Figure 7
Figure 7. IFN-α response in Arid3a KO cells. (A) Immunoblot for phospho-Stat1 and Stat1 in Arid3a +/− and −/− AGMs treated with IFN-α. (B) Immunoblot confirmation of ARID3A KD in K562 cells via shRNAs. (C) Immunoblot for phospho-Stat1 and Stat1 in ARID3A KD cells showing response to IFN-α. (D) Representative model indicating the role of IFN-α during embryonic hematopoiesis. In contrast to IFN-γ, which promotes HSC emergence, IFN-α promotes partial maturation of AGM HSCs. Arid3a is a transcription co-regulator of IFN effector genes. When Arid3a is absent, inflammatory signaling via IFNs is dampened. Saturating the system with Stat1 via exogenous IFN-α treatment is able to overcome this defect. KD, knockdown; sh, short hairpin.

IFN-α response in Arid3a KO cells. (A) Immunoblot for phospho-Stat1 and Stat1 in Arid3a+/− and −/− AGMs treated with IFN-α. (B) Immunoblot confirmation of ARID3A KD in K562 cells via shRNAs. (C) Immunoblot for phospho-Stat1 and Stat1 in ARID3A KD cells showing response to IFN-α. (D) Representative model indicating the role of IFN-α during embryonic hematopoiesis. In contrast to IFN-γ, which promotes HSC emergence, IFN-α promotes partial maturation of AGM HSCs. Arid3a is a transcription co-regulator of IFN effector genes. When Arid3a is absent, inflammatory signaling via IFNs is dampened. Saturating the system with Stat1 via exogenous IFN-α treatment is able to overcome this defect. KD, knockdown; sh, short hairpin.

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