Figure 1
Figure 1. Hdac1 knock-down accelerates APL development. (A) Immunoblot analysis of Hdac1, 2, and 3 expression, and histone 3H/H4 acetylation in GFP+ lin− cells derived from mCGPR/PR mice and transduced with the indicated retroviral vectors. Total histone 3H served as a loading control. (B) Leukemia-free survival curves of mice transplanted with the indicated GFP+ lin− cells. HDAC1-KDA and HDAC1-KDB indicate 2 different shRNA against Hdac1 (supplemental Table 4). CTRL vs Hdac1: P < .0001. (C) Hdac1, Hdac2, and Hdac3 expression in bone marrows of leukemic mice. Vinculin was used as a loading control. (D) Cytologic analysis of APL blasts from the spleens of moribund animals. Original magnification ×1000, May Grünwald-Giemsa staining, Olympus BX51. (E) Representative immunophenotype of leukemic cells derived from the spleens of moribund animals.

Hdac1 knock-down accelerates APL development. (A) Immunoblot analysis of Hdac1, 2, and 3 expression, and histone 3H/H4 acetylation in GFP+ lin cells derived from mCGPR/PR mice and transduced with the indicated retroviral vectors. Total histone 3H served as a loading control. (B) Leukemia-free survival curves of mice transplanted with the indicated GFP+ lin cells. HDAC1-KDA and HDAC1-KDB indicate 2 different shRNA against Hdac1 (supplemental Table 4). CTRL vs Hdac1: P < .0001. (C) Hdac1, Hdac2, and Hdac3 expression in bone marrows of leukemic mice. Vinculin was used as a loading control. (D) Cytologic analysis of APL blasts from the spleens of moribund animals. Original magnification ×1000, May Grünwald-Giemsa staining, Olympus BX51. (E) Representative immunophenotype of leukemic cells derived from the spleens of moribund animals.

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