Chemical modification of the brown-fat-mitochondrial uncoupling protein with tetranitromethane and N-ethylmaleimide. A cysteine residue is implicated in the nucleotide regulation of anion permeability

Eur J Biochem. 1986 Dec 15;161(3):689-94. doi: 10.1111/j.1432-1033.1986.tb10494.x.

Abstract

Treatment of brown adipose tissue mitochondria with tetranitromethane or N-ethylmaleimide decreases the affinity with which inhibitory nucleotide GDP binds to the tissue-specific uncoupling protein. Both reagents modify cysteine residues which are 'accessible' and 'buried' to 5,5'-dithio-bis(2-nitrobenzoic acid) (Nbs2). Modification of the single Nbs2-accessible residue correlates with the loss of high-affinity binding sites for GDP. Tetranitromethane does not affect the Cl- or H+ permeability of the protein in the absence of nucleotide, while N-ethylmaleimide increases both by 70-80%. Bound GDP is a less effective inhibitor of Cl- permeability after N-ethylmaleimide or tetranitromethane treatment, but retains much of the ability to inhibit H+ permeation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adipose Tissue, Brown / metabolism*
  • Animals
  • Carrier Proteins*
  • Chlorides / metabolism
  • Cricetinae
  • Cysteine / metabolism
  • Ethylmaleimide* / pharmacology
  • Guanosine Diphosphate / metabolism
  • Ion Channels
  • Male
  • Membrane Proteins / metabolism*
  • Mesocricetus
  • Methane* / analogs & derivatives
  • Mitochondria / metabolism*
  • Mitochondrial Proteins
  • Permeability
  • Protein Binding / drug effects
  • Protons
  • Tetranitromethane* / pharmacology
  • Uncoupling Protein 1

Substances

  • Carrier Proteins
  • Chlorides
  • Ion Channels
  • Membrane Proteins
  • Mitochondrial Proteins
  • Protons
  • Uncoupling Protein 1
  • Guanosine Diphosphate
  • Tetranitromethane
  • Cysteine
  • Ethylmaleimide
  • Methane