The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.
Alteration of reproductive function but not prenatal sexual development after insertional disruption of the mouse estrogen receptor gene.
Open accessAbstract
Estrogen receptor and its ligand, estradiol, have long been thought to be essential for survival, fertility, and female sexual differentiation and development. Consistent with this proposed crucial role, no human estrogen receptor gene mutations are known, unlike the androgen receptor, where many loss of function mutations have been found. We have generated mutant mice lacking responsiveness to estradiol by disrupting the estrogen receptor gene by gene targeting. Both male and female animals survive to adulthood with normal gross external phenotypes. Females are infertile; males have a decreased fertility. Females have hypoplastic uteri and hyperemic ovaries with no detectable corpora lutea. In adult wild-type and heterozygous females, 3-day estradiol treatment at 40 micrograms/kg stimulates a 3- to 4-fold increase in uterine wet weight and alters vaginal cornification, but the uteri and vagina do not respond in the animals with the estrogen receptor gene disruption. Prenatal male and female reproductive tract development can therefore occur in the absence of estradiol receptor-mediated responsiveness.
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Citations
Cites
The Skipping of Constitutive Exons in Vivo Induced by Nonsense Mutations
Dietz, H. C., Valle, D., Francomano, C. A., Kendzior, R. J., Pyeritz, R. E., & Cutting, G. A. (1993) · Science · doi:10.1126/science.8430317 · Cited by 417
Cited by
Kuiper, G. G. J. M., Carlsson, B., Grandien, K., Enmark, E., Häggblad, J., Nilsson, S., & Gustafsson, J.-A. (1997) · Endocrinology · doi:10.1210/endo.138.3.4979 · Cited by 4,442
Estrogen Resistance Caused by a Mutation in the Estrogen-Receptor Gene in a Man
Smith, E. P., Boyd, J., Frank, G. R., Takahashi, H., Cohen, R. M., Specker, B., Williams, T. C., Lubahn, D. B., & Korach, K. S. (1994) · New England Journal of Medicine · doi:10.1056/nejm199410203311604 · Cited by 2,471
Self-citationEstrogen Receptor Null Mice: What Have We Learned and Where Will They Lead Us?
Couse, J. F., & Korach, K. S. (1999) · Endocrine Reviews · doi:10.1210/edrv.20.3.0370 · Cited by 2,045
Self-citationEstrogen receptors: how do they signal and what are their targets
Heldring, N., Pike, A., Andersson, S., Matthews, J., Cheng, G., Hartman, J., Tujague, M., Ström, A., Treuter, E., Warner, M., et al. (2007) · Physiological Reviews · doi:10.1152/physrev.00026.2006 · Cited by 1,857
Luo, X., Ikeda, Y., & Parker, K. L. (1994) · Cell · doi:10.1016/0092-8674(94)90211-9 · Cited by 1,631
Metadata
- Authors
- Lubahn, D. B., Moyer, J. S., Golding, T. S., Couse, J. F., Korach, K. S., & Smithies, O.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 1993-12
- Volume
- 90
- Issue
- 23
- Pages
- 11162-11166
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W2141269411
- Cited by
- 1,898
- References
- 1
- FWCI
- 15.37
- Type
- journal article
- Language
- en
- Open access
- green
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- Lubahn, D. B., Moyer, J. S., Golding, T. S., Couse, J. F., Korach, K. S., & Smithies, O. (1993). Alteration of reproductive function but not prenatal sexual development after insertional disruption of the mouse estrogen receptor gene. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.90.23.11162
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