Steroid receptor knockouts

Current Opinion in Endocrinology and Diabetes

Volumn 3, Issue 5, 1996, Pages 363-368

  Cole, Timothy J ^a  

^a BAKER IDI HEART AND DIABETES INSTITUTE   (Australia)

Author keywords

[No Author keywords available]

Indexed keywords

EID: 0006035776     PISSN: 10683097     EISSN: None     Source Type: Journal    
DOI: 10.1097/00060793-199610000-00002     Document Type: Article

References (38)

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18. Threadgill DW, Dlugosz AA, Hansen LA, Tennenbaum T, Lichti U, Yee D, LaMantia C, Mourton T, Herrup K, Harris RC, Barnard JA, Yuspa SH, Coffey RJ, Magnuson T: Targeted disruption of the mouse EGF receptor: effect of genetic background on mutant phenotype. Science 1995, 269:230-234. The targeted mutation of the mouse epidermal growth factor receptor was placed in three genetic backgrounds, producing three different phenotypes. In the CF-1 background there was peri-implantation lethality, in the 129/sv background there was midgestation lethality, and in the CD-1 background there was perinatal lethality.
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27. Lydon JP, DeMayo FJ, Funk CR, Mani SK, Hughes AR, Montgomery CA Jr, Shyamala G, Conneely OM, O'Malley BW: Mice lacking progesterone receptor exhibit pleiotropic reproductive abnormalities. Genes Dev 1995, 9:2266-2278. Targeted disruption of PR produced infertile female mice but normal fertile males. Adult female PR knockout mice had an inability to ovulate, uterine hyperplasia and inflammation, limited mammary gland development, and an inability to exhibit sexual behavior.
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32. Taplin M-E, Bubley GJ, Shuster TD, Frantz ME, Spooner AE, Ogata GK, Keer HN, Balk SP: Mutation of the androgen-receptor gene in metastatic androgen-independent prostate cancer. N Engl J Med 1995, 332:1393-1398.
33. Gerlai R: Gene-targeting studies of mammalian behavior: is it mutation or the background genotype? Trends Neurosci 1996, 19:177-181.
34. Rozmahel R, Wilschanski M, Matin A, Plyte S, Oliver M, Auerbach W, Moore A, Forstner J, Dune P, Nadeau J, Bear C, Tsui L-C: Modulation of disease severity in cystic fibrosis transmembrane conductance regulator deficient mice by a secondary genetic factor. Nat Gen 1996, 12:280-287. The phenotype of Cftr mice, generated by gene targeting, showed variations in different inbred genetic backgrounds. Genome scanning allowed isolation of a modifier locus on chromosome 7 that was identified as a calcium-activated Cl-conductor that, when more active, promoted survival of Cftr-deficient mice.
35. Logie C, Stewart AF: Ligand-regulated site-specific recombination. Proc Natl Acad Sci U S A 1995, 92:5940-5944. Demonstration of ligand-dependent induction of Flp-recombinase activity in vivo using an Flp-recombinase-estrogen receptor ligand binding domain fusion protein.
36. Metzger D, Clifford J, Chiba H, Chambon P: Conditional site-specific recombination in mammalian cells using a ligand-dependent chimeric Cre recombinase. Proc Natl Acad Sci U S A 1995, 92:6991-6995. Reports the use of a Cre-recombinase-estrogen receptor ligand binding domain fusion protein to allow ligand-induced site-specific recombination in F9 cells.
37. Dymecki SM: Flp recombinase promotes site-specific DNA recombination in embryonic stem cells and transgenic mice. Proc Natl Acad Sci U S A 1996, 93:6191-6196. Demonstrates that Flp-recombinase expression in mice is compatible with normal development and survival and, more important, that it can excise DNA in transgenic mice.
38. Kellendonk C, Tronche F, Monaghan A-P, Angrand P-O, Stewart F, Schütz G: Regulation of Cre recombinase activity by the synthetic steroid RU 486. Nucleic Acids Res 1996, 24:1404-1411. Describes a strategy for inducible gene targeting in mouse embryonic stem cells using the Cre-recombinase joined to a mutated PR ligand binding domain that is activated by concentrations of the synthetic steroid mifepristone.