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. 2005 Apr 28;1(4):27-55.
doi: 10.1901/jaba.2005.1-27.

Molecular Basis of Steroid Action in the Prostate

Yuan-Shan Zhu  1
Affiliations

Molecular Basis of Steroid Action in the Prostate

Yuan-Shan Zhu. Cellscience. .
No abstract available

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Figures

Figure 1
Figure 1
Schematic illustration of the location, exon structure and protein domain structure of the AR gene. (Top) The location of AR gene at the q11-12 of X chromosome. (Middle) The AR gene and its mRNA. The AR gene consists of 8 exons (boxes) and 7 introns (line), and the size of each exon and introns is indicated in kbases. (Bottom) The AR protein. The domains of AR are indicated. Relative positions of glutamine (Gln), proline (Pro) and glycine (Gly) repeats within the N-terminal domain are shown by the indicated boxes. The transactivation function domains, AF-1 and AF-2 are located within the N-terminal domain and ligand-binding domain, respectively. Two zinc fingers in the DNA binding domain and a PEST sequence in hinge region are indicated.
Figure 2
Figure 2
Illustrations of the molecular events of androgen-AR action in a target cell, and the 5α-reductase action. When testosterone (T) enters the cell, it can be converted to dihydrotestosterone (DHT) in the cell by 5α-reductases (5αRD) (top panel). Both T and DHT bind to androgen receptor (AR), resulting in a conformational change in AR and translocation of the receptor complex to nucleus. This complex interacts with androgen response element (ARE) on the target gene, and regulates gene expression in concert with co-regulators (CoR), transcription factors (TF) and the general transcription complex. The changes in androgen-target proteins in the cell eventually affect cellular structure and function related to male sexual differentiation, physiology, and pathophysiology. The function of AR can be activated or modified by non-ligand factors such as growth factors, EGF and IGF-1. GTFs – general transcription factors; ARA – androgen receptor associated proteins; P- phosphorylation; TFs – transcription factors; hsp – heat shock protein.
Figure 3
Figure 3
Comparison of prostate sizes between age-matched normal adult males and 5α-reductase-2 deficient patients before (5α-RD) and after (5α-RD/DHT) DHT treatment for 3 to 6 months. Panels A and B show representative sonograms of prostate in a 5α-reductase-2 deficient patient pre-DHT treatment (A) and post 2% DHT cream (B) applied to the genital area for approximately 3 months. Note the crosses at the outer edges of the prostate. Panel C shows the prostate volume as determined by sonogram in 5α-reductase-2 deficient patients and age-matched normal male controls.
Figure 4
Figure 4
A structural comparison of human ERα and ERβ. A schematic structural comparison of human ERα and ERβ. Receptor domains are illustrated with different colored boxes, and the approximate size of each domain is indicated.
Figure 5
Figure 5
A graphic illustration of ligand-AR and ER cross-talk in the prostate cells. A graphic illustration of ligand-AR and ER cross-talk in the prostate cells. T – testosterone, E2 – estrogens, and 5αRD - 5α-reductase.
Figure 6
Figure 6
Illustration of the direct and indirect actions of estrogens in the modulation of androgen actions in the prostate cell.
See this image and copyright information in PMC

References

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