Ca2+ regulates the subcellular localization of adenomatous polyposis coli tumor suppressor protein
| Autor: | Tatsuru Togo |
|---|---|
| Rok vydání: | 2009 |
| Předmět: |
Adenomatous polyposis coli
Xenopus Adenomatous Polyposis Coli Protein Cell Biophysics Transfection Biochemistry Cell membrane Glycogen Synthase Kinase 3 chemistry.chemical_compound medicine Animals Molecular Biology GSK3B Cells Cultured Glycogen Synthase Kinase 3 beta biology Cell Membrane Cell Biology Protein-Tyrosine Kinases biology.organism_classification Molecular biology Cell biology Blot medicine.anatomical_structure chemistry Ionomycin biology.protein Calcium Tyrosine kinase |
| Zdroj: | Biochemical and Biophysical Research Communications. 388:12-16 |
| ISSN: | 0006-291X |
| DOI: | 10.1016/j.bbrc.2009.07.114 |
| Popis: | Microtubule (MT) plus-end tracking proteins (+TIPs) are involved in the regulation of MT plus-end dynamics and stabilization. It was reported previously that an increase in intracellular Ca(2+) concentration ([Ca(2+)](i)) induced by disruption of the plasma membrane stimulates rearrangement of MTs [T. Togo, Disruption of the plasma membrane stimulates rearrangement of microtubules and lipid traffic toward the wound site, J. Cell Sci. 119 (2006) 2780-2786], suggesting that some +TIPs are regulated by Ca(2+). In the present study, the behavior of adenomatous polyposis coli (APC) following an increase in [Ca(2+)](i) was observed using Xenopus A6 epithelial cell expressing GFP-tagged APC. An increase in [Ca(2+)](i) by cell membrane disruption or by ionomycin treatment induced dissociation of APC without depolymerizing MTs. Inhibition of a tyrosine kinase and GSK-3beta suppressed APC dissociation upon an increase in [Ca(2+)](i). Western blotting analysis showed that Ca(2+) transients activated GSK-3beta through a tyrosine kinase. These results suggest that Ca(2+) stimulates redistribution of APC through a tyrosine kinase- and GSK-3beta-dependent pathway. |
| Databáze: | OpenAIRE |
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