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자료유형
학술저널
저자정보
Hye-Rim Lee (충북대학교) Tae-Hee Kim (순천향대학교) Kyung-Chul Choi (충북대학교)
저널정보
한국실험동물학회 Laboratory Animal Research Laboratory Animal Research Vol.28 No.2
발행연도
2012.6
수록면
71 - 76 (6page)

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Estrogens, a class of steroid hormones, regulate the growth, development, and physiology of the human reproductive system. Estrogens also involve in the neuroendocrine, skeletal, adipogenesis, and cardiovascular systems. Estrogen signaling pathways are selectively stimulated or inhibited depending on a balance between the activities of estrogen receptor (ER) α or ERβ in target organs. ERs belong to the steroid hormone superfamily of nuclear receptors, which act as transcription factors after binding to estrogen. The gene expression regulation by ERs is to modulate biological activities, such as reproductive organ development, bone modeling, cardiovascular system functioning, metabolism, and behavior in both females and males. Understanding of the general physiological roles of ERs has been gained when estrogen levels were ablated by ovariectomy and then replenished by treatment with exogenous estrogen. This technique is not sufficient to fully determine the exact function of estrogen signaling in general processes in living tissues. However, a transgenic mouse model has been useful to study gene-specific functions. ERα and ERβ have different biological functions, and knockout and transgenic animal models have distinct phenotypes. Analysis of ERα and ERβ function using knockout mouse models has identified the roles of estrogen signaling in general physiologic processes. Although transgenic mouse models do not always produce consistent results, they are the useful for studying the functions of these genes under specific pathological conditions.

목차

The reproductive system in ER knockout mice
Fertility
Reproductive organs
Mammary gland
Male reproduction
Bone development and maintenance in ER knockout mice
Cardiovascular tissues and metabolism in ER knockout mice
Brain and behavior
Summary
Acknowledgments
References

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UCI(KEPA) : I410-ECN-0101-2013-510-002637085