Nuclear Jak2 and Transcription Factor Nf1-c2: a Novel Mechanism of Prolactin Signaling in Mammary Epithelial Cells.
From: Department of CMB/Molecular Biology, Box 462, S-405 30 Göteborg, Sweden.
Molecular and cellular biology
- Publish Date: Aug 2006
- ISSN: 0270-7306
- Volume: 26
- Issue: 15
- Pages: 5663-74
- Medium: Print
- Language: English
- Citation (JAMA): Nilsson Jeanette, Bjursell Gunnar, Kannius-Janson Marie, et al. Nuclear Jak2 and Transcription Factor Nf1-c2: a Novel Mechanism of Prolactin Signaling in Mammary Epithelial Cells.. Mol. Cell. Biol. Aug 2006;26:5663-74
Abstract
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.
Mesh Headings (Keywords): Animals, Cell Line, Cell Nucleus, Epithelial Cells, Humans, Janus Kinase 2, Lipase, Mammary Glands, Human, Mice, NFI Transcription Factors, Phosphorylation, Prolactin, Proteasome Endopeptidase Complex, Protein-Tyrosine Kinases, Proto-Oncogene Proteins, RNA Interference, Signal Transduction, Tumor Suppressor Protein p53, Two-Hybrid System Techniques, Tyrosine
Check for Full Text / PubMed Unique Identifier (PMID): 16847321
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