Figure 2
Increased coimmunoprecipitation (co-IP) of endogenous corepressor (Eto2, Sin3A, and Hdac2) with Pu.1 in Runx1-deficient cells. (A) Increased co-IP of endogenous corepressor with Pu.1 from PUER shRunx1 compared with PUER empty vector (control) cells. Input indicates nonimmunoprecipitated cell lysate; IgG, control IP with isotype antibody; C, PUER control; and shR, PUER shRunx1. Cells were lysed 4 hours after addition of OHT. (B) Runx1 protein expression is decreased in primary Runx1 haploinsufficient (Runx1+/−) compared with wild-type littermate control (WT) bone marrow cells. Mice were genotyped as previously described.28 (C) Co-IP of endogenous corepressor with endogenous Pu.1 from Runx1+/− compared with WT bone marrow. Lysates were generated from freshly harvested bone marrow.

Increased coimmunoprecipitation (co-IP) of endogenous corepressor (Eto2, Sin3A, and Hdac2) with Pu.1 in Runx1-deficient cells. (A) Increased co-IP of endogenous corepressor with Pu.1 from PUER shRunx1 compared with PUER empty vector (control) cells. Input indicates nonimmunoprecipitated cell lysate; IgG, control IP with isotype antibody; C, PUER control; and shR, PUER shRunx1. Cells were lysed 4 hours after addition of OHT. (B) Runx1 protein expression is decreased in primary Runx1 haploinsufficient (Runx1+/−) compared with wild-type littermate control (WT) bone marrow cells. Mice were genotyped as previously described.28  (C) Co-IP of endogenous corepressor with endogenous Pu.1 from Runx1+/− compared with WT bone marrow. Lysates were generated from freshly harvested bone marrow.

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