Regulation of Leukemic Cell Differentiation through the Vitamin D Receptor at the Levels of Intracellular Signal Transduction, Gene Transcription, and Protein Trafficking and Stability

<table>Expression of VDR protein in AML cells exposed to 1,25(OH)<sub>2</sub>D. AML cells after incubation for indicated times with 10 nM 1,25(OH)<sub>2</sub>D were lysed and fractionated into the cytoplasmic (C) and nuclear (N) fractions. The lysates from equal numbers of cells were separated in SDS-PAGE and blotted to the membrane. The membrane was probed with anti-VDR. Actin was probed as a control of equal loading and transfer of proteins. (a) HL60 cells, (b) THP-1, MV4-11 cells, and (c) AML-M4 blasts from patient’s peripheral blood. Based on [<a href="713243.html#B44">41</a>, <a href="713243.html#B46">42</a>] and on unpublished data.</table>

Leukemia Research and Treatment

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Figure 5

Figure 5: Regulation of Leukemic Cell Differentiation through the Vitamin D Receptor at the Levels of Intracellular Signal Transduction, Gene Transcription, and Protein Trafficking and Stability 

Figure 5 | Regulation of Leukemic Cell Differentiation through the Vitamin D Receptor at the Levels of Intracellular Signal Transduction, Gene Transcription, and Protein Trafficking and Stability 