Alterations of adenylyl cyclase-linked G proteins in rat liver during aging

Ann T. Eakes, Tazuko K. Hymer, Mark J. Rosenthal, Joel Moss, Michael S. Katz

Research output: Contribution to journalArticlepeer-review

7 Scopus citations


β-Adrenergic stimulation of adenylyl cyclase in rat liver increases during aging. We examined whether this increase is related to alterations in the stimulatory and inhibitory G proteins (G(s) and G(i)) linked to adenylyl cyclase. Levels of immunoreactive α- and β-subunits of G(s) and G(i) in liver plasma membranes from 6-, 12-, 18-, and 24-mo-old rats were unchanged with age, as was pertussis toxin-catalyzed [32P]ADP ribosylation of G(i)α. Cholera toxin-catalyzed [32P]ADP ribosylation of G(s)α and G(s) bioactivity, assessed as reconstitution of adenylyl cyclase activity in S49 cyc cell membranes, increased two- to threefold between 6 and 12-18 mo, and declined by 24 mo. Recombinant ADP ribosylation factor (ARF) enhanced cholera toxin labeling of G(s)α at all ages, yet abolished the increase in toxin labeling at 12-18 mo. Auto-ADP ribosylation of the cholera toxin A1 peptide also increased transiently with age. Alteration of G(s)α, as reflected by increased cholera toxin labeling and G(s) bioactivity, may be involved in the regulation of β-adrenergic-responsive adenylyl cyclase in rat liver during aging. Moreover, changes in endogenous ARF levels could contribute to age differences in cholera toxin labeling of G(s)α.

Original languageEnglish (US)
Pages (from-to)E126-E132
JournalAmerican Journal of Physiology - Endocrinology and Metabolism
Issue number1 33-1
StatePublished - 1996


  • adenosine 5'- diphosphate ribosylation factor
  • cholera toxin
  • pertussis toxin
  • β-adrenergic receptor

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Physiology
  • Physiology (medical)


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