دورية
Agonists Cause Nuclear Translocation of Phosphatidylinositol 3-Kinase γ
| العنوان: | Agonists Cause Nuclear Translocation of Phosphatidylinositol 3-Kinase γ |
|---|---|
| المؤلفون: | Metjian, Ara, Roll, Richard L., Ma, Alice D., Abrams, Charles S. |
| المصدر: | Journal of Biological Chemistry; September 1999, Vol. 274 Issue: 39 p27943-27947, 5p |
| مستخلص: | In hematopoietic cells, the signals initiated by activation of the phosphoinositide 3-kinase (PI3K) family have been implicated in cell proliferation and survival, membrane and cytoskeletal reorganization, chemotaxis, and the neutrophil respiratory burst. Of the four isoforms of human PI3K that phosphorylate phosphatidylinositol 4,5-bisphosphate, only p110γ (or PI3Kγ) is associated with the regulatory subunit, p101, and is stimulated by G protein βγ heterodimers. We performed immunolocalization of transfected p110γ in HepG2 cells and found that, under resting conditions, p110γ was present in a diffuse cytoplasmic pattern, but translocated to the cell nucleus after serum stimulation. Serum-stimulated p110γ translocation was inhibited by pertussis toxin and could also be induced by overexpression of Gβγ in the absence of serum. In addition, we found that deletion of the amino-terminal 33 residues of p110γ had no effect on association with p101 or on its agonist-regulated translocation, but truncation of the amino-terminal 82 residues yielded a p110γ variant that did not associate with p101 and was constitutively localized in the nucleus. This finding implies that the intracellular localization of p110γ is regulated by p101 as well as Gβγ. The effect of PI3Kγ in the nucleus is an area of active investigation. |
| قاعدة البيانات: | Supplemental Index |
Full Text Finder | تدمد: | 00219258 1083351X |
|---|---|
| DOI: | 10.1074/jbc.274.39.27943 |