National Academy of Sciences, Proceedings of the National Academy of Sciences, 4(99), p. 2175-2180, 2002
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Studies of SOCS-1 -deficient mice have implicated Socs-1 in the suppression of JAK-STAT (Janus tyrosine kinase-signal transducers and activators of transcription) signaling and T cell development. It has been suggested that the levels of Socs-1 protein may be regulated through the proteasome pathway. Here we show that Socs-1 interacts with members of the Pim family of serine/threonine kinases in thymocytes. Coexpression of the Pim kinases with Socs-1 results in phosphorylation and stabilization of the Socs-1 protein. The protein levels of Socs-1 are significantly reduced in the Pim-1 −/− , Pim-2 −/− mice as compared with wild-type mice. Similar to Socs-1 −/− mice, thymocytes from Pim-1 −/− , Pim-2 −/− mice showed prolonged Stat6 phosphorylation upon IL-4 stimulation. These data suggest that the Pim kinases may regulate cytokine-induced JAK-STAT signaling through modulation of Socs-1 protein levels.