Display Settings:

Format

Send to:

Choose Destination
See comment in PubMed Commons below
Exp Cell Res. 2002 Apr 1;274(2):178-88.

dlk modulates mitogen-activated protein kinase signaling to allow or prevent differentiation.

Author information

  • 1Laboratory of Immunobiology, Division of Monoclonal Antibodies, Center for Biologics Evaluation and Research, 1401 Rockville Pike, HFM 564, Rockville, Maryland, USA.

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.

Copyright 2002 Elsevier Science (USA).

PMID:
11900478
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Write to the Help Desk