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Publication : Cutting edge: Transcriptional activity of NFATc1 is enhanced by the Pim-1 kinase.

First Author  Rainio EM Year  2002
Journal  J Immunol Volume  168
Issue  4 Pages  1524-7
PubMed ID  11823475 Mgi Jnum  J:74465
Mgi Id  MGI:2158519 Doi  10.4049/jimmunol.168.4.1524
Citation  Rainio EM, et al. (2002) Cutting Edge: Transcriptional Activity of NFATc1 Is Enhanced by the Pim-1 Kinase. J Immunol 168(4):1524-7
abstractText  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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