The leukemia-associated fusion protein MN1-TEL blocks TEL-specific recognition sequences
| Autor: | Jacqueline Bonten, Marjolein J. F. W. Janssen, Bart Geverts, Adriaan B. Houtsmuller, Ellen C. Zwarthoff, Gerard Grosveld, Karel H. M. van Wely, Claudia C. M. M. Schot, W. Martijn ter Haar, Magda A. Meester-Smoor |
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| Přispěvatelé: | Pathology |
| Jazyk: | angličtina |
| Rok vydání: | 2012 |
| Předmět: |
Acute Myeloid Leukemia
Oncogene Proteins Fusion Repressor lcsh:Medicine Plasma protein binding Biology Biochemistry Hematologic Cancers and Related Disorders chemistry.chemical_compound Mice Transcription (biology) hemic and lymphatic diseases DNA-binding proteins Leukemias Transcriptional regulation Animals lcsh:Science Recombinant proteins Oncogene Proteins Multidisciplinary Proto-Oncogene Proteins c-ets Tumor Suppressor Proteins lcsh:R Fluorescence recovery after photobleaching Proteins Cancers and Neoplasms Molecular biology Fusion protein Repressor Proteins chemistry Oncology Computer Science NIH 3T3 Cells Trans-Activators Medicine lcsh:Q Monte Carlo Method DNA Research Article Computer Modeling Fluorescence Recovery After Photobleaching Protein Binding |
| Zdroj: | PLoS ONE, Vol 7, Iss 9, p e46085 (2012) PLoS ONE PLoS One (print), 7(9). Public Library of Science |
| ISSN: | 1932-6203 |
| Popis: | The leukemia-associated fusion protein MN1-TEL combines the transcription-activating domains of MN1 with the DNA-binding domain of the transcriptional repressor TEL. Quantitative photobleaching experiments revealed that similar to 20% of GFP-tagged MN1 and TEL is transiently immobilised, likely due to indirect or direct DNA binding, since transcription inhibition abolished immobilisation. Interestingly, similar to 50% of the MN1-TEL fusion protein was immobile with much longer binding times than unfused MN1 and TEL. MN1-TEL immobilisation was not observed when the TEL DNA-binding domain was disrupted, suggesting that MN1-TEL stably occupies TEL recognition sequences, preventing binding of factors required for proper transcription regulation, which may contribute to leukemogenesis. |
| Databáze: | OpenAIRE |
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