Table 1.

Down-regulation of chimeric receptors is not affected by type I TGF-β receptor tyrosine mutations

Cell line	Slope	Percent receptor binding at 4 h	n
A105	−0.661  ± 0.082	32.2  ± 2.7	3
A-Y182S	−0.664  ± 0.057	26.6  ± 5.7	3
A-Y249S	−0.962  ± 0.090	25.7  ± 4.0	3
M-Heteromer	−1.301  ± 0.067	17.1  ± 2.3	2
M-Y182S	−0.981  ± 0.082	18.4  ± 0.8	2
M-Y249S	−0.906  ± 0.059	26.2  ± 2.1	2

Decreased surface binding of ¹²⁵I-GM-CSF was determined for AKR-2B and Mv1Lu clones expressing a wild-type chimeric type II TGF-β receptor and a type I TGF-β receptor with tyrosine to serine mutations at either Y182 or Y249, when treated with 10 ng/ml GM-CSF at 37°C. Down-regulation of the normal mesenchymal (A105) and epithelial (M-Heteromer) heteromer containing wild-type type I and type II chimeric receptors is shown for comparison. The rate of down-regulation was determined from the slope of the line calculated from four data points over the first 60 min. Data for the mesenchymal cells represent 1 AKR-2B clone for each receptor type (A105, Y182S-1, and Y249S-7), whereas the epithelial cell data represent the mean of 2 M-heteromers (MB-9 and -18) and three separate M-Y182S (Y182S-1, -4, and -9) and Y249S (Y249S-8, -16, and -22) mutant clones. Assays from the indicated (n) number of experiments were each performed in duplicate.