Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The production of adenosine 3',5'-monophosphate (cyclic AMP) in a membrane preparation from human liver homogenate has been studied. Cyclic AMP production was enhanced by glucagon, guanylyl 5'-imidodiphosphate (GMP-PNP), or fluoride, or combinations of these. Adenosine, adenosine monophosphate (AMP) and adenosine diphosphate (ADP) at a concentration of 10(-3) mol/l antagonized the effects of all stimulants. These data suggest that inhibitory effects are exercised at the catalytic moiety of the adenylate cyclase system, or at the transducer function between hormone receptor and catalytic unit. In contrast, adenosine at a concentration of 10(-5) mol/l antagonized glucagon- but not fluoride-stimulated adenylate cyclase activity.
 ...
PMID:Adenylate cyclase activity in human liver membranes and its inhibition by adenosine and adenine nucleotides. 21 Apr 96

The basal adenylate cyclase activity of the rat heart increases with the age of the animal. By itself, 10(-5) M glucagon activates only adenylate cyclase activity from adult rat hearts. In contrast, 10(-5) M glucagon in the presence of 10(-4)M 5'-guanylylimidodiphosphate (GMP-PNP) clearly activates adenylates cyclase activity in the 14-day-old rat heart, with some activation being evident in hearts of 7-day-old animals. GMP-PNP, 10(-4) M, activates adenylate cyclase activity by itself at ages of 14 days and older, but to a far lesser degree than in combination with 10(-5) M glucagon. Activity elicited by NaF increases throughout the neonatal period. The ratio of NaF-stimulated activity to basal activity increases from 6.3 at 2 days to 10.0 in the adult, a change which is not statistically significant. We conclude that a cardiac receptor for glucagon is present early in neonatal period of the rat, but this receptor cannot effect activation of adenylate cyclase and an increase in heart rate, or depletion of glycogen. Even in the presence of 10(-4) GMP-PNP, the response to glucagon by cardiac adenylate cyclase depends on the age of the rat. In heart cells from a 7-day-old rat, the response is barely measurable but the magnitude of the response increases each week.
 ...
PMID:Development of guanylylimidodiphosphate-dependent activation of adenylate cyclase by glucagon in the neonatal rat heart. 97 86

The major histocompatibility complex of mice, the H-2 complex, regulates the steady-state level of adenosine cyclic 3',5'-monophosphate (cAMP) in liver. This effect of H-2 may be due to an effect on hormone binding to receptors. Here we show that liver membranes from animals of different H-2 types differ in their sensitivity to glucagon stimulation of adenylate cyclase and in the affinity of their receptors for glucagon. No H-2-associated differences are seen in basal, NaF-stimulated, or GMP-PNP-stimulated adenylate cyclase.
 ...
PMID:Influence of the mouse major histocompatibility complex, H-2, on liver adenylate cyclase activity and on glucagon binding to liver cell membranes. 624 75

Glucagon-like peptide-1 (GLP-1) acts through its G-protein-coupled receptor to enhance glucose-stimulated insulin secretion from pancreatic beta-cells. This is believed to result from modulation of at least two ion channels: ATP-sensitive K(+) (K(ATP)) channels and voltage-dependent Ca(2+) channels. Here, we report that GLP-1 receptor signaling also regulates the activity of beta-cell voltage-dependent K(+) (K(V)) channels, themselves potent glucose-dependent regulators of insulin secretion. GLP-1 receptor activation with exendin 4 (10(-8) mol/l) in rat beta-cells antagonized K(V) currents by 43.3 +/- 6.3%, whereas the GLP-1 receptor antagonist exendin 9-39 had no effect. The effect of GLP-1 receptor activation on K(V) currents could be replicated (current reduction of 55.7 +/- 6.0%) by G-protein activation with GMP-PNP (10 nmol/l). The cAMP pathway antagonist Rp-cAMPS (100 micro mol/l) prevented current inhibition by exendin 4, implicating cAMP signaling in GLP-1 receptor modulation of beta-cell K(V) currents. Finally, exendin 4 (10(-8) mol/l) increased the amplitude (130 +/- 5.7%) and duration (285 +/- 15.9%) of the beta-cell depolarization response to current injection, independent of any effect on K(ATP) or Ca(2+) channels. The present results demonstrate that GLP-1 receptor signaling can antagonize beta-cell repolarization by reducing voltage-dependent K(+) currents, an effect likely to contribute to GLP-1's glucose-dependent insulinotropic effect.
 ...
PMID:Glucagon-like peptide-1 receptor activation antagonizes voltage-dependent repolarizing K(+) currents in beta-cells: a possible glucose-dependent insulinotropic mechanism. 1247 88