Figure 3
Figure 3. Nrf2 reduces the erythroid phenotype of Trsp-deficient mice. (A-B) Flow cytometric analysis of immature-erythroid (c-Kit+/CD71+) and mature-erythroid (CD71+/Ter119+) lineages in bone marrows, respectively. Representative data are presented from more than 3 independent experiments. Frequencies of cells in the indicated fraction are shown in the panels. (C-D) ROS production in c-Kit+/CD71+ (C) and CD71+/Ter119+ cells (D) of Trspfl/del and Trspfl/del:Mx1-Cre mice on Nrf2+/+ (top) or Nrf2–/– (bottom) background. (E-F) Expressions of Nrf2 target gene mRNA levels in c-Kit+/CD71+ (E) and CD71+/Ter119+ cells (F) were examined by real-time RT-PCR. Ribosomal 18S subunit was used as an internal control.

Nrf2 reduces the erythroid phenotype of Trsp-deficient mice. (A-B) Flow cytometric analysis of immature-erythroid (c-Kit+/CD71+) and mature-erythroid (CD71+/Ter119+) lineages in bone marrows, respectively. Representative data are presented from more than 3 independent experiments. Frequencies of cells in the indicated fraction are shown in the panels. (C-D) ROS production in c-Kit+/CD71+ (C) and CD71+/Ter119+ cells (D) of Trspfl/del and Trspfl/del:Mx1-Cre mice on Nrf2+/+ (top) or Nrf2–/– (bottom) background. (E-F) Expressions of Nrf2 target gene mRNA levels in c-Kit+/CD71+ (E) and CD71+/Ter119+ cells (F) were examined by real-time RT-PCR. Ribosomal 18S subunit was used as an internal control.

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