1. Expression and signal transduction of the glucagon receptor in betaTC3 cells
- Author
-
Alicia Rodriguez-Gabin, Jing Li, Jorge N. Larocca, and Maureen J. Charron
- Subjects
endocrine system ,medicine.medical_specialty ,Inositol Phosphates ,Gene Expression ,Stimulation ,Biology ,Glucagon ,Glucagon receptor ,Polymerase Chain Reaction ,Cell Line ,Internal medicine ,medicine ,Cyclic AMP ,Receptors, Glucagon ,Northern blot ,RNA, Messenger ,Inositol phosphate ,Molecular Biology ,Glucagon-like peptide 1 receptor ,chemistry.chemical_classification ,Cell Biology ,Blotting, Northern ,Endocrinology ,βTC3 cells ,chemistry ,Type C Phospholipases ,Signal transduction ,hormones, hormone substitutes, and hormone antagonists ,Intracellular ,Adenylyl Cyclases ,Signal Transduction - Abstract
The expression and signal transduction of the glucagon receptor (GR) have been studied in β TC3 cells. Northern blot and RT-PCR analysis indicated the expression of the GR gene in β TC3 cells. One-5 nM glucagon stimulated a 2.5-fold increase in the IP s production. At glucagon concentrations higher than 5 nM, the production of IP s was blunted but not abolished. The accumulation of intracellular cAMP was observed following the stimulation with 5 nM of glucagon. A maximal 4.5-fold increase in cAMP was observed using 250 nM glucagon and higher. Comparative studies using a glucagon anatogonist, des-His 1 [Glu] 9 glucagon, showed no effect on intracellular cAMP and IPs in β TC3 cells. Our data shows that the GR gene is expressed in β TC3 cells. The GR in β TC3 cells transmits its intracellular signal by causing the accumulation of both IP s and cAMP.
- Published
- 1997