Partial deficiency of Thyroid transcription factor 1 produces predominantly neurological defects in humans and mice
J. Clin. Invest. Joachim Pohlenz, et al. 109:469 doi:10.1172/JCI14192 [Go to this article.]

Figure 2
Functional analysis of the mutTTF1 as compared with the wtTTF1. (a) DNA binding was assessed by electrophoresis mobility shift assay using α³²P-labeled oligonucleotide primer (oligonucleotide C), containing the TTF1 binding sequence (see Methods), and TTF1 synthesized in reticulocyte lysate. The amounts of lysate (in μl) added to each lane and its origin is indicated below the gel image generated by phosphorimaging of the electrophoresed gel. Note that the mutTTF1 does not bind to oligonucleotide C and does not interfere with the binding of the wtTTF1. The same results were obtained with the addition of an equal amount (shown) and twice and four times the amount of the mutTTF1 as compared with wtTTF1 (see also Results and Discussion) (b) The transactivation properties of the mutTTF1 and wtTTF1 were tested by their cotransfection with a reporter luciferase expression vector driven by the human thyroglobulin enhancer/promoter. Note that the mutTTF1 completely lacks activity and does not interfere with that of the wtTTF1. AU, arbitrary units; 1× and 3×, amount of mutTTF1 relative to wtTTF1.