Call us toll-free

T1 - Regulation of prolactin synthesis by estrogen

Prolactin Physiology: The Synthesis, Secretion, and Actions of Prolactin

Approximate price

Pages:

275 Words

$19,50

is the site of prolactin synthesis

AB - There is an increasing body of evidence implicating estradiol in the regulation of prolactin synthesis. We have recently demonstrated that treatment of rats with estradiol specifically increased the incorporation of precursors into prolactin and led to the accumulation of preprolactin mRNA. These effects of estradiol could be due either to a direct action on the pituitary or to an indirect effect mediated by the hypothalamus. To distinguish between these possibilities, we studied the response of dispersed rat pituitary cells maintained in culture. We found that cultured pituitary cells respond to estradiol by increased incorporation of precursors into prolactin but not into the bulk of other cellular proteins. The rate of increase in prolactin synthesis is dose dependent, reaching maximal levels in the physiological range of estradiol. At a concentration of 10-9M, estradiol, estriol and diethylstilbestrol are stimulatory whereas androgens, progesterone and cortisone have no significant effect. Exposure of cells to 10-8M, estradiol results in a 500% stimulation of prolactin synthesis after 7 days of culture. The time course and magnitude of response to estradiol in cultured pituitary cells is comparable to the response seen in vivo. Our findings indicate that estradiol can stimulate prolactin synthesis through a direct action on the pituitary.

The Biosynthesis of Prolactin | SpringerLink

The principal site of prolactin action is the mammary gland, where the hormone initiates and maintains lactation after childbirth. Major stimuli for breast development are estrogen, progesterone, prolactin, and placental mammotropic hormones. Other stimuli include insulin, cortisol, and thyroid hormone.

16/01/2018 · The Biosynthesis of Prolactin

A specific, high affinity, saturable binding site for the 160 kilodalton fragment of prolactin on capillary endothelial cells.

There are at least three different isoforms of PRLR differing mainly in their cytoplasmic domain: long (90 kDa), intermediate, and short (40kDa) isoform.

N2 - There is an increasing body of evidence implicating estradiol in the regulation of prolactin synthesis. We have recently demonstrated that treatment of rats with estradiol specifically increased the incorporation of precursors into prolactin and led to the accumulation of preprolactin mRNA. These effects of estradiol could be due either to a direct action on the pituitary or to an indirect effect mediated by the hypothalamus. To distinguish between these possibilities, we studied the response of dispersed rat pituitary cells maintained in culture. We found that cultured pituitary cells respond to estradiol by increased incorporation of precursors into prolactin but not into the bulk of other cellular proteins. The rate of increase in prolactin synthesis is dose dependent, reaching maximal levels in the physiological range of estradiol. At a concentration of 10-9M, estradiol, estriol and diethylstilbestrol are stimulatory whereas androgens, progesterone and cortisone have no significant effect. Exposure of cells to 10-8M, estradiol results in a 500% stimulation of prolactin synthesis after 7 days of culture. The time course and magnitude of response to estradiol in cultured pituitary cells is comparable to the response seen in vivo. Our findings indicate that estradiol can stimulate prolactin synthesis through a direct action on the pituitary.

Regulation of prolactin synthesis by estrogen — …

T1 - Synthesis and storage of prolactin in the pituitary gland of bullfrog tadpoles during metamorphosis

The driving forces underlying this cycle are the hormones related to puberty, pregnancy, and lactation. From puberty on, the waxing and waning (think of moon phases) of estrogen and progesterone during the menstrual cycle slowly develops the ducts and alveoli; this subtle stimulation of the glands continues until about age 30. Pregnancy stimulates a large rise in both of these hormones, as well as the production of prolactin, human placental lactogen, human chorionic gonadotropin (HCG), and growth hormone, which all help to stimulate alveolar growth. Research has shown that the changes in breast size (volume) that women experience during pregnancy are most closely related to the concentration of human placental lactogen, which is produced only by the placenta and therefore only during pregnancy. At the same time, the glandular tissue of the breast also becomes sensitive to insulin, the hormone that helps bring fuel (glucose) to the cells, while also playing a role in the making, or synthesizing, of milk. Full maturation of the milk-making tissue requires the hormones insulin, cortisol, thyroxine, prolactin, and growth hormone.


There is an increasing body of evidence implicating estradiol in the regulation of prolactin synthesis. We have recently demonstrated that treatment of rats with estradiol specifically increased the incorporation of precursors into prolactin and led to the accumulation of preprolactin mRNA. These effects of estradiol could be due either to a direct action on the pituitary or to an indirect effect mediated by the hypothalamus. To distinguish between these possibilities, we studied the response of dispersed rat pituitary cells maintained in culture. We found that cultured pituitary cells respond to estradiol by increased incorporation of precursors into prolactin but not into the bulk of other cellular proteins. The rate of increase in prolactin synthesis is dose dependent, reaching maximal levels in the physiological range of estradiol. At a concentration of 10-9M, estradiol, estriol and diethylstilbestrol are stimulatory whereas androgens, progesterone and cortisone have no significant effect. Exposure of cells to 10-8M, estradiol results in a 500% stimulation of prolactin synthesis after 7 days of culture. The time course and magnitude of response to estradiol in cultured pituitary cells is comparable to the response seen in vivo. Our findings indicate that estradiol can stimulate prolactin synthesis through a direct action on the pituitary.

ALBS is a member of the family of high affinity membrane-associated binding sites called antiestrogen binding sites (AEBS) (124).
Order now
  • Prolactin (PRL), also known as ..

    The intermediate form is a deletion mutant of the long form, lacking 198 aminoacids in its cytoplasmic domain.

  • Prolactin: Synthesis, Fate and Actions | SpringerLink

    1977, Effects of estradiol-17ß and pimozide on prolactin synthesis in male and ..

  • Prolactin - Colorado State University

    There is an increasing body of evidence implicating estradiol in the regulation of prolactin synthesis

Order now

(FINAL) CH16: The Endocrine System Flashcards | Quizlet

N2 - A hypothetical model of the ligand interaction with the estrogen receptor binding site has been developed to describe the structural features necessary to initiate or to inhibit prolactin synthesis in vitro. The biological potency of the binding ligands is directly related to their relative binding affinity (RBA) for the estrogen receptor. The relative potencies of antiestrogens to inhibit estradiol-stimulated prolactin synthesis was trans-monohydroxytamoxifen ≡ LY117018 > trioxifene > enclomiphene ≡ cis-monohydroxytamoxifen ≡ tamoxifen, consistent with their RBAs for uterine estrogen receptor. Similarly the relative potency of estrogens to stimulate prolactin synthesis was diethylstilbestrol ≡ estradiol > ICI 77,949 > ICI 47,699 ≡ zuclomiphene, consistent with their RBAs. The compound LY126412 (trioxifene without the aminoethoxy side chain) did not interact with the estrogen receptor at the concentrations tested (10-8-10-6 M) or exhibit estrogenic or antiestrogenic properties using the prolactin synthesis assay. Overall, the ligand-receptor model stresses the structural requirement for high affinity binding and the critical positioning of the alkylaminoethoxy side chain in space (in relation to the ligand-binding site on the estrogen receptor) to prevent prolactin synthesis.

Start studying (FINAL) CH16: The Endocrine System

AB - A hypothetical model of the ligand interaction with the estrogen receptor binding site has been developed to describe the structural features necessary to initiate or to inhibit prolactin synthesis in vitro. The biological potency of the binding ligands is directly related to their relative binding affinity (RBA) for the estrogen receptor. The relative potencies of antiestrogens to inhibit estradiol-stimulated prolactin synthesis was trans-monohydroxytamoxifen ≡ LY117018 > trioxifene > enclomiphene ≡ cis-monohydroxytamoxifen ≡ tamoxifen, consistent with their RBAs for uterine estrogen receptor. Similarly the relative potency of estrogens to stimulate prolactin synthesis was diethylstilbestrol ≡ estradiol > ICI 77,949 > ICI 47,699 ≡ zuclomiphene, consistent with their RBAs. The compound LY126412 (trioxifene without the aminoethoxy side chain) did not interact with the estrogen receptor at the concentrations tested (10-8-10-6 M) or exhibit estrogenic or antiestrogenic properties using the prolactin synthesis assay. Overall, the ligand-receptor model stresses the structural requirement for high affinity binding and the critical positioning of the alkylaminoethoxy side chain in space (in relation to the ligand-binding site on the estrogen receptor) to prevent prolactin synthesis.

B) is partly contained within the infundibulum.

A hypothetical model of the ligand interaction with the estrogen receptor binding site has been developed to describe the structural features necessary to initiate or to inhibit prolactin synthesis in vitro. The biological potency of the binding ligands is directly related to their relative binding affinity (RBA) for the estrogen receptor. The relative potencies of antiestrogens to inhibit estradiol-stimulated prolactin synthesis was trans-monohydroxytamoxifen ≡ LY117018 > trioxifene > enclomiphene ≡ cis-monohydroxytamoxifen ≡ tamoxifen, consistent with their RBAs for uterine estrogen receptor. Similarly the relative potency of estrogens to stimulate prolactin synthesis was diethylstilbestrol ≡ estradiol > ICI 77,949 > ICI 47,699 ≡ zuclomiphene, consistent with their RBAs. The compound LY126412 (trioxifene without the aminoethoxy side chain) did not interact with the estrogen receptor at the concentrations tested (10-8-10-6 M) or exhibit estrogenic or antiestrogenic properties using the prolactin synthesis assay. Overall, the ligand-receptor model stresses the structural requirement for high affinity binding and the critical positioning of the alkylaminoethoxy side chain in space (in relation to the ligand-binding site on the estrogen receptor) to prevent prolactin synthesis.

Order now
  • Kim

    "I have always been impressed by the quick turnaround and your thoroughness. Easily the most professional essay writing service on the web."

  • Paul

    "Your assistance and the first class service is much appreciated. My essay reads so well and without your help I'm sure I would have been marked down again on grammar and syntax."

  • Ellen

    "Thanks again for your excellent work with my assignments. No doubts you're true experts at what you do and very approachable."

  • Joyce

    "Very professional, cheap and friendly service. Thanks for writing two important essays for me, I wouldn't have written it myself because of the tight deadline."

  • Albert

    "Thanks for your cautious eye, attention to detail and overall superb service. Thanks to you, now I am confident that I can submit my term paper on time."

  • Mary

    "Thank you for the GREAT work you have done. Just wanted to tell that I'm very happy with my essay and will get back with more assignments soon."

Ready to tackle your homework?

Place an order