Arrestin is required for agonist-induced trafficking of voltage-dependent calcium channels

J Biol Chem. 2006 Oct 13;281(41):31131-41. doi: 10.1074/jbc.M605000200. Epub 2006 Aug 15.

Abstract

Many metabotropic receptors in the nervous system act through signaling pathways that result in the inhibition of voltage-dependent calcium channels. Our previous findings showed that activation of seven-transmembrane receptors results in the internalization of calcium channels. This internalization takes place within a few seconds, raising the question of whether the endocytic machinery is in close proximity to the calcium channel to cause such rapid internalization. Here we show that voltage-dependent calcium channels are pre-associated with arrestin, a protein known to play a role in receptor trafficking. Upon GABAB receptor activation, receptors are recruited to the arrestin-channel complex and internalized. beta-Arrestin 1 selectively binds to the SNARE-binding region of the calcium channel. Peptides containing the arrestin-binding site of the channel disrupt agonist-induced channel internalization. Taken together these data suggest a novel neuronal role for arrestin.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Retracted Publication

MeSH terms

  • Animals
  • Arrestin / metabolism
  • Arrestin / physiology*
  • Binding Sites
  • Calcium Channels / metabolism*
  • Calcium Channels, N-Type / metabolism
  • Chick Embryo
  • Endocytosis
  • Neurons / metabolism
  • Peptides / chemistry
  • Protein Binding
  • Protein Transport
  • Signal Transduction

Substances

  • Arrestin
  • Calcium Channels
  • Calcium Channels, N-Type
  • Peptides