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. 2007 Mar;170(3):1041–1053. doi: 10.2353/ajpath.2007.060804

Figure 1.

Figure 1

Characterization of the GR(C656G) point mutation and generation of the superTGR rats. A: Western blot analysis of the three Jurkat cell lines E6.1, J.Gr, and J.Gr* for GR expression. β-Tubulin served as a loading control. B: The survival of J.Gr and J.Gr* cells cultured for 48 hours in the presence of serial dilutions of dexamethasone was determined by flow cytometry. Survival in control cultures was set at 100%. C: Structure of the transgene vector consisting of the proximal lck promoter, the mutant mGR(C656G) cDNA, and a hGH minigene. D: Analysis of GR mRNA expression in thymocytes and lymph node T cells from wild-type and transgenic rats. The cDNA was amplified using GR-specific primers and the PCR products digested with PstI. The smaller band is derived from the mutant GR encoded by the transgene (mut), whereas the larger band stems from the endogenous GR (wt). E: Western blot analysis of thymocytes and lymph node T cells using antibodies against GR and lck as a loading control.