Answers are grounded in this paper and cite their sources.
In vitro mutational analysis reveals that third cytoplasmic loop deletions impair Hm1 receptor internalization in U293 cells, indicating a specific domain governs receptor uptake.
The m1 muscarinic receptor was previously shown to stimulate phosphatidyl inositol (PI) turnover and to internalize rapidly upon agonist activation. Three receptor mutants with large deletions of the third cytoplasmic loop (i3) of human Hm1, leaving only 11 and 8 amino acids at the amino and carboxy terminal junctions of i3, respectively, retained full ability to stimulate PI turnover, when expressed in U293 cells, but receptor internalization was greatly reduced in two mutants with deletions reaching close to the NH2 terminal of i3. We propose that a receptor domain located toward the amino terminal junction of i3 plays a role in Hm1 internalization.
No takes yet. Share an insight, caveat, or question.
Maeda et al. (1990) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: