Central pore residues mediate the p97/VCP activity required for ERAD.

@article{DeLaBarre2006CentralPR,
  title={Central pore residues mediate the p97/VCP activity required for ERAD.},
  author={Byron DeLaBarre and John C Christianson and Ron R. Kopito and Axel T Brunger},
  journal={Molecular cell},
  year={2006},
  volume={22 4},
  pages={
          451-62
        }
}

• Byron DeLaBarre, John C Christianson, +1 author Axel T Brunger
• Published 2006 in Molecular cell

The AAA-ATPase p97/VCP facilitates protein dislocation during endoplasmic reticulum-associated degradation (ERAD). To understand how p97/VCP accomplishes dislocation, a series of point mutants was made to disrupt distinguishing structural features of its central pore. Mutants were evaluated in vitro for ATPase activity in the presence and absence of synaptotagmin I (SytI) and in vivo for ability to process the ERAD substrate TCRalpha. Synaptotagmin induces a 4-fold increase in the ATPase… CONTINUE READING

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