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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概要

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• In this study, we established rat 3Y1 embryo cell lines expressing FosB and ΔFosB as fusion proteins (ER-FosB, ER-ΔFosB) 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-ΔFosB, 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-ΔFosB and ER-FosB after one round of cell division triggered by estrogen administration. The cells expressing ER-ΔFosB 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-ΔFosB, 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.

• 社団法人 日本生化学会の論文

著者

• Nakabeppu Yusaku

  Division Of Neurofunctional Genomics Department Of Immunobiology And Neuroscience Medical Institute

• Sakumi Kunihiko

  Division of Neurofunctional Genomics, Medical Institute of Bioregulation, Kyushu University, and CRE

• Kadoya Toshihiko

  Pharmaceutical Laboratory Kirin Brewery Co. Ltd

• Miura Tomofumi

  Division of Gastroenterology and Hepatology, Nagaoka Red Cross Hospital, Japan

• Miura Tomofumi

  Division of Neurofunctional Genomics, Medical Institute of Bioregulation, Kyushu University

• Nishioka Tomoko

  Division of Neurofunctional Genomics, Medical Institute of Bioregulation, Kyushu University

• Tahara Kazuki

  Division of Neurofunctional Genomics, Medical Institute of Bioregulation, Kyushu University

• Horie Hidenori

  Advanced Research Center for Biological Science, Waseda University

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