FIGURE 7.

Tel-PdgfRβ increased activity of the PTPN13 promoter. A, Tel-PdgfRβ increased PTPN13 promoter activity in a kinase-independent manner. U937 cells that were stably transfected with a vector to express Tel-PdgfRβ, a kinase inactive form of Tel-PdgRβ (KD-Tel-PdgfRβ), or control expression vector were co-transfected with a reporter vector with 670 bp of the PTPN13 promoter (ptpn13GL3) or control reporter vector. Activity from the empty reporter vector was <10% of the ptpn13GL3, which was subtracted as background. Differences in reporter activity not statistically significantly different (p > 0.6) are indicated by a lowercase a. Statistically significant differences (p < 0.0001) in reporter activity are indicated by *. B, Tel-PdgfRβ increased Fap1 protein expression in a tyrosine kinase-independent manner. U937 myeloid cells were stably transfected with a vector to express Tel-PdgfRβ, KD-Tel-PdgfRβ, or empty control vector. Total cell lysates were analyzed by Western blots (WB), which were serially probed with antibodies to PdgfRβ, Fap1, or tubulin (as a loading control). The anti-PdgfRβ antibodies used in this experiment recognize both endogenous PdgfRβ and the product of the Tel-PdgfRβ transgene. This blot represents transfectants performed at the same time as one of the reporter gene assays from A.