Download Acute Promyelocytic Leukemia: Molecular Genetics, Mouse by Pier Paolo Pandolfi (Editor), Peter K. Vogt (Editor) PDF

By Pier Paolo Pandolfi (Editor), Peter K. Vogt (Editor)

ISBN-10: 3540345922

ISBN-13: 9783540345923

ISBN-10: 3540345949

ISBN-13: 9783540345947

Over the last 10 years, paintings on acute promyelocytic leukemia (APL) has develop into the paradigm of translational learn that started with the invention of a recurrent chromosomal translocation, through the id of the genes and proteins concerned, discovering their molecular capabilities in transcriptional keep watch over, constructing mouse types and culminating within the improvement  of detailed treatment.

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Extra resources for Acute Promyelocytic Leukemia: Molecular Genetics, Mouse Models and Targeted Therapy (Current Topics in Microbiology and Immunology 313)

Sample text

Among the areas that animal models will be used for in the coming years are: 1. Developing a better understanding of the cells from which relapses arise in APL and other AMLs. ) 2. Identifying the critical transcriptional targets repressed by X-RARα proteins. 3. Elucidating effects on PML and its interaction partners that facilitate leukemic transformation. 4. Delineating how events cooperate at a molecular level to block differentiation and deregulate proliferation and survival. 5. Extending differentiation therapy to other leukemias.

Proc Natl Acad Sci U S A 96:14831–14836 Dhordain P, Albagli O, Honore N, Guidez F, Lantoine D, Schmid M, de Thé HD, Zelent A, Koken MH (2000) Colocalization and heteromerization between the two human oncogene POZ/zinc finger proteins, LAZ3 (BCL6) and PLZF. Oncogene 19:6240–6250 Dong S, Zhu J, Reid A, Strutt P, Guidez F, Zhong HJ, Wang ZY, Licht J, Waxman S, Chomienne C, et al (1996) Amino-terminal protein-protein interaction motif (POZ-domain) is responsible for activities of the promyelocytic leukemia zinc finger-retinoic acid receptor-alpha fusion protein.

Promoter activity is reduced when the PLZF site is lost, and PLZF is necessary for increasing p85α PI3K levels [70]. Transcriptional upregulation of CBFA1 [RUNX2] was demonstrated by forced PLZF expression in C2C12 cells [35]. 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.

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