Example sentences for: gonadotropes

How can you use “gonadotropes” in a sentence? Here are some example sentences to help you improve your vocabulary:

  • Previously, we showed that RSG3 was expressed endogenously in rat pituitary cells and, when experimentally co-expressed together with GnRH receptors in a heterologous cell line (COS1), it suppressed GnRH-stimulated inositol trisphosphate production [ 9 ] . Here, those studies have been extended to include GnRH-stimulated LH secretion using adenovirus-mediated gene transfer of RGS3 complementary DNA into normal rat pituitary gonadotropes.

  • Because of the evidence that the signal transduction pathway for GnRH in gonadotropes involves the GnRH receptor, Gqα, phospholipase Cβ, and cellular IP 3 release [ 39 40 ] , we determined the effect of RGS3 on GnRH-stimulated LH secretion using adenoviral-mediated gene transfer in rat pituitary cells (Fig.

  • Two molecular loci recently have been implicated as potential modulators of GnRH receptor signaling: one is the receptor itself [ 23 ] , and the other is the G protein that transduces the signal generated by binding of the receptor to its agonist [ 9 ] . With respect to the former locus, G protein coupled receptor kinases (GRKs) act in an agonist-specific manner to phosphorylate intracellular regions of the receptor thus permitting β arrestin binding that sterically inhibits G protein association with the receptor [ 1 45 ] . We have reported previously that experimental expression of GRKs in GnRH receptor-expressing heterologous cells (COS-1) suppressed GnRH-stimulated IP 3 production, and that co-expression of GRK2 and β-arrestin 2 suppressed GnRH receptor signaling more than that of either alone [ 23 ] . Stronger evidence that the GRK/β arrestin paradigm may play a role in regulating GnRH receptor signaling is our recent finding that adenovirus-mediated gene transfer of GRK2 into normal pituitary gonadotropes suppressed GnRH-stimulated LH secretion and IP 3 production [ 31 ] . However, no evidence has been presented for a direct interaction between β-arrestin and the GnRH receptor.

  • However, a calcium ionophore stimulated LH secretion in RGS3-expressing gonadotropes, confirming a specific site of action occurring at phospholipase Cβ or earlier in the signal transduction pathway.

  • With respect to the G protein as a locus for modulation of GnRH receptor signaling, we reported earlier that experimental expression of RGS3 but not RGS1, 2, or 4 in GnRH receptor expressing COS-1 cells suppressed GnRH-stimulated IP 3 production [ 9 ] . In the current report, we present evidence strengthening the hypothesis of a regulatory role for RGS3 in GnRH receptor signaling: adenovirus-mediated expression of RGS3 in normal pituitary gonadotropes profoundly inhibited GnRH-stimulated LH secretion and 3H-inositol phosphate accumulation.


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