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M300311200v1
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Papers In Press, published online ahead of print March 5, 2003
J. Biol. Chem, 10.1074/jbc.M300311200
Submitted on January 10, 2003
Revised on March 3, 2003
Accepted on March 4, 2003

A winged helix forkhead (FOXD2) tunes sensitivity to cAMP in T lymphocytes through regulation of PKA RIalpha

Carl Christian Johansson, Maria K. Dahle, Sandra Rodrigo Blomqvist, Line M. Gronning, Elinar M. Aandahl, Sven Enerbäck, and Kjetil Tasken

Medical Biochemistry, University of Oslo, Blindern, Oslo N-0317

Corresponding Author: kjetil.tasken{at}basalmed.uio.no

Forkhead/winged helix (FOX) transcription factors are essential for control of the cell cycle and metabolism. Here, we show that spleens from Mf2-/- (FOXD2-/-) mice have reduced mRNA (50%) and protein (35%) levels of the RIalpha subunit of the cAMP-dependent protein kinase (PKA). In T cells from Mf2-/- mice, reduced levels of RIalpha translates functionally into approximately 2-fold less sensitivity to cAMP-mediated inhibition of proliferation triggered through the T cell receptor/CD3 complex. In Jurkat T cells, FOXD2 over-expression increased the endogenous levels of RIalpha through induction of the RIalpha1b promoter. FOXD2 over-expression also increased the sensitivity of the promoter to cAMP. Finally, co-expression experiments demonstrated that PKBalpha/Akt1 work together with FOXD2 in order to induce the RIĄ1b promoter (10-fold) and increase endogenous RIalpha protein levels further. Taken together, our data indicate that FOXD2 is a physiological regulator of the RIalpha1b promoter in vivo working synergistically with PKB in order to induce PKA RIalpha expression, which increases cAMP sensitivity and sets the threshold for cAMP-mediated negative modulation of T cell activation.


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