Role for the C-terminus in agonist-induced mu opioid receptor phosphorylation and desensitization

Biochemistry. 2000 May 9;39(18):5492-9. doi: 10.1021/bi991938b.

Abstract

Determining which domains and amino acid residues of the mu opioid receptor are phosphorylated is critical for understanding the mechanism of mu opioid receptor phosphorylation. The role of the C-terminus of the receptor was investigated by examining the C-terminally truncated or point-mutated mu opioid receptors in receptor phosphorylation and desensitization. Both wild-type and mutated receptors were stably expressed in Chinese hamster ovary (CHO) cells. The receptor expression was confirmed by receptor radioligand binding and immunoblottting. After exposure to 5 microM of DAMGO, phosphorylation of the C-terminally truncated receptor and the mutant receptor T394A was reduced to 40 and 10% of that of the wild-type receptor, respectively. Mutation effects on agonist-induced desensitization were studied using adenylyl cyclase inhibition assays. The C-terminally truncated receptor and mutant receptor T394A both showed complete loss of DAMGO-induced desensitization, while the mutant T/S-7A receptor only lost part of its ability to desensitize. Taken together, these results suggest that the C-terminus of the mu opioid receptor participates in receptor phosphorylation and desensitization with threonine 394, a crucial residue for both features. DAMGO-induced mu opioid receptor phosphorylation and desensitization are associated and appear to involve both the mu opioid receptor C-terminus and other domains of the receptor.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adenylyl Cyclases / metabolism
  • Amino Acid Sequence
  • Animals
  • CHO Cells
  • Colforsin / pharmacology
  • Cricetinae
  • Enkephalin, Ala(2)-MePhe(4)-Gly(5)- / metabolism
  • Humans
  • Molecular Sequence Data
  • Mutation
  • Phosphorylation
  • Protein Binding / genetics
  • Receptors, Opioid, mu / chemistry
  • Receptors, Opioid, mu / genetics*
  • Transfection

Substances

  • Receptors, Opioid, mu
  • Enkephalin, Ala(2)-MePhe(4)-Gly(5)-
  • Colforsin
  • Adenylyl Cyclases