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J Biochem. 2002 May;131(5):653-61.

FosB gene products trigger cell proliferation and morphological alteration with an increased expression of a novel processed form of galectin-1 in the rat 3Y1 embryo cell line.

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  • 1Division of Neurofunctional Genomics, Medical Institute of Bioregulation, Kyushu University, and CREST, Japan Science and Technology Corporation, Maidashi, Higashi-ku, Fukuoka 812-8582.


In this study, we established rat 3Y1 embryo cell lines expressing FosB and DeltaFosB as fusion proteins (ER-FosB, ER-DeltaFosB) with the ligand-binding domain of human estrogen receptor (ER). The binding of estrogen to the fusion proteins resulted in their nuclear translocation. After estrogen administration, exponentially growing cells expressing ER-DeltaFosB, and to a lesser extent ER-FosB, underwent morphological alteration from the flat fibroblastic shape to an extended bipolar shape, and ceased proliferating. Such morphological alteration was also induced in quiescent cells expressing ER-DeltaFosB and ER-FosB after one round of cell division triggered by estrogen administration. The cells expressing ER-DeltaFosB changed shape frequently, and the content of F-actin in the cytoplasm detected by binding of Alexa 488-phalloidin significantly decreased after the morphological alteration. By two-dimensional gel electrophoresis analysis of cellular proteins from the cells expressing ER-DeltaFosB, we identified several proteins whose expression either increased or decreased after estrogen administration. Two of these proteins were identified from their amino acid sequences as novel processed form of galectin-1.

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