23-07-2014, 05:19
Although complicated it's a great illustration:
![[Image: attachment.php?aid=7503]](http://www.breastnexus.com/attachment.php?aid=7503)
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23-07-2014, 05:30
Selective progesterone receptor modulator
Mechanism of action
Synthetic SPRMs differ in chemical structure from the endogenous hormone progesterone, but nevertheless bind to the same progesterone receptor. In humans, there is only one gene (PGR) that codes for the receptor, but two splice variants (PR-A and -B) arising from this single gene each with a somewhat different tissue distribution and intrinsic functional activity in response to ligand binding (agonist vs. antagonist). In addition, synthetic SPRMs may have some binding selectivity between the two isoforms, although this is unlikely as the ligand binding domains of the two isoforms are identical.
A more likely origin of the tissue selectivity of SPRMs is what conformational preference these ligands induce in the receptor. The ligand binding domain of the receptor is in equilibrium between two different conformations. The first is an agonist conformation which favors the binding of coactivator proteins which in turn favors upregulation of gene transcription. The second is an antagonistic conformation which in contrast favors the binding of corepressors and as a consequence down regulation of gene expression. Full agonists such as progesterone which display agonist properties in all tissues, strongly shift the conformational equilibrium in the agonist direction. Conversely full antagonists such as aglepristone strongly shift the equilibrium in the antagonist direction. Finally, the overall ratio of concentrations of coactivator to corepressor may differ in different cell types.
When SPRMs bind to the progesterone receptor, the equilibrium between the two conformational states is more closely balanced and hence more easily perturbed by differences in the cellular environment. In tissues where the concentration of coactivators is higher than corepressors, the excess coactivators drive the equilibrium in the agonist direction. Conversely in tissues where corepressor concentration is higher the equilibrium is driven in the antagonist direction.[5][6] Hence SPRMs display agonist activity in tissues where coactivators predominate and antagonist activity where corepressors are in excess.
http://wikipedia.org/wiki/Selective_prog..._modulator
Mechanism of action
Synthetic SPRMs differ in chemical structure from the endogenous hormone progesterone, but nevertheless bind to the same progesterone receptor. In humans, there is only one gene (PGR) that codes for the receptor, but two splice variants (PR-A and -B) arising from this single gene each with a somewhat different tissue distribution and intrinsic functional activity in response to ligand binding (agonist vs. antagonist). In addition, synthetic SPRMs may have some binding selectivity between the two isoforms, although this is unlikely as the ligand binding domains of the two isoforms are identical.
A more likely origin of the tissue selectivity of SPRMs is what conformational preference these ligands induce in the receptor. The ligand binding domain of the receptor is in equilibrium between two different conformations. The first is an agonist conformation which favors the binding of coactivator proteins which in turn favors upregulation of gene transcription. The second is an antagonistic conformation which in contrast favors the binding of corepressors and as a consequence down regulation of gene expression. Full agonists such as progesterone which display agonist properties in all tissues, strongly shift the conformational equilibrium in the agonist direction. Conversely full antagonists such as aglepristone strongly shift the equilibrium in the antagonist direction. Finally, the overall ratio of concentrations of coactivator to corepressor may differ in different cell types.
When SPRMs bind to the progesterone receptor, the equilibrium between the two conformational states is more closely balanced and hence more easily perturbed by differences in the cellular environment. In tissues where the concentration of coactivators is higher than corepressors, the excess coactivators drive the equilibrium in the agonist direction. Conversely in tissues where corepressor concentration is higher the equilibrium is driven in the antagonist direction.[5][6] Hence SPRMs display agonist activity in tissues where coactivators predominate and antagonist activity where corepressors are in excess.
http://wikipedia.org/wiki/Selective_prog..._modulator
23-07-2014, 05:51
The pathways of progesterone action in target tissues are not well defined and, in many respects, distinctions remain to be made between the direct downstream targets of progesterone action and indirect consequences of progesterone regulation. Furthermore, as the effects of progesterone are mediated by its receptor and as PR is induced by estrogen in most target tissues, the delineation of specific progesterone effects, as distinct from those of estrogen, is similarly not clear. A number of reviews have described the molecular mechanisms of PR action (2, 3, 4), progesterone and progesterone antagonist effects on cellular proliferation (5, 6), and regulation of the concentration of progesterone-responsive proteins (7, 8). This review does not seek to replicate existing reviews of the molecular biology of PR action but will provide an overview of the physiological action of progesterone and its regulation of gene expression in target tissues.
Physiological Action of Progesterone in Target Tissues
http://press.endocrine.org/doi/full/10.1....18.4.0308
25-07-2014, 20:00
(23-07-2014, 05:03)lovely11 Wrote:(23-07-2014, 04:56)Lotus Wrote: It is not a sex hormone, it plays no part in the secondary sexual characteristics which develop at puberty
It is not a sex hormone, true, but it does play a role in secondary sexual characteristics which develop at puberty.
Actually it's estrogen that plays the role in developing secondary sexual characteristics.
(25-07-2014, 20:00)Lotus Wrote: Actually it's estrogen that plays the role in developing secondary sexual characteristics.
Estrogen yes. If breasts are considered Secondary sexual characteristics, then progesterone is yes too. If the breasts are more of a nursing, instead of secondary sexual characteristic, then perhaps progesterone is not. The breasts are definitely not a Primary sexual characteristics, but they are a definitely reproductive characteristics
25-07-2014, 20:52
(25-07-2014, 20:23)lovely11 Wrote:(25-07-2014, 20:00)Lotus Wrote: Actually it's estrogen that plays the role in developing secondary sexual characteristics.
Estrogen yes. If breasts are considered Secondary sexual characteristics, then progesterone is yes too. If the breasts are more of a nursing, instead of secondary sexual characteristic, then perhaps progesterone is not. The breasts are definitely not a Primary sexual characteristics, but they are a definitely reproductive characteristics
Primary and secondary sexual characteristics occur and develop at puberty, breasts are secondary.
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