Abstract：
:NPS(o-nitrophenyl sulfenyl)-ACTH stimulated steroidogenesis in Y1 cells to the same maximum level as did ACTH, but with a 60-fold lower potency than the native hormone. NPS-ACTH also stimulated the extracellular accumulation of cAMP in Y1 cells with lower potency than the unmodified hormone. The amount of cAMP accumulated in the presence of NPS-ACTH approached 75% of the maximum with ACTH. In Y1 plasma membranes, NPS-ACTH was a partial agonist of adenylate cyclase activity, witn an efficacy dependent upon the type of guanyl nucleotide present. The steroidogenic responses of two Y1(Kin) mutants and two Y1(Cyc) mutants to NPS-ACTH paralleled their responses to ACTH and reflected closely their defects in cAMP-dependent protein kinase and ACTH-sensitive adenylate cyclase activity. These data imply an obligatory role for adenylate cyclase and cAMP-dependent protein kinase activities in stimulation of steroidogenesis in Y1 cells by NPA-ACTH.
journal_name
Mol Cell Endocrinoljournal_title
Molecular and cellular endocrinologyauthors
Rae PA,Zinman H,Ramachandran J,Schimmer BPdoi
10.1016/0303-7207(80)90111-2subject
Has Abstractpub_date
1980-03-01 00:00:00pages
171-9issue
3eissn
0303-7207issn
1872-8057journal_volume
17pub_type
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journal_title：Molecular and cellular endocrinology
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更新日期：2012-06-05 00:00:00
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journal_title：Molecular and cellular endocrinology
pub_type： 杂志文章,评审
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更新日期：2011-03-15 00:00:00
