Estradiol-17β receptors in the immature rat ovary

Saiduddin, Syed; Zassenhaus, Hans Peter

doi:10.1016/0039-128x(77)90039-3

Cited by 45 publications

(23 citation statements)

References 17 publications

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“…Therefore, normal ovarian function appears to be dependent on a multitude of auto-and paracrine actions of estradiol that act in concert with the gonadotropins secreted from the anterior pituitary to provide for successful folliculogenesis and steroid production. Nonetheless, immunohistochemical detection and characterization of ER in the different ovarian compartments have proven difficult, although studies employing binding assays with radiolabeled ligands report the presence of ER in ovarian granulosa cells of the rat (216,(233)(234)(235), mouse (236), rabbit (236), and pig (235).…”

Section: Review Of Intraovarian Estrogen Actionsmentioning

confidence: 99%

Estrogen Receptor Null Mice: What Have We Learned and Where Will They Lead Us?

1999

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Section: Review Of Intraovarian Estrogen Actionsmentioning

confidence: 99%

Estrogen Receptor Null Mice: What Have We Learned and Where Will They Lead Us?

1999

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“…These effects are partly exerted through ovarian steroid receptors (Schreiber et al, 1980). Many published data deal with rat ovarian steroid receptors (Schreiber and Hsueh, 1979;Schreiber and Erickson, 1979;Sakabe et al, 1983;Fujii-Hanamoto et al, 1985;Hamilton et al, 1977;Saiduddin and Zassenhaus, 1977;Saiduddin and Zassenhaus, 1978), but the effect of gonadotropins on immature rat ovarian vs. uterine receptors of steroid hormones still remains to be clarified. The serum P4 level for group B was higher than that for group A, but the difference was not significant (Fig.…”

mentioning

confidence: 99%

“…Ginsburg (Ginsburg et al, 1975) reported that the Kd value for rat uterine ER was constant in the estrous cycle. The Kd value for the ER of pregnant rat corpus luteum was reported to be 0.22nM (Saiduddin et al, 1977) and that of immature rat was 0.413nM (Richards, 1974). These values are fairly close.…”

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confidence: 99%

Steroid Hormone Receptors in the Uterus and Ovary of Immature Rats Treated with Gonadotropins.

et al. 1989

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We administered either saline (group A) or 10 IU of pregnant mare serum gonadotropin (PMS; groups B and C) to female immature rats. Fifty-three hours later, the rats were injected with saline (groups A and B) or 30 IU of human chorionic gonadotropin (hCG; group C). The rats were decapitated 17 h after the last treatment, and the serum levels of progesterone (P4) and estradiol (E2) were measured by specific radioimmunoassays (RIA). The receptor levels of progesterone (PR) and estrogen (ER) in the uterus and ovaries were measured and the dissociation constant (Kd) of PR was obtained.The highest serum level of P4 was found in group C and that of E2 in group B. Cytsol levels of PR and ER in the uterus and ovary of the group B were the highest.It was indicated that the PMS treated-group (B), which had developing follicles in the ovary and the high serum level of E2, showed the highest concentration of ER and PR in both the ovary and the uterus. In the PMS and hCG-treated group (C), the uterine and ovarian steroid receptors decreased probably because of the luteinization and the high serum level of P4. The Kd uterine PR value was less than that of ovarian PR.

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“…When ERb was cloned and expressed in insect cells, it was found that this new ER sediments at 4S regardless of the salt concentrations in the buffer [12][13][14]. Before 1995, there are some reports in the literature where 4S 17b -estradiol binding peaks were found when tissues were analyzed [15][16][17][18][19]. These results were not understood, but today we know that these are ERb-containing tissues, and the 4S peak was probably ERb.…”

Section: Gl01-03mentioning

confidence: 91%

General Lectures (GL)

2003

European Journal of Biochemistry

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Ca2+ inside cells must be regulated around 10 )7 nM, since enzyme targets respond to the calcium signal in this concentration range. Regulation is achieved through the reversible complexation to several classes of Ca 2+ binding proteins, the best known of which is that of the EF-hand proteins. However, the most important task of these proteins is not the buffering of Ca 2+ but the processing of the information it carries. These proteins decode the Ca 2+ signal by undergoing conformational changes, at the end of which Ca 2+ information is transferred to the target protein. The buffering of cell Ca 2+ is instead the sole role of proteins intrinsic to membranes, which bind Ca 2+ at one side of the membrane, transport it across, and discharge it to the other side. These proteins are located in the plasma membrane and membrane organelles, and belong to several classes: channels, ATPases (pumps), Na The completion of the human and mouse genome projects has revealed the presence of more than 30 000 genes in vertebrates and many more encoded mRNAs and proteins. The next formidable and most challenging task is to determine the physiological and pathophysiological functions of these genes within living organisms. This will be achieved by interfering with the expression of individual genes using genetic and pharmacological approaches. In this respect, germ line-targeted mutagenesis through gene disruption (knock-out) in murine embryonic stem (ES) cells has been widely used during the last decade.However, there are a number of limitations (embryonic lethality, functional redundancies between related genes, compensatory mechanisms during development, impossibility to discriminate between cell-autonomous and noncell-autonomous events) that preclude a simple genetic analysis of gene function in vivo through conventional gene knock-out approaches. In fact, only targeted spatio-temporally-controlled somatic mutations that are generated in animal models in given cell-type/tissues and at chosen times during pre-and post-natal life can lead to the functional dissection of complex regulatory networks, thus revealing the physiological and pathophysiological functions of the genes involved. To generate such somatic mutations, we have developed a new genetic tool based on the bacteriophage P1-Cre/lox system. A conditional ligandinducible Cre recombinase, Cre-ER T2 , has been generated by fusing Cre with a mutated ligand binding domain of the human oestrogen receptor (ER) that binds the synthetic ligand tamoxifen, but not estradiol. Upon tamoxifen administration the Cre activity is induced, and ÔÔfloxedÕÕ DNA segments flanked by loxP sites are efficiently excised. This somatic conditional mutagenesis approach is illustrated by describing our recent mouse studies that are aimed at dissecting the retinoid signaling pathway, a complex regulatory network involved in vertebrate morphogenesis, organogenesis, growth, cellular differentiation and homeostasis. These studies have revealed the physiological and pathophysiological functions of the ...

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Estradiol-17β receptors in the immature rat ovary

Cited by 45 publications

References 17 publications

Estrogen Receptor Null Mice: What Have We Learned and Where Will They Lead Us?

Estrogen Receptor Null Mice: What Have We Learned and Where Will They Lead Us?

Steroid Hormone Receptors in the Uterus and Ovary of Immature Rats Treated with Gonadotropins.

General Lectures (GL)

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