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Similarities in the modulation of pituitary and prostatic FSH by inhibin and related peptides
Author(s) -
Shah Madhavi G.,
Sheth Anil R.
Publication year - 1991
Publication title -
the prostate
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.295
H-Index - 123
eISSN - 1097-0045
pISSN - 0270-4137
DOI - 10.1002/pros.2990180102
Subject(s) - endocrinology , medicine , tyrosine , peptide , in vitro , cysteine , anterior pituitary , chemistry , hormone , pituitary gland , residue (chemistry) , peptide hormone , prostate , biology , biochemistry , enzyme , cancer
Prostatic inhibin peptide (PIP) suppresses the synthesis as well as release of FSH from the rat pituitary whereas the carboxy terminal nonapeptide (86–94) of PIP elevated the release of pituitary FSH. Addition of a tyrosine residue at the NH 2 ‐terminal end of nonapeptide and blocking the sulfydryl group of the cysteine residue at position 87 resulted in a decapeptide having the property of suppressing FSH release from rat pituitary. Human prostate has been shown to synthesize FSH in vitro. PIP, nonapeptide, and decapeptide modulate the prostatic FSH biosynthesis, the pattern of which was similar to that observed for pituitary.