Related Experiment Video
Updated: Feb 9, 2026

Rescue of Recombinant Newcastle Disease Virus from cDNA
Published on: October 11, 2013
Rab1a rescues the toxicity of PRAF3
Hiroyuki Oshikane1, Masahiko Watabe1,2, Kazue Kikuchi-Utsumi1
1Department of Pharmacology, Teikyo University School of Medicine, Kaga 2-11-1, Itabashi-ku, Tokyo 173-8605, Japan.
Abstract:
The PRA1-superfamily member PRAF3 plays pivotal roles in membrane traffic as a GDI displacement factor via physical interaction with a variety of Rab proteins, as well as in the modulation of antioxidant glutathione through its interaction with EAAC1 (SLC1A1). Overproduction of PRAF3 is known to be toxic to the host cells, although the factors capable of cancelling the toxicity remained unknown. We here show that Rab1a can rescue the cytotoxicity caused by PRAF3 possibly by "positively" regulating ER-Golgi trafficking, cancelling the "negative" modulation by PRAF3. Our results illuminate the close physiological relationship between PRAF3 and Rab proteins.
Related Concept Videos
Toxic Reactions: Overview
Toxicity falls into two primary categories: local and systemic.
Local toxicity appears at the exposure site, such as protein denaturation caused by caustic substances.
In contrast, systemic toxicity requires the toxic agent's absorption and distribution,...
Frequency-dependent Selection
Predator-Prey Interactions
Responses to Salt Stress
Comparative Excretory Systems
The Stanford Prison Experiment

