Diego Maritano1, 2, 7, Michelle L Sugrue2, 6, 7, Silvia Tininini2, Sarah Dewilde1, Birgit Strobl3, 6, XinPing Fu2, Victoria Murray-Tait2, Roberto Chiarle4, 5
& Valeria Poli1, 2, 51
Department of Genetics, Biology and Biochemistry, University of Turin, 10126
Turin, Italy.
2
School of Life Sciences, Wellcome Trust Biocentre, University of Dundee, Dow Street, DD1 5EH
Scotland.
3
Cancer Research United Kingdom London Research Institute, 44 Lincoln's Inn Fields, London
WC2A 3PX, UK.
4
Department of Biomedical Sciences and Human Oncology, University of Turin, Turin, Italy.
5
Center for Experimental Research and Medical Studies, Turin, Italy.
6
Present addresses: Division of Endocrinology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts
02215, USA (M.L.S.) and Institute of Animal Breeding and Genetics, Veterinaerplatz, A-1210
Vienna, Austria (B.S.).
7
These authors contributed equally to this work.
Correspondence should be addressed to Valeria Poli valeria.poli@unito.it
and 
have unique and specific functions
and the truncated STAT3
, generally thought to act as a dominant negative factor. To assess their relative functions, we ablated the expression of either isoform by gene targeting. We show here that in vivo STAT3
