Shiga toxin 'goes retro' in human primary kidney cells.
The pathway and the efficiency of intracellular trafficking of Shiga toxin differ between cell types, and this impacts on susceptibility to cytotoxicity. Warnier et al. demonstrate that in cell types targeted during human disease, Shiga toxin undergoes retrograde transport via the trans-Golgi network to the endoplasmic reticulum, albeit less efficiently than in HeLa cells.
Paton
J C
JC
School of Molecular and Biomedical Science, University of Adelaide, Adelaide, Australia. james.paton@adelaide.edu.au
Paton
A W
AW
D001692:Biological Transport / Q000502:physiology; D002478:Cells, Cultured; D006801:Humans; D007668:Kidney / Q000166:cytology* / Q000378:metabolism*; D022603:Shiga Toxins / Q000493:pharmacokinetics* / Q000633:toxicity*
D022603:Shiga Toxins