dlk modulates mitogen-activated protein kinase signaling to allow or prevent differentiation |
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Authors: | Ruiz-Hidalgo María José Gubina Elena Tull Lori Baladrón Victoriano Laborda Jorge |
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Institution: | Laboratory of Immunobiology, Division of Monoclonal Antibodies, Center for Biologics Evaluation and Research, 1401 Rockville Pike, HFM 564, Rockville, Maryland, USA. |
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Abstract: | The EGF-like membrane protein dlk plays a crucial role in the control of cell differentiation. Overexpression of the protein prevents, whereas inhibition of its expression increases, adipocyte differentiation of 3T3-L1 cells in response to Insulin-like Growth Factor I (IGF-1) or insulin. We have investigated whether dlk modulates the signaling pathways known to control this process. We found that the levels of dlk expression modulated signaling through the IGF-1 receptor, causing changes in the activation levels and kinetics of Extracellular-Regulated Kinase/Mitogen-Activated Protein Kinase (ERK/MAPK) that correlated with differentiation outcome. These changes occurred in response to IGF-1 or insulin but not in response to Epidermal Growth Factor. However, the levels of expression of IGF-1 receptor, or the activation of Insulin Receptor Substrate-1 in response to IGF-1, were not affected by the levels of dlk expression. Therefore, dlk appears to modulate ERK/MAPK signaling in response to specific differentiation signals. |
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Keywords: | dlk cell differentiation ERK/MAPK signaling adipogenesis cell to cell communication |
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