@article{taylor_cowin_couse_korach_risbridger_2006, title={17 beta-Estradiol induces apoptosis in the developing rodent prostate independently of ER alpha or ER beta}, volume={147}, ISSN={["1945-7170"]}, DOI={10.1210/en.2005-0683}, abstractNote={Estrogens induce both proliferative and antiproliferative responses in the prostate gland. To date, antiproliferative effects of estrogens are generally considered to be due to systemic antiandrogenic actions. However, estrogen action mediated through estrogen receptor (ER) β was recently suggested as another mechanism of induction of apoptosis in the prostate. This study aimed to explore the hypothesis that the antiproliferative effects of estrogen are directly mediated through ERβ using a prostate organ culture system. We previously reported effects of 17β-estradiol (E2) using rat ventral prostate (VP) tissues, and adapted the system for culturing mouse tissues. In both rat and mouse models, estrogen-induced apoptosis was detected that was spatially and regionally localized to the epithelium of the distal tips. Using organ cultures of αER knockout (αERKO) and βERKO prostates, we failed to demonstrate that apoptosis induced by E2 was mediated through either receptor subtype. Activation of ER-selective ligands (ERα, propyl pyrazole triol, ERβ, diaryl-proprionitrile, and 5α-androstane-3β,17β-diol) in organ culture experiments failed to induce apoptosis, as did the membrane impermeable conjugate E2:BSA, discounting the possibility of nongenomic effects. Consequently, E2 regulation of androgen receptor (AR) expression was examined and, in the presence of nanomolar testosterone levels, E2 caused a specific reduction in AR protein expression in wild-type, αERKO, and βERKO mice, particularly in the distal region where apoptosis was detected. This down-regulation of AR protein provides a possible mechanism for the proapoptotic action of E2 that is independent of ERs or nongenomic effects.}, number={1}, journal={ENDOCRINOLOGY}, author={Taylor, RA and Cowin, P and Couse, JF and Korach, KS and Risbridger, GP}, year={2006}, month={Jan}, pages={191–200} }
 @article{couse_korach_2004, title={Estrogen receptor-alpha-mediates the detrimental effects of neonatal diethylstilbestrol (DES) exposure in the murine reproductive tract}, volume={205}, number={02-Jan}, journal={Toxicology (Amsterdam, Netherlands)}, author={Couse, J. F. and Korach, K. S.}, year={2004}, pages={55–63} }
 @article{couse_yates_walker_korach_2003, title={Characterization of the hypothalamic-pituitary-gonadal axis in estrogen receptor (ER) null mice reveals hypergonadism and endocrine sex reversal in females lacking ER alpha but not ER beta}, volume={17}, number={6}, journal={Molecular Endocrinology (Baltimore, Md.)}, author={Couse, J. F. and Yates, M. M. and Walker, V. R. and Korach, K. S.}, year={2003}, pages={1039–1053} }
 @inbook{couse_korach_2001, title={Contrasting phenotypes in reproductive tissues of female estrogen receptor null mice}, volume={948}, number={2001}, booktitle={Environmental hormones: The scientific basis of endocrine disruption}, publisher={New York, NY: New York Academy of Sciences}, author={Couse, J. F. and Korach, K. S.}, year={2001}, pages={1–8} }
 @article{prins_birch_couse_choi_katzenellenbogen_korach_2001, title={Estrogen imprinting of the developing prostate gland is mediated through stromal estrogen receptor alpha: Studies with alpha ERKO and beta ERKO mice}, volume={61}, number={16}, journal={Cancer Research}, author={Prins, G. S. and Birch, L. and Couse, J. F. and Choi, I. and Katzenellenbogen, B. and Korach, K. S.}, year={2001}, pages={6089–6097} }
 @article{couse_mahata_eddy_korach_2001, title={Molecular mechanism of estrogen action in the male: insights from the estrogen receptor null mice}, volume={13}, ISSN={["1031-3613"]}, DOI={10.1071/RD00128}, abstractNote={
Until recently, 17β-estradiol was thought to be of little importance
in male fertility. However, the descriptions of testicular dysfunction and
behavioral deficits leading to complete infertility in male mice lacking
estrogen receptor α (ERα) have indicated the importance of
estrogen action in fertility of the male rodent. In contrast, male mice
lacking the newly discovered estrogen receptor β (ERβ)
exhibit no compromised fertility. Recently, elaborate sperm transplantation
studies have shown that the altered sperm function characteristic of the
ERα knockout male are the result of the loss of ERα
actions in the supporting somatic cells of the testis and epididymis rather
than in the germ cell. This brief review will discuss the roles of estrogen
action in male reproduction as revealed by mice lacking both known forms of
the ER. A brief review of the estrogen signaling system is also included.
}, number={4}, journal={REPRODUCTION FERTILITY AND DEVELOPMENT}, author={Couse, JF and Mahata, D and Eddy, EM and Korach, KS}, year={2001}, pages={211–219} }
 @article{dixon_couse_korach_1997, title={Highlights of contemporary genetically altered models: disruption of the estrogen receptor in mice}, volume={25}, number={1997}, journal={Toxicologic Pathology}, author={Dixon, D. and Couse, J.F. and Korach, K.S.}, year={1997}, pages={518–520} }