Defective relocalization of ALS2/alsin missense mutants to Rac1-induced macropinosomes accounts for loss of their cellular function and leads to disturbed amphisome formation.

@article{Otomo2011DefectiveRO,
  title={Defective relocalization of ALS2/alsin missense mutants to Rac1-induced macropinosomes accounts for loss of their cellular function and leads to disturbed amphisome formation.},
  author={Asako Otomo and Ryota Kunita and Kyoko Suzuki-Utsunomiya and Joh-E Ikeda and Shinji Hadano},
  journal={FEBS letters},
  year={2011},
  volume={585 5},
  pages={730-6}
}
Loss of ALS2/alsin function accounts for several recessive motor neuron diseases. ALS2 is a Rab5 activator and its endosomal localization is regulated by Rac1 via macropinocytosis. Here, we show that the pathogenic missense ALS2 mutants fail to be localized to Rac1-induced macropinosomes as well as endosomes, which leads to loss of the ALS2 function as a Rab5 activator on endosomes. Further, these mutants lose the competence to enhance the formation of amphisomes, the hybrid-organelle formed… CONTINUE READING
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