A1 Vertaisarvioitu alkuperäisartikkeli tieteellisessä lehdessä
Cutting edge: Transcriptional activity of NFATc1 is enhanced by the Pim-1 kinase
Tekijät: Rainio EM, Sandholm J, Koskinen PJ
Kustantaja: AMER ASSOC IMMUNOLOGISTS
Julkaisuvuosi: 2002
Journal: Journal of Immunology
Tietokannassa oleva lehden nimi: JOURNAL OF IMMUNOLOGY
Lehden akronyymi: J IMMUNOL
Vuosikerta: 168
Numero: 4
Aloitussivu: 1524
Lopetussivu: 1527
Sivujen määrä: 4
ISSN: 0022-1767
DOI: https://doi.org/10.4049/jimmunol.168.4.1524
Tiivistelmä
Pim-1 is an oncogenic serine/threonine kinase implicated in cytokine-induced signal transduction and in development of lymphoid malignancies. However, its precise function as well as physiological substrates have remained unknown. In this study we demonstrate that Pim-1 can physically interact with the NFATc1 transcription factor and phosphorylate it in vitro on several serine residues. In contrast to previously recognized NFATc kinases, wild-type Pim-1 enhances NFATc-dependent transactivation and IL-2 production in Jurkat T cells, while kinase-deficient Pim-1 mutants inhibit them in a dominant negative fashion. Our results reveal a novel, phosphorylation-dependent regulatory mechanism targeting NFATc1 through which Pim-1 acts as a downstream effector of Ras to facilitate IL-2-dependent proliferation and/or survival of lymphoid cells.
Pim-1 is an oncogenic serine/threonine kinase implicated in cytokine-induced signal transduction and in development of lymphoid malignancies. However, its precise function as well as physiological substrates have remained unknown. In this study we demonstrate that Pim-1 can physically interact with the NFATc1 transcription factor and phosphorylate it in vitro on several serine residues. In contrast to previously recognized NFATc kinases, wild-type Pim-1 enhances NFATc-dependent transactivation and IL-2 production in Jurkat T cells, while kinase-deficient Pim-1 mutants inhibit them in a dominant negative fashion. Our results reveal a novel, phosphorylation-dependent regulatory mechanism targeting NFATc1 through which Pim-1 acts as a downstream effector of Ras to facilitate IL-2-dependent proliferation and/or survival of lymphoid cells.
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