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M. E. Jones, A. W. Thorburn, K. L. Britt, K. N. Hewitt, N. G. Wreford, J. Proietto, O. K. Oz, B. J. Leury, K. M. Robertson, S. Yao and E. R. Simpson, “Aromatase-Deficient (ArKO) Mice Have a Phenotype of Increased Adiposity,” Proceedings of the National Academy of Sciences of the United States of America, Vol. 97, No. 23, 2000, pp. 12735-12740. doi:10.1073/pnas.97.23.12735
has been cited by the following article:
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TITLE:
The Transactivating Function 2 (AF-2) of Estrogen Receptor (ER) α Is Indispensable for ERα-Mediated Physiological Responses and AF-1 Activity
AUTHORS:
Yukitomo Arao, Katherine J. Hamilton, Kenneth S. Korach
KEYWORDS:
Knock-In Mouse; SERMs; Antagonist Reversal
JOURNAL NAME:
Open Journal of Endocrine and Metabolic Diseases,
Vol.3 No.4B,
August
6,
2013
ABSTRACT: Estrogen
has various physiological functions and the estrogen receptor (ER) is a key
regulator of those functions. ERα is a ligand-dependent transcription factor and that activity is mediated
by the transactivating
function-1 (AF-1) in the N-terminal domain and transactivating function-2 (AF-2) in the C-terminal ligand-binding domain. The functions of ERα AF-1 and AF-2 have been characterized by various in vitro experiments, however, there is
still less information about the in vivo physiological functions of ERα AF-1 and
AF-2. Recently, we established a genetically mutated ERα AF-2 knock-in mouse (AF2ERKI) that possessed L543A,
L544A mutated-ERα. This AF-2 core mutation disrupted AF-2 function and resulted in ERα null phenotypes. This mouse model
revealed that proper AF-2 core structure and function were indispensable for ERα-mediated
physiological responses and
AF-1 functionality. AF2ER mutation reverses the ERα antagonists to agonists and that activity is mediated by AF-1
solely. The pure antagonist, ICI182780/fulvestrant, activated several
estrogen-mediated physiological responses in the AF2ERKI mouse. The AF2ERKI
mouse model will be useful to discern estrogen physiological functions which
involve AF-1.