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During the last 10 years, paintings on acute promyelocytic leukemia (APL) has develop into the paradigm of translational study that started with the invention of a recurrent chromosomal translocation, through the identity of the genes and proteins concerned, discovering their molecular capabilities in transcriptional regulate, developing mouse types and culminating within the improvement of distinctive remedy.
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Additional resources for Acute Promyelocytic Leukemia: Molecular Genetics, Mouse Models and Targeted Therapy (Current Topics in Microbiology and Immunology 313)
Since VDUP1 binds thioredoxin, it is intriguing to speculate that thioredoxin could affect the redox state of PLZF, or link PLZF function to the cellular redox state. PLZF can also interact with the LIM (Lin11, Isl-1, and Mec-3) domain protein DRAL/FHL2, an interaction that requires both the BTB domain and the second repression domain of PLZF . Co-expression of DRAL augmented transcriptional repression by PLZF. DRAL was localized in both the nucleus and cytoplasm, and serum stimulation of cells increased nuclear accumulation of DRAL, further increasing PLZF repression.
Although these systems do not provide a mechanism, or even evidence, of direct activation of gene expression by PLZF, the possibility that PLZF acts as a bifunctional transcription factor is intriguing. Work underway in our laboratory to purify interaction partners for PLZF may help address the possible mechanism of PLZF-mediated transcriptional activation. 38 M. J. McConnell · J. D. Licht There is a growing body of evidence that, in addition to the nucleus, PLZF can be found in the cytoplasm. In a process called “ectodomain shedding,” a membrane-anchored ligand for the epidermal growth factor receptor (EGFR) HB-EGF (heparin-binding EGF-like growth factor) is cleaved, generating a small, roughly 7-kDa fragment of HB-EGF in the cytoplasm of the cell.
A RA-resistant leukemia that arose in an MRP8 PML-RARAm4 transgenic mouse was examined in engrafted histocompatible recipients (Guillemin et al. 2002). Mice were treated with a low toxicity cAMP analog, [8-chloro-adenosine 3 -5 cyclic monophosphate (8Cl-cAMP)], alone or in combination with ATRA or arsenic. Treatment with 8Cl-cAMP had a moderate effect, whereas the combination of 8-Cl-cAMP with ATRA induced differentiation of the ATRA-resistant leukemic cells. Theophylline, an inhibitor of phosphodiesterase able to boost cAMP levels, has subsequently been used as an adjunct to therapy in some AML patients.