The Soluble Heparin-Binding EGF-Like Growth Factor Stimulates EGF Receptor Trafficking to the Nucleus.
| Autor: | Korotkevych NV; Molecular Immunology Department, Palladin Institute of Biochemistry of the National Academy of Sciences of Ukraine, Kyiv, Ukraine., Labyntsev AJ; Molecular Immunology Department, Palladin Institute of Biochemistry of the National Academy of Sciences of Ukraine, Kyiv, Ukraine., Kolybo DV; Molecular Immunology Department, Palladin Institute of Biochemistry of the National Academy of Sciences of Ukraine, Kyiv, Ukraine., Komisarenko SV; Molecular Immunology Department, Palladin Institute of Biochemistry of the National Academy of Sciences of Ukraine, Kyiv, Ukraine. |
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| Jazyk: | angličtina |
| Zdroj: | PloS one [PLoS One] 2015 May 27; Vol. 10 (5), pp. e0127887. Date of Electronic Publication: 2015 May 27 (Print Publication: 2015). |
| DOI: | 10.1371/journal.pone.0127887 |
| Abstrakt: | Most ligands of epidermal growth factor receptor (EGFR) have the ability to induce EGFR translocation into the nucleus, where EGFR acts as an important transcriptional regulator. Soluble form of heparin-binding EGF-like growth factor (sHB-EGF) is one of the ligands for EGFR in many cell types; however, there is no evidence for the ability of sHB-EGF to induce EGFR nuclear importation. Here, we demonstrated that treatment of A431 cells with sHB-EGF resulted in nuclear localization of EGFR and such translocation occurs via retrograde pathway. It was shown by confocal microscopy and co-immunoprecipitation assay that the translocation complex consisted of both ligand and receptor. The chromatin immunoprecipitation assay showed the association of sHB-EGF-EGFR complex with promoter region of cyclin D1 in the cell nucleus and this association was prevented by application of EGFR kinase inhibitor AG-1478. The obtained data suggest that sHB-EGF acts similarly to other EGFR ligands and is capable to induce EGFR nuclear translocation as a part of ligand-receptor complex in a tyrosine phosphorylation-dependent manner. |
| Databáze: | MEDLINE |
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