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Autoiduction of androgen receptor mRNA n primary cultures of hamster (Mesocricetus auratus) harderian gland
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The hamster androgen receptor promoter: a molecular analysis
No full textThe steroid/thyroid hormone receptors are members of a very large family of nuclear-activated transcription factors. These receptors play a crucial role in most biological function, including regulation of development, metabolism, behaviour and reproduction. Among androgen receptor (AR), we have recently demonstrated that its expression in the Harderian gland (HG) of the male hamster is under a well-co-ordinated cross-talk between various steroid hormone receptors. Here, are presented data on the sequence of hamster AR promoter region (5’UTR) and the molecular tools of its regulation. The 5’UTR is 1585 bp. The promoter region shows various responsive elements. Two putative CREM elements are present at −71 and −1576 bp. A putative retinoic acid responsive element is present at −1476 bp. An androgen/glucocorticoid responsive element is present at −473 bp. A putative thyroid hormone-responsive element at −381 bp and an estrogen responsive element at −230 bp. Also, a homopurinic stretch is evident between −1199 and −1118. Furthermore, Sp1 sites are also spread along the sequence. As well as for human, mouse, rat and pig, the hamster lacks the canonical promoter TATA and CCAAT boxes. Gel retardation experiments confirm the presence of active responsive elements for AR, estrogen receptor, glucocorticoid receptor and thyroid hormone receptor. Previous data on the regulation of expression of AR by other members of steroid/thyroid hormone receptors well correlate with sequence analysis and gel retardation experiments. Thus, androgens, thyroid hormone, stimulate the AR transcription, while synthetic glucocorticoid (Dex) and estrogen are potent inhibitors of AR expression. The comparison of hamster AR promoter sequence with other AR promoter shows an 89, 82, 84 and 84% identity with human, rat, mouse and pig AR promoter, respectively. These results, in the light of the extreme plasticity of hamster HG, suggest that the comparative study of expression and regulation of AR gene in the HG of the hamster offers a useful tool to approach the normal and pathological phenotype in human
The androgen receptor mRNA is up-regulated by testosterone in both the Harderian gland and thumb pad of the frog, Rana esculenta
No full textAutoinduction of estrogen receptor is associated with FOSP-1 mRNA induction by estrogen in primary cultures of Xenopus oviduct cells
No full textAutoregulation of androgen and estrogen receptor mRNAs and down regulation by estrogen of androgen receptor mRNA in lizard testis
No full textAutoregulation of estrogen and androgen receptor mRNAs and downregulation of androgen receptor mRNA by estrogen in primary cultures of lizard testis cells
No full textSeasonal fluctuations in plasma progesterone concentrations in Gentile-di-Puglia and Ile-de-France ewes in southern Italy
No full textHormonal regulation and characterization of MHG30 gene, a desaturase-like gene of hamster harderian gland.
No full textThe harderian gland (HG) is an orbital gland of the vast majority of land vertebrates. In the Syrian hamster these glands display a marked sexual dimorphism. Here we present data on a male specific clone named MHG30. The MHG30 cDNA (1470 bp) has significant sequence homologies with human #15μ10#Δ6-desaturase enzymes. The expression of MHG30 has been found in male HG and in the liver of both sexes, no other tissue showing the presence of MHG30 mRNA. Castration brings the MHG30 levels below detectable level in about 7 days. In in vitro cultures of male hamster HG cells, androgens (A) determine an enhancement of MHG30 expression in a time-dependent manner. Conversely, a continuous decrement has been observed in control cells and in cells treated with A plus flutamide (F) or with A and cycloheximide (Cy). Incubation of cells in cultures supplemented with desamethason (Dex) or thyroid hormone (T3) also increases MHG30 expression while 17β-estradiol prevents the stimulatory effect exerted by A, Dex and T3. Findings strongly suggest that the MHG30 gene could be involved in supporting the sexual dimorphism and its expression is likely triggered by a series of hormonal interactions
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