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. 2018 Jun 11;293(30):11659–11673. doi: 10.1074/jbc.RA118.002482

Figure 6.

Figure 6.

Jarid2 represses the Isl1 reporter gene. A, pGL3, pGL3-Isl1 including the −0.5–kb region (−0.9/+0.15 kb) or without the −0.5–kb region (−0.12/+0.15 kb) was transfected into 10T1/2 cells with increasing amounts of Jarid2 (μg). B, a schematic diagram shows Jarid2, and Jarid2 mutants (N-term, 1–528 aa; TR, 1–222 aa; C-term, 529–1234 aa; NLS/C-term, 1–130/529-1234 aa). Jarid2 (0.2 μg) was transfected into 10T1/2 cells with the pGL3-Isl1 (−0.9/+0.15 kb) reporter. TR, transcription repression domain; JN, Jumonji N domain; JC, Jumonji C domain; ARID, AT-rich interaction domain. C, pGL3-Isl1 (−0.9/+0.15 kb) reporter was transfected into 10T1/2 cells with Jarid2, EED, and/or EZH2 at a low dose (50 ng). D, the TR domain of Jarid2 (1–222 aa, 25 ng) was transfected into 10T1/2 cells with or without EED and/or EZH2 (50 ng) for luciferase activity assays of pGL3-Isl1 (−0.9/+0.15 kb). Luciferase activity was normalized to the reporter gene alone. Asterisks indicate a significant difference compared with the reporter gene alone (*, p ≤ 0.05; **, p ≤ 0.01, n = 3). A number sign indicates a significant difference between a combination of any two factors and all three factors together.