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rdf:type
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Description
| - Histone acetylation plays an important role in regulation of transcription and is particularlry relevant to the regulation and pathology of hematopoiesis. In the present study, we examined the contribution of elevated histone acetylation to the differentiation of BM2 monoblasts. Inhibition of the activity of endogenous histone deacetylases by trichostatin A (TSA) resulted in histone hyperacetylation causing cell cycle arrest and differentiation of BM2 cells into macrophage polykaryons. TSA did not affect the level of v-Myb protein in BM2 cells, but it downregulated its transcription activation capability. This suggests that chromatin remodeling can be significantly engaged in regulation of proliferation and differentiation of leukemic cells.
- Histone acetylation plays an important role in regulation of transcription and is particularlry relevant to the regulation and pathology of hematopoiesis. In the present study, we examined the contribution of elevated histone acetylation to the differentiation of BM2 monoblasts. Inhibition of the activity of endogenous histone deacetylases by trichostatin A (TSA) resulted in histone hyperacetylation causing cell cycle arrest and differentiation of BM2 cells into macrophage polykaryons. TSA did not affect the level of v-Myb protein in BM2 cells, but it downregulated its transcription activation capability. This suggests that chromatin remodeling can be significantly engaged in regulation of proliferation and differentiation of leukemic cells. (en)
- Histone acetylation plays an important role in regulation of transcription and is particularlry relevant to the regulation and pathology of hematopoiesis. In the present study, we examined the contribution of elevated histone acetylation to the differentiation of BM2 monoblasts. Inhibition of the activity of endogenous histone deacetylases by trichostatin A (TSA) resulted in histone hyperacetylation causing cell cycle arrest and differentiation of BM2 cells into macrophage polykaryons. TSA did not affect the level of v-Myb protein in BM2 cells, but it downregulated its transcription activation capability. This suggests that chromatin remodeling can be significantly engaged in regulation of proliferation and differentiation of leukemic cells. (cs)
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Title
| - Trichostatin A suppresses transformation by the v-myb oncogene in BM2 cells
- Trichostatin A suppresses transformation by the v-myb oncogene in BM2 cells (en)
- Trichostatin A suppresses transformation by the v-myb oncogene in BM2 cells (cs)
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skos:prefLabel
| - Trichostatin A suppresses transformation by the v-myb oncogene in BM2 cells
- Trichostatin A suppresses transformation by the v-myb oncogene in BM2 cells (en)
- Trichostatin A suppresses transformation by the v-myb oncogene in BM2 cells (cs)
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skos:notation
| - RIV/00216224:14310/03:00008979!RIV09-MSM-14310___
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http://linked.open...avai/riv/aktivita
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http://linked.open...avai/riv/aktivity
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http://linked.open...iv/cisloPeriodika
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http://linked.open...vai/riv/dodaniDat
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http://linked.open...aciTvurceVysledku
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http://linked.open.../riv/druhVysledku
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http://linked.open...iv/duvernostUdaju
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http://linked.open...titaPredkladatele
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http://linked.open...dnocenehoVysledku
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http://linked.open...ai/riv/idVysledku
| - RIV/00216224:14310/03:00008979
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http://linked.open...riv/jazykVysledku
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http://linked.open.../riv/klicovaSlova
| - myb; histone acetylation; trichostatin A; cyclin D (en)
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http://linked.open.../riv/klicoveSlovo
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http://linked.open...odStatuVydavatele
| - US - Spojené státy americké
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http://linked.open...ontrolniKodProRIV
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http://linked.open...i/riv/nazevZdroje
| - Journal of Hematotherapy Stem Cell Research
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http://linked.open...in/vavai/riv/obor
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http://linked.open...ichTvurcuVysledku
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http://linked.open...cetTvurcuVysledku
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http://linked.open...UplatneniVysledku
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http://linked.open...v/svazekPeriodika
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http://linked.open...iv/tvurceVysledku
| - Kubala, Lukáš
- Souček, Karel
- Šmarda, Jan
- Nemajerová, Alice
- Šmardová, Jana
- Jurdic, Pierre
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http://linked.open...n/vavai/riv/zamer
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issn
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number of pages
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http://localhost/t...ganizacniJednotka
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