Titlebook: Gene Regulation by Steroid Hormones III; Arun K. Roy,James H. Clark Conference proceedings 1987 Springer-Verlag New York Inc. 1987 Activat

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moribund

Pregnancy in Chronic Kidney Diseasen vitro incubations (Loosfelt et al., 1984). Questions also persist about the mechanisms by which progesterone converts the receptors from loose to tight chromatin-binding proteins, and virtually nothing is known about the means by which the actions of the nuclear hormone-receptor complexes are term

大罵

Obstreperous

Christine El-Yahchouchi,Antoun Naderly owing to our poor understanding of receptor structure and receptor interactions with the transcriptional apparatus. Moreover, many genes appear to be regulated in a complex fashion in which regulatory mechanisms distinct from direct transcriptional activation by the steroid-receptor complex may b

先兆

Engaged

C. Figarella,D. Basso,O. Guy-Crotteratory were directed to explore the molecular mechanism of steroidal regulation of α.-globulin synthesis in the rat liver. Further studies of the α.-globulin model led to the appreciation of the multihormonal regulation of α.-globulin gene expression (Roy, 1979; Roy et al., 1983). In this chapter we

overwrought

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nt. These findings, although controversial, will lead to a reassessment of many of the previous concepts of steroid-receptor interactions and regulation. The way in which these observations at the of physiology, molecular and cellular levels fit into the overall scheme development, and evolution are continuin978-1-4612-9114-5978-1-4612-4686-2

Rodent

Ofelia O. Villero,Nancy J. Burkeittle-studied properties of estrogen receptors—properties arising from their interactions with other common molecules which may play a role in their interactions with chromatin and are likely to influence the cascading genetic events.

bioavailability

Masayuki Miyasaka,Kiyoshi Takatsunuclear response to estrogenic hormones that is highly correlated with uterine hypertrophy and hyperplasia (Markaverich et al., 1981a,b,c). Likewise, nuclear type II sites are elevated in neoplastic tissues such as mouse mammary tumors (Watson et al., 1977; Watson and Clark, 1980; Watson et al., 1981) and human breast cancer (Syne et al., 1982).