By T. Haferlach, C. Schoch, W. Hiddemann (auth.), Prof. Dr. med. Wolfgang Hiddemann, Prof. Dr. Dr. med. phil. Torsten Haferlach, Dr. med. Michael Unterhalt, Prof. Dr. med. Thomas Büchner, Prof. Dr. med. Jörg Ritter (eds.)
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Extra info for Acute Leukemias IX: Basic Research, Experimental Approaches and Novel Therapies
1999). , 1999). The GAL4-inv(l6) chimeric proteins repressed transcription 5-6-fold. Unexpectedly, the C-terminal 160 aa of the smooth muscle myosin heavy chain (which is normally a cytoplasmic protein) were required for repression. Thus, like the t(8;21) and t(l2;21) fusion proteins, the inv(l6) encoded protein also actively represses the transcription of AML-l-regulated genes. The t(8;21) and the t(12;21) fusion proteins repress transcription by interacting with 23 the nuclear hormone co-repressors, mSin3A or mSin3B, and histone deacetylases.
The salient features of cell line MUTZ-S are summarized in Table 2. References Bene MC, Castoldi G, Knapp W, Ludwig WD, Matutes E, Orfao A, Van't Veer MB, European Group for the Immunological Characterization of Leukemia 18 (1995) Proposals for the immunological classification of acute leukemias. Leukemia 9: 1783-1786 Drexler HG (2000) The Leukemia-Lymphoma Cell Line FactsBook. Academic Press, London Drexler HG, Matsuo Y (1999) Guidelines for the characterization and publication of human malignant hematopoietic cell lines.
1998a). The MYND motif is required for repression of basal transcription from the multidrug resistance-I promoter by the t(8;21) fusion protein, Mol Cell BioI 18, 3601-3611. , Westendorf, I. , and Hiebert, S. W. (2000). A mechanism of repression by acute myeloid leukemia-I, the target of multiple chromosomal translocations in acute leukemia, I BioI Chern 275,651-6. , Westendorf, J. , Davie, I. , Huynh, K. , Bardwell, V. , Lavinsky, R. , Rosenfeld, M. , et al. (1998b). ETO, a target of t(8;21) in acute leukemia, interacts with the N-CoR and mSin3 corepressors, Mol Cell BioI 18,7176-84.