Figure 1
Figure 1. RARα-PML cDNA isoforms and Kaplan-Meier analysis of APL disease in transgenic animals. (A) Diagram of the structural features of bcr-1 and bcr-3 isoforms. The identical portion of RARα is expressed in both isoforms of RP (breakpoint in RARα is indicated by the arrow), whereas the expressed PML domains are different because of the locations of the breakpoints in PML (indicated by the dashed lines). DB indicates DNA binding; LB, ligand binding; Dimer, dimerization; P, proline rich; R, ring finger; BB, B-box; CC, coiled-coil; AH, alpha helix; NLS, nuclear localization signal; SP, serine-proline rich. (B) Data represent the complete study of the first intercross (PR×RP1, line 9). The number of animals per group is indicated. The cumulative probability of death resulting from APL is not significantly different in PR animals than it is in PR×RP1 animals (P = .19).

RARα-PML cDNA isoforms and Kaplan-Meier analysis of APL disease in transgenic animals. (A) Diagram of the structural features of bcr-1 and bcr-3 isoforms. The identical portion of RARα is expressed in both isoforms of RP (breakpoint in RARα is indicated by the arrow), whereas the expressed PML domains are different because of the locations of the breakpoints in PML (indicated by the dashed lines). DB indicates DNA binding; LB, ligand binding; Dimer, dimerization; P, proline rich; R, ring finger; BB, B-box; CC, coiled-coil; AH, alpha helix; NLS, nuclear localization signal; SP, serine-proline rich. (B) Data represent the complete study of the first intercross (PR×RP1, line 9). The number of animals per group is indicated. The cumulative probability of death resulting from APL is not significantly different in PR animals than it is in PR×RP1 animals (P = .19).

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