Deficient activity of the adenylate cyclase stimulatory coupling protein (N(s)) has been demonstrated in many patients with pseudohypoparathyroidism type I (PHP) who have Albright's hereditary osteodystrophy and multiple hormone resistance. Since an abnormality in the activity of the related adenylate cyclase inhibitory coupling protein (N(i)) could influence hormone responsiveness, we measured pertussis toxin-catalyzed [32P]ADP ribosylation of the 40,000-dalton α-subunit of N(i) (N(i)α) in erythrocyte membranes from patients with PHP and normal subjects. There were no significant differences in the amounts of N(i)α in membranes from normal subjects, patients with PHP who have low N(s) associated with Albright's hereditary osteodystrophy and multiple hormone resistance, and patients with PHP who have normal N(s). Abnormal N(i) is not likely to cause hormone resistance in patients with PHP who have normal N(s) to influence hormone responsiveness in patients with PHP who have low N(s).
|Original language||English (US)|
|Number of pages||4|
|Journal||Journal of Clinical Endocrinology and Metabolism|
|State||Published - 1985|
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism