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Rafting with cholera toxin: endocytosis and trafficking from plasma membrane to ER

期刊

FEMS MICROBIOLOGY LETTERS
卷 266, 期 2, 页码 129-137

出版社

OXFORD UNIV PRESS
DOI: 10.1111/j.1574-6968.2006.00545.x

关键词

cholera toxin; lipid raft; retrograde pathway; GM1; AB(5) toxin; endocytosis

资金

  1. NIDDK NIH HHS [R01 DK057827, DK57827, DK34854, R01 DK084424, R01 DK048106, R37 DK048106, P30 DK034854, DK48106] Funding Source: Medline
  2. NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [P30DK034854, R01DK048106, R01DK084424, R01DK057827, R37DK048106] Funding Source: NIH RePORTER

向作者/读者索取更多资源

Cholera toxin (CT), and members of the AB(5) family of toxins enter host cells and hijack the cell's endogenous pathways to induce toxicity. CT binds to a lipid receptor on the plasma membrane (PM), ganglioside GM1, which has the ability to associate with lipid rafts. The toxin can then enter the cell by various modes of receptor-mediated endocytosis and traffic in a retrograde manner from the PM to the Golgi and the endoplasmic reticulum (ER). Once in the ER, a portion of the toxin is unfolded and retro-translocated to the cytosol so as to induce disease. GM1 is the vehicle that carries CT from PM to ER. Thus, the toxin pathway from PM to ER is a lipid-based sorting pathway, which is potentially meditated by the determinants of the GM1 ganglioside structure itself.

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