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  Differential expression of receptors for Shiga and Cholera toxin is regulated by the cell cycle

Majoul, I., Schmidt, T., Pomasanova, M., Boutkevich, E., Kozlov, Y., & Soeling, H. D. (2002). Differential expression of receptors for Shiga and Cholera toxin is regulated by the cell cycle. Journal of Cell Science, 115(4), 817-826. Retrieved from http://jcs.biologists.org/cgi/reprint/115/4/817.

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Item Permalink: http://hdl.handle.net/11858/00-001M-0000-0012-F43E-D Version Permalink: http://hdl.handle.net/11858/00-001M-0000-0028-9CE6-3
Genre: Journal Article

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599689.pdf (Publisher version), 604KB
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 Creators:
Majoul, I.1, Author              
Schmidt, T., Author
Pomasanova, M., Author
Boutkevich, E.1, Author              
Kozlov, Y., Author
Soeling, H. D.1, Author              
Affiliations:
1Department of Neurobiology, MPI for biophysical chemistry, Max Planck Society, ou_578595              

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Free keywords: AB5-toxins; glycosphingolipid receptors; cell cycle; Golgi
 Abstract: Cholera and Shiga toxin bind to the cell surface via glycolipid receptors GM1 and Gb3, respectively. Surprisingly, the majority of Vero cells from a non-synchronized population bind either Cholera or Shiga toxin but not both toxins. The hypothesis that the differential expression of toxin receptors is regulated by the cell cycle was tested. We find that Cholera toxin binds preferentially in G0/G1, with little binding through S-phase to telophase, whereas Shiga toxin binds maximally through G2 to telophase but does not bind during G0/G1 and S-phase. The changes result from the corresponding changes in Gb3 and GM1 synthesis, not from variations of receptor transport to the cell surface. The changes do not reflect competition of Gb3 and GM1 synthesis for lactosylceramide. Cells as diverse as Vero cells, PC12 cells and astrocytes show the same cell-cycle- dependent regulation of glycosphingolipid receptors, suggesting that this novel phenomenon is based on a conserved regulatory mechanism.

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Language(s): eng - English
 Dates: 2002-02-15
 Publication Status: Published in print
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 Rev. Method: Peer
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Title: Journal of Cell Science
Source Genre: Journal
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Pages: - Volume / Issue: 115 (4) Sequence Number: - Start / End Page: 817 - 826 Identifier: -