an early event in IL-l signaling mechanism, and may be involved in transcriptional activation.
112
631
640
Phosphatidylinositol 3-kinase translocation to the nucleus is induced by interleukin 1 and prevented by mutation of interleukin 1 receptor in human osteosarcoma Saos-2 cells / A., Bavelloni; S., Santi; A., Sirri; Riccio, Massimo; I., Faenza; N., Zini; S., Cecchi; A., Ferri; P., Auron; N. M., Maraldi; Marmiroli, Sandra. - In: JOURNAL OF CELL SCIENCE. - ISSN 0021-9533. - STAMPA. - 112:(1999), pp. 631-640.
A., Bavelloni; S., Santi; A., Sirri; Riccio, Massimo; I., Faenza; N., Zini; S., Cecchi; A., Ferri; P., Auron; N. M., Maraldi; Marmiroli, Sandra
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11380/797696
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