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Statements

Subject Item
n2:RIV%2F00216208%3A11110%2F14%3A10282399%21RIV15-MSM-11110___
rdf:type
skos:Concept n20:Vysledek
rdfs:seeAlso
http://dx.doi.org/10.1371/journal.pone.0087448
dcterms:description
CCCTC-binding factor (CTCF) can both activate as well as inhibit transcription by forming chromatin loops between regulatory regions and promoters. In this regard, Ctcf binding on non-methylated DNA and its interaction with the Cohesin complex results in differential regulation of the H19/Igf2 locus. Similarly, a role for CTCF has been established in normal hematopoietic development; however its involvement in leukemia remains elusive. Here, we show that Ctcf binds to the imprinting control region of H19/Igf2 in AML blasts. We also demonstrate that Smarca5, which also associates with the Cohesin complex, facilitates Ctcf binding to its target sites on DNA. Furthermore, Smarca5 supports Ctcf functionally and is needed for enhancer-blocking effect at ICR. We next asked whether CTCF and SMARCA5 control the expression of key hematopoiesis regulators. In normally differentiating myeloid cells both CTCF and SMARCA5 together with members of the Cohesin complex are recruited to the SPI1 gene, a key hematopoiesis regulator and leukemia suppressor. Due to DNA methylation, CTCF binding to the SPI1 gene is blocked in AML blasts. Upon AZA-mediated DNA demethylation of human AML blasts, CTCF and SMARCA5 are recruited to the -14.4 Enhancer of SPI1 gene and block its expression. Our data provide new insight into complex SPI1 gene regulation now involving additional key epigenetic factors, CTCF and SMARCA5 that control PU. 1 expression at the -14.4 Enhancer. CCCTC-binding factor (CTCF) can both activate as well as inhibit transcription by forming chromatin loops between regulatory regions and promoters. In this regard, Ctcf binding on non-methylated DNA and its interaction with the Cohesin complex results in differential regulation of the H19/Igf2 locus. Similarly, a role for CTCF has been established in normal hematopoietic development; however its involvement in leukemia remains elusive. Here, we show that Ctcf binds to the imprinting control region of H19/Igf2 in AML blasts. We also demonstrate that Smarca5, which also associates with the Cohesin complex, facilitates Ctcf binding to its target sites on DNA. Furthermore, Smarca5 supports Ctcf functionally and is needed for enhancer-blocking effect at ICR. We next asked whether CTCF and SMARCA5 control the expression of key hematopoiesis regulators. In normally differentiating myeloid cells both CTCF and SMARCA5 together with members of the Cohesin complex are recruited to the SPI1 gene, a key hematopoiesis regulator and leukemia suppressor. Due to DNA methylation, CTCF binding to the SPI1 gene is blocked in AML blasts. Upon AZA-mediated DNA demethylation of human AML blasts, CTCF and SMARCA5 are recruited to the -14.4 Enhancer of SPI1 gene and block its expression. Our data provide new insight into complex SPI1 gene regulation now involving additional key epigenetic factors, CTCF and SMARCA5 that control PU. 1 expression at the -14.4 Enhancer.
dcterms:title
Epigenetic Control of SPI1 Gene by CTCF and ISWI ATPase SMARCA5 Epigenetic Control of SPI1 Gene by CTCF and ISWI ATPase SMARCA5
skos:prefLabel
Epigenetic Control of SPI1 Gene by CTCF and ISWI ATPase SMARCA5 Epigenetic Control of SPI1 Gene by CTCF and ISWI ATPase SMARCA5
skos:notation
RIV/00216208:11110/14:10282399!RIV15-MSM-11110___
n3:aktivita
n9:I n9:S n9:P
n3:aktivity
I, P(ED1.1.00/02.0109), P(GAP305/12/1033), S
n3:cisloPeriodika
2
n3:dodaniDat
n13:2015
n3:domaciTvurceVysledku
n5:9620680 n5:4065352 n5:9952349 n5:7931360 n5:7099568 n5:9497307
n3:druhVysledku
n8:J
n3:duvernostUdaju
n15:S
n3:entitaPredkladatele
n16:predkladatel
n3:idSjednocenehoVysledku
14853
n3:idVysledku
RIV/00216208:11110/14:10282399
n3:jazykVysledku
n6:eng
n3:klicovaSlova
insulator; cells; cohesin; methylation; leukemia; expression; differentiation; pu.1; transcription-factor; chromatin remodeling complex
n3:klicoveSlovo
n4:transcription-factor n4:cohesin n4:methylation n4:chromatin%20remodeling%20complex n4:pu.1 n4:leukemia n4:insulator n4:cells n4:expression n4:differentiation
n3:kodStatuVydavatele
US - Spojené státy americké
n3:kontrolniKodProRIV
[27011EC1E353]
n3:nazevZdroje
PLoS ONE
n3:obor
n14:FD
n3:pocetDomacichTvurcuVysledku
6
n3:pocetTvurcuVysledku
6
n3:projekt
n18:ED1.1.00%2F02.0109 n18:GAP305%2F12%2F1033
n3:rokUplatneniVysledku
n13:2014
n3:svazekPeriodika
9
n3:tvurceVysledku
Čuřík, Nikola Jonášová, Anna Stopka, Tomáš Dluhošová, Martina Zikmund, Tomáš Vargová, Jarmila
n3:wos
000330626900070
s:issn
1932-6203
s:numberOfPages
11
n11:doi
10.1371/journal.pone.0087448
n7:organizacniJednotka
11110