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Downregulation of myc promoter-binding protein 1 (MBP-1) in growth-arrested malignant B cells
Daniel Tvrdík, Pavel Dundr, Ctibor Povýšil, Petr Přikryl, Štěpánka Melčáková, Martina Planková
Language English Country Czech Republic
NLK
Free Medical Journals
from 2000
Freely Accessible Science Journals
from 2000
ProQuest Central
from 2005-01-01
Health & Medicine (ProQuest)
from 2005-01-01
ROAD: Directory of Open Access Scholarly Resources
from 2000
- MeSH
- Electrophoresis, Gel, Two-Dimensional methods utilization MeSH
- Financing, Organized utilization MeSH
- Lymphoma, Follicular genetics immunology MeSH
- Polymerase Chain Reaction methods utilization MeSH
- Promoter Regions, Genetic MeSH
- Proto-Oncogene Proteins c-myc genetics immunology MeSH
- Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization methods utilization MeSH
- TATA Box genetics immunology MeSH
- Transforming Growth Factor beta1 genetics immunology MeSH
- Blotting, Western methods utilization MeSH
Normal human B lymphocytes are sensitive to the growth-inhibitory action of TGF-beta1 whereas malignant B lymphoma cells are mostly resistant to TGF-beta1 effects. We have shown in our previous work that, TGF-beta1 treatment resulted in significant growth inhibition of the DoHH2 cell line. In the present study we showed that TGF-beta1-induced growth arrest was associated with notable downregulation of the myc-binding protein-1 (MBP-1). Moreover, our results indicated that c-Myc overexpression in TGF-beta1-arrested malignant B cells is mediated by binding of MBP-1, as a transcription repressor, to the (+118/+153) element of the promoter region of the myc gene.
Lit.: 45
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- $a Institute of Pathology, Charles University in Prague, 1st Faculty of Medicine and General Teaching Hospital, Prague
- 504 __
- $a Lit.: 45
- 520 9_
- $a Normal human B lymphocytes are sensitive to the growth-inhibitory action of TGF-beta1 whereas malignant B lymphoma cells are mostly resistant to TGF-beta1 effects. We have shown in our previous work that, TGF-beta1 treatment resulted in significant growth inhibition of the DoHH2 cell line. In the present study we showed that TGF-beta1-induced growth arrest was associated with notable downregulation of the myc-binding protein-1 (MBP-1). Moreover, our results indicated that c-Myc overexpression in TGF-beta1-arrested malignant B cells is mediated by binding of MBP-1, as a transcription repressor, to the (+118/+153) element of the promoter region of the myc gene.
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