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Chromatin remodeling and SWI/SNF2 factors in human disease
Juraj Kokavec, Jarmila Podskocova, Jiri Zavadil, Tomas Stopka
Language English Country United States
Document type Review
Grant support
NR9021
MZ0
CEP Register
- MeSH
- Chromatin metabolism MeSH
- Chromosomal Proteins, Non-Histone metabolism MeSH
- DNA, Neoplasm metabolism MeSH
- DNA Helicases genetics metabolism MeSH
- DNA metabolism MeSH
- Financing, Organized MeSH
- Genetic Diseases, Inborn genetics metabolism MeSH
- Histones metabolism MeSH
- Nuclear Proteins genetics metabolism MeSH
- Leukemia genetics metabolism MeSH
- Humans MeSH
- Neoplasms genetics metabolism MeSH
- Transcription Factors genetics metabolism MeSH
- Check Tag
- Humans MeSH
- Publication type
- Review MeSH
Chromatin structure and its changes or maintenance throughout developmental checkpoints play indispensable role in organismal homeostasis. Chromatin remodeling factors of the SWI/SNF2 superfamily use ATP hydrolysis to change DNA-protein contacts, and their loss-of-function or inappropriate increase leads to distinct human pathologic states. In this review, we focus on the translational view of human pathologic physiology involving SWI/SNF2 superfamily, combining latest finding from basic and clinical research. We discuss in mechanistic terms the consequences resulting from dose alteration of the SWI/SNF2 superfamily ATPases and emphasize the necessity of future human subject-based studies.
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- $a Kokavec, Juraj. $7 _AN046347 $u Pathologic Physiology and Center for Experimental Hematology, Charles University in Prague, First Faculty of Medicine, Prague, Czech Republic
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- $a Pathologic Physiology and Center for Experimental Hematology, Charles University in Prague, First Faculty of Medicine, U nemocnice 5, Prague 12853, Czech Republic.
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- $a Chromatin structure and its changes or maintenance throughout developmental checkpoints play indispensable role in organismal homeostasis. Chromatin remodeling factors of the SWI/SNF2 superfamily use ATP hydrolysis to change DNA-protein contacts, and their loss-of-function or inappropriate increase leads to distinct human pathologic states. In this review, we focus on the translational view of human pathologic physiology involving SWI/SNF2 superfamily, combining latest finding from basic and clinical research. We discuss in mechanistic terms the consequences resulting from dose alteration of the SWI/SNF2 superfamily ATPases and emphasize the necessity of future human subject-based studies.
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