Interaction of suppressor of cytokine signalling 3 with cavin-1 links SOCS3 function and cavin-1 stability

Jamie J. L. Williams (), Nasser Alotaiq, William Mullen, Richard Burchmore, Libin Liu, George S. Baillie, Fred Schaper, Paul F. Pilch and Timothy M. Palmer ()
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Jamie J. L. Williams: University of Bradford
Nasser Alotaiq: University of Glasgow
William Mullen: University of Glasgow
Richard Burchmore: University of Glasgow
Libin Liu: Boston University School of Medicine
George S. Baillie: University of Glasgow
Fred Schaper: Otto-von-Guericke-University Magdeburg
Paul F. Pilch: Boston University School of Medicine
Timothy M. Palmer: University of Bradford

Nature Communications, 2018, vol. 9, issue 1, 1-17

Abstract: Abstract Effective suppression of JAK–STAT signalling by the inducible inhibitor “suppressor of cytokine signalling 3” (SOCS3) is essential for limiting signalling from cytokine receptors. Here we show that cavin-1, a component of caveolae, is a functionally significant SOCS3-interacting protein. Biochemical and confocal imaging demonstrate that SOCS3 localisation to the plasma membrane requires cavin-1. SOCS3 is also critical for cavin-1 stabilisation, such that deletion of SOCS3 reduces the expression of cavin-1 and caveolin-1 proteins, thereby reducing caveola abundance in endothelial cells. Moreover, the interaction of cavin-1 and SOCS3 is essential for SOCS3 function, as loss of cavin-1 enhances cytokine-stimulated STAT3 phosphorylation and abolishes SOCS3-dependent inhibition of IL-6 signalling by cyclic AMP. Together, these findings reveal a new functionally important mechanism linking SOCS3-mediated inhibition of cytokine signalling to localisation at the plasma membrane via interaction with and stabilisation of cavin-1.

Date: 2018
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DOI: 10.1038/s41467-017-02585-y

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