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Fig. S1 Testosterone increases hematocrit, hemoglobin (A), and serum iron (B) in castrated (Cx) male mice.

Fig. S2 Hepatic hepcidin mRNA expression level in female wild-type (wt) mice and the female mice with silent (Tg−) and constitutively active (Tg+) transgenic hepcidin expression.

Fig. S3 Constitutive over-expression of a hepcidin transgene in Tg+ mice attenuates testosterone-induced increase of hematocrit and completely blocks the rise of hemoglobin (N = 6 for each group).

Fig. S4 Effects of testosterone administration on hypoxia sensing mechanisms.

Fig. S5 Testosterone does not affect mRNA expression of Smad1, 4, 8, Hjv, TMRPSS6, and BMP6, but it significantly reduced the expression of Smad7 in the liver of female mice 2 days after testosterone injection, a time point when hepcidin expression was downregulated (mean ± SE, = 6 for each group).

Fig. S6 ChIP analysis of liver tissue isolated from mice treated with either vehicle (C) or testosterone (T) four 48 h.

Fig. S7 AR antagonist flutamide does not change basal or BMP2-induced hepcidin promoter activity.

Fig. S8 AR/DHT does not affect hepcidin mRNA stability: time-dependent changes in hepcidin mRNA in HepG2 cells expressing vector (C) or ectopic AR after RNA synthesis was blocked by actinomycin D (1 μg mL−1).

Fig. S9 Representative DNA gel pattern after chromatin digestion by micrococcal nuclease at 37°C for 30 min (10 min longer than protocol recommended), with frequent flicking.

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