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J. Biol. Chem., Vol. 267, Issue 2, 913-921, 01, 1992
F Leidig, AR Shepard, WG Zhang, A Stelter, PA Cattini, JD Baxter and NL Eberhardt
Triiodothyronine (T3) induces the transcription of the human chorionic
somatomammotropin (hCS) promoter transfected into rat pituitary (GC) cells,
but does not stimulate the homologous human growth hormone (hGH) promoter.
As demonstrated by forward and reverse mutagenesis, this differential T3
responsiveness is due to subtle structural differences in a T3 response
element located between nucleotides -64 and -44 of the 5'-flanking DNA of
the hGH and hCS promoters. Synthetic hCS(-70/-40) DNA binds thyroid hormone
receptors with a 4-fold higher affinity than the corresponding hGH T3
response element, indicating that small differences in receptor binding
properties are reflected by major differences in T3 responsiveness.
Analysis of circular permutation fragments containing the native hGH and
hCS or mutated hCS(-70/-40) sequences demonstrates that the thyroid hormone
receptor induces DNA bending. The extent of bending shows a possible
correlation with the function of these sequences, suggesting that the
receptor-induced changes in DNA conformation may be required for thyroid
hormone receptor action.
Thyroid hormone responsiveness in human growth hormone-related genes. Possible correlation with receptor-induced DNA conformational changes
Department of Medicine, Mayo Clinic, Rochester, Minnesota 55905.
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