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Bulldog_10
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I saw one yesterday about oxandrolone...want it?
Abstracts Please
- Thread starter Bulldog_10
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Bulldog_10
New member
hmmm...i cant actually find the one I'm looking for...but I found a study that mentions that oxandrolone and fluoxymesterone have a lower AR affinity testosterone.
It's not proof of it, but it is something that says that it is an accepted fact.
Here it is...I'll try to find that other one.
Title: Distinguishing androgen receptor agonists and antagonists: Distinct mechanisms of activation by medroxyprogesterone acetate and dihydrotestosterone.
Author, Editor, Inventor: Kemppainen-Jon-A; Langley-Elizabeth {a}; Wong-Choi-iok; Bobseine-Kathy; Kelce-William-R; Wilson-Elizabeth-M {a}
Author Address: {a} Laboratories for Reproductive Biology, University of North Carolina, Room 374, Medical Sciences Research Building, Chapel Hill, NC, 27599, USA
Source: Molecular-Endocrinology. March, 1999; 13 (3) 440-454.
Publication Year: 1999
Document Type: Article-
ISSN (International Standard Serial Number): 0888-8809
Language: English
Language of Summary: English
Abstract: Natural and pharmacological androgen receptor (AR) ligands were tested for their ability to induce the AR NH2-terminal and carboxyl-terminal (N/C) interaction in a two-hybrid protein assay to determine whether N/C complex formation distinguishes in vivo AR agonists from antagonists. High-affinity agonists such as dihydrotestosterone, mibolerone, testosterone, and methyltrienolone at concentrations between 0.1 and 1 nm induce the N/C interaction more than 40-fold. The lower affinity anabolic steroids, oxandrolone and fluoxymesterone, require concentrations of 10-100 nm for up to 23-fold induction of the N/C interaction. However no N/C interaction was detected in the presence of the antagonists, hydroxyflutamide, cyproterone acetate, or RU56187, at concentrations up to 1 muM, or with 1 muM estradiol, progesterone, or medroxyprogesterone acetate; each of these steroids at 1-500 nm inhibited the dihydrotestosterone-induced N/C interaction, with medroxyprogesterone acetate being the most effective. In transient and stable cotransfection assays using the mouse mammary tumor virus reporter vector, all ligands displayed concentration-dependent AR agonist activity that paralleled induction of the N/C interaction, with antagonists and weaker agonists failing to induce the N/C interaction. AR dimerization and DNA binding in mobility shift assays and AR stabilization reflected, but were not dependent on, the N/C interaction. The results indicate that the N/C interaction facilitates agonist potency at low physiological ligand concentrations as detected in transcription, dimerization/DNA binding, and stabilization assays. However the N/C interaction is not required for agonist activity at sufficiently high ligand concentrations, nor does its inhibition imply antagonist activity.
It's not proof of it, but it is something that says that it is an accepted fact.
Here it is...I'll try to find that other one.
Title: Distinguishing androgen receptor agonists and antagonists: Distinct mechanisms of activation by medroxyprogesterone acetate and dihydrotestosterone.
Author, Editor, Inventor: Kemppainen-Jon-A; Langley-Elizabeth {a}; Wong-Choi-iok; Bobseine-Kathy; Kelce-William-R; Wilson-Elizabeth-M {a}
Author Address: {a} Laboratories for Reproductive Biology, University of North Carolina, Room 374, Medical Sciences Research Building, Chapel Hill, NC, 27599, USA
Source: Molecular-Endocrinology. March, 1999; 13 (3) 440-454.
Publication Year: 1999
Document Type: Article-
ISSN (International Standard Serial Number): 0888-8809
Language: English
Language of Summary: English
Abstract: Natural and pharmacological androgen receptor (AR) ligands were tested for their ability to induce the AR NH2-terminal and carboxyl-terminal (N/C) interaction in a two-hybrid protein assay to determine whether N/C complex formation distinguishes in vivo AR agonists from antagonists. High-affinity agonists such as dihydrotestosterone, mibolerone, testosterone, and methyltrienolone at concentrations between 0.1 and 1 nm induce the N/C interaction more than 40-fold. The lower affinity anabolic steroids, oxandrolone and fluoxymesterone, require concentrations of 10-100 nm for up to 23-fold induction of the N/C interaction. However no N/C interaction was detected in the presence of the antagonists, hydroxyflutamide, cyproterone acetate, or RU56187, at concentrations up to 1 muM, or with 1 muM estradiol, progesterone, or medroxyprogesterone acetate; each of these steroids at 1-500 nm inhibited the dihydrotestosterone-induced N/C interaction, with medroxyprogesterone acetate being the most effective. In transient and stable cotransfection assays using the mouse mammary tumor virus reporter vector, all ligands displayed concentration-dependent AR agonist activity that paralleled induction of the N/C interaction, with antagonists and weaker agonists failing to induce the N/C interaction. AR dimerization and DNA binding in mobility shift assays and AR stabilization reflected, but were not dependent on, the N/C interaction. The results indicate that the N/C interaction facilitates agonist potency at low physiological ligand concentrations as detected in transcription, dimerization/DNA binding, and stabilization assays. However the N/C interaction is not required for agonist activity at sufficiently high ligand concentrations, nor does its inhibition imply antagonist activity.
Bulldog_10
New member
haha...i JUST read that one zyg.
