Elizabeth M. Wilson
University of North Carolina at Chapel Hill
198 Papers
3.1K Citations
Elizabeth M. Wilson is an academic researcher from University of North Carolina at Chapel Hill. The author has contributed to research in topics: Androgen receptor & Androgen. The author has an hindex of 75, co-authored 195 publications. Previous affiliations of Elizabeth M. Wilson include University at Buffalo.
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Papers
The putative androgen receptor-A form results from in vitro proteolysis
TL;DR: The results suggest that AR forms with gel mobility similar to that of the previously described 87 kDa AR-A result from in vitro proteolytic cleavage of NH(2)- or carboxyl-terminal regions during cell extraction and storage and that smaller forms with increased transcriptional activity do not occur in vivo.
Molecular basis of androgen insensitivity
Frank S. French,Dennis B. Lubahn,Terry R. Brown,Jorge A. Simental,Charmian A. Quigley,Wendell G. Yarbrough,Jiann An Tan,Madhabananda Sar,David R. Joseph,Bronwyn A.J. Evans,I A Hughes,Claude J. Migeon,Elizabeth M. Wilson +12 more
TL;DR: Clinical indications can be abnormal sexual development of individuals with a predominant male phenotype with severe hypospadias and micropenis or of Individuals with a predominantly female phenotype with cliteromegaly, ambiguous genitalia, and gynecomastia.
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A complex response element in intron 1 of the androgen-regulated 20-kDa protein gene displays cell type-dependent androgen receptor specificity
Kuo-Chieh Ho,Keith B. Marschke,Jiann-An Tan,Stephen G.A. Power,Elizabeth M. Wilson,Frank S. French +5 more
TL;DR: The androgen-regulated 20-kDa protein gene consists of four exons that code for a major secretory protein of rat ventral prostate that contains putative response elements for the transcription factors AP1, CREB, AP2, OCT-1, C/EBP, and a number of inverted and direct repeats.
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Epidermal Growth Factor-Dependent Phosphorylation and Ubiquitinylation of MAGE-11 Regulates Its Interaction with the Androgen Receptor
Suxia Bai,Elizabeth M. Wilson +1 more
TL;DR: It is demonstrated that epidermal growth factor signaling increases androgen-dependent AR transcriptional activity through the posttranslational modification of MAGE-11, and sequence conservation of the Mage-11 phosphorylation and ubiquitinylation sites throughout the MAGE gene family suggests common regulatory mechanisms for this group of cancer-testis antigens.
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Partial androgen insensitivity with phenotypic variation caused by androgen receptor mutations that disrupt activation function 2 and the NH(2)- and carboxyl-terminal interaction.
Charmian A. Quigley,Jiann An Tan,Bin He,Zhong Xun Zhou,Farida Mebarki,Yves Morel,Maguelone G. Forest,Pierre Chatelain,E. Martin Ritzén,Frank S. French,Elizabeth M. Wilson +10 more
TL;DR: The studies indicate that the function of an AR AF2 mutant in male development can vary greatly depending on the genetic background.
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