Glucagon desensitization of adenylate cyclase and stimulation of inositol phospholipid metabolism does not involve the inhibitory guanine nucleotide regulatory protein Gi, which is inactivated upon challenge of hepatocytes with glucagon.

Antzeko izenburuak

• The rapid desensitization of glucagon-stimulated adenylate cyclase is a cyclic AMP-independent process that can be mimicked by hormones which stimulate inositol phospholipid metabolism.
  nork: Murphy, G J, et al.
  Argitaratua: (1987)
• Treatment of streptozotocin-diabetic rats with metformin restores the ability of insulin to inhibit adenylate cyclase activity and demonstrates that insulin does not exert this action through the inhibitory guanine nucleotide regulatory protein Gi.
  nork: Gawler, D, et al.
  Argitaratua: (1988)
• Insulin and glucagon attenuate the ability of cholera toxin to activate adenylate cyclase in intact hepatocytes.
  nork: Irvine, F J, et al.
  Argitaratua: (1988)
• Diabetes abolishes the GTP-dependent, but not the receptor-dependent inhibitory function of the inhibitory guanine-nucleotide-binding regulatory protein (Gi) on adipocyte adenylate cyclase activity.
  nork: Strassheim, D, et al.
  Argitaratua: (1990)
• Challenge of hepatocytes by glucagon triggers a rapid modulation of adenylate cyclase activity in isolated membranes.
  nork: Heyworth, C M, et al.
  Argitaratua: (1983)