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Molecular and Cellular Biology, August 2006, p. 5663-5674, Vol. 26, No. 15
0270-7306/06/$08.00+0     doi:10.1128/MCB.02095-05
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Nuclear Jak2 and Transcription Factor NF1-C2: a Novel Mechanism of Prolactin Signaling in Mammary Epithelial Cells

Jeanette Nilsson, Gunnar Bjursell, and Marie Kannius-Janson*

Department of CMB/Molecular Biology, Box 462, S-405 30 Göteborg, Sweden

Received 28 October 2005/ Returned for modification 2 December 2005/ Accepted 5 May 2006

The classical mechanism by which prolactin transduces its signal in mammary epithelial cells is by activation of cytosolic signal transducer and activator of transcription 5 (Stat5) via a plasma membrane-associated prolactin receptor-Janus kinase 2 (Jak2) complex. Here we describe an alternative pathway through which prolactin via Jak2 localized in the nucleus activates the transcription factor nuclear factor 1-C2 (NF1-C2). Previous reports have demonstrated a nuclear localization of Jak2, but the physiologic importance of nuclear Jak2 has not been clear. We demonstrate that nuclear Jak2 regulates the amount of active NF1-C2 through tyrosine phosphorylation and proteasomal degradation. Our data also demonstrate a link between prolactin and p53 as well as the milk gene carboxyl ester lipase through nuclear Jak2 and NF1-C2. Hence, we describe a novel pathway through which nuclear Jak2 is subject to regulation by prolactin in mammary epithelial cells.

* Corresponding author. Mailing address: Department of CMB/Molecular Biology, Box 462, S-405 30 Göteborg, Sweden. Phone: 46 31 7733805. Fax: 46 31 7733801. E-mail: marie.kannius{at}molbio.gu.se.

Molecular and Cellular Biology, August 2006, p. 5663-5674, Vol. 26, No. 15
0270-7306/06/$08.00+0     doi:10.1128/MCB.02095-05
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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