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Molecular and Cellular Biology, April 2002, p. 2586-2597, Vol. 22, No. 8
0270-7306/02/$04.00+0     DOI: 10.1128/MCB.22.8.2586-2597.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Cripto-1 Activates Nodal- and ALK4-Dependent and -Independent Signaling Pathways in Mammary Epithelial Cells

Caterina Bianco,1 Heather B. Adkins,1,2 Christian Wechselberger,1 Masaharu Seno,3 Nicola Normanno,4 Antonella De Luca,4 Youping Sun,1 Nadia Khan,1 Nicholas Kenney,5 Andreas Ebert,6 Kevin P. Williams,2 Michele Sanicola,2* and David S. Salomon1*

Tumor Growth Factor Section, Basic Research Laboratory, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892,1 Department of Bioscience and Biotechnology, Faculty of Engineering, Okayama University, Okayama 700-8530, Japan,3 Oncologia Sperimentale D, ITN-Fondazione Pascale, 80131 Naples, Italy,4 Department of Biological Science, Hampton University, Hampton, Virginia 23668,5 Department of Obstetrics and Gynecology, Free University of Berlin, Berlin, Germany,6 Biogen Inc., Cambridge, Massachusetts 021422

Received 24 August 2001/ Returned for modification 19 October 2001/ Accepted 15 January 2002

Cripto-1 (CR-1), an epidermal growth factor-CFC (EGF-CFC) family member, has a demonstrated role in embryogenesis and mammary gland development and is overexpressed in several human tumors. Recently, EGF-CFC proteins were implicated as essential signaling cofactors for Nodal, a transforming growth factor ß family member whose expression has previously been defined as embryo specific. To identify a receptor for CR-1, a human brain cDNA phage display library was screened using CR-1 protein as bait. Phage inserts with identity to ALK4, a type I serine/threonine kinase receptor for Activin, were identified. CR-1 binds to cell surface ALK4 expressed on mammalian epithelial cells in fluorescence-activated cell sorter analysis, as well as by coimmunoprecipitation. Nodal is coexpressed with mouse Cr-1 in the mammary gland, and CR-1 can phosphorylate the transcription factor Smad-2 in EpH-4 mammary epithelial cells only in the presence of Nodal and ALK4. In contrast, CR-1 stimulation of mitogen-activated protein kinase and AKT in these cells is independent of Nodal and ALK4, suggesting that CR-1 may modulate different signaling pathways to mediate its different functional roles.

* Corresponding author. Mailing address for David S. Salomon: TGFS, BRL, NCI, NIH, Bldg. 10 Rm. 5B39, 9000 Rockville Pike, Bethesda, MD 20892. Phone: (301) 496-9536. Fax: (301) 402-8656. E-mail: davetgfa{at}helix.nih.gov. Mailing address for Michele Sanicola: Biogen Inc., Cambridge, MA 02142. Phone: (617) 673-3307. Fax: (617) 679-2617. E-mail: michele_sanicola{at}biogen.com.

Molecular and Cellular Biology, April 2002, p. 2586-2597, Vol. 22, No. 8
0022-538X/02/$04.00+0     DOI: 10.1128/MCB.22.8.2586-2597.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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