Fig. 4.
Fig. 4. Induction of RARα2 by RA in RA-responsive, but not RA-resistant, leukemic cell lines. / (A) RT-PCR analysis of RARα1 and α2 expression in NB4 and HL60 cells that are sensitive (lanes 1-2 and 7-8) and resistant (lanes 3-6 and 9-10) to differentiation induction with RA. (B) Schematic diagram illustrating differential and lineage-specific effects of hematopoietic GFs on RARα expression. Given limiting RXR levels and the role of RXR as an obligatory heterodimerization partner for granulopoiesis- and erythropoisis-associated RAR and TR, respectively, the effects of hematopietic GFs on progenitor cell differentiation may, at least in part, be mediated by facilitating the formation of appropriate NR heterodimers.

Induction of RARα2 by RA in RA-responsive, but not RA-resistant, leukemic cell lines.

(A) RT-PCR analysis of RARα1 and α2 expression in NB4 and HL60 cells that are sensitive (lanes 1-2 and 7-8) and resistant (lanes 3-6 and 9-10) to differentiation induction with RA. (B) Schematic diagram illustrating differential and lineage-specific effects of hematopoietic GFs on RARα expression. Given limiting RXR levels and the role of RXR as an obligatory heterodimerization partner for granulopoiesis- and erythropoisis-associated RAR and TR, respectively, the effects of hematopietic GFs on progenitor cell differentiation may, at least in part, be mediated by facilitating the formation of appropriate NR heterodimers.

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