Linked Life Data

20030931

Source:http://linkedlifedata.com/resource/pubmed/id/20030931

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2009-12-24
pubmed:abstractText
This study was purposed to investigate the effect of AML1-ETO fusion protein resulted from hematopoietic transcription factor (AML1) and acute myeloid leukemia M(2b)(AML-M(2b)) on transcription activity of nucleobindin 2 (nucb2) promoter, and to explore the role of AML1-ETO in molecular pathogenesis of AML-M(2b). The real-time RT-PCR was used to study the regulation of AML1-ETO on nucb2 at transcription level in AML1-ETO inducible leukemia cell line, the chromatin immunoprecipitation (ChIP)-based qPCR was used to investigate the direct in vivo interaction between the AML1, AML1-ETO and nucb2 promoter in AML1-ETO positive leukemia cell line, the luciferase report gene assay was used to detect the regulation of AML1, AML1-ETO on the transcription activity of nucb2 promoter. The results showed that the expression level of nucb2 was reduced with the increase of AML1-ETO. The promoter of nucb2 could be bound by both AML1 and AML1-ETO. The promoter of nucb2 was trans-repressed by AML1 and AML1-ETO respectively. It is concluded that the nucb2 is the direct target gene of AML1 and AML1-ETO, the transcription regulation of AML1, AML1-ETO on nucb2 is carried out via repressing its promoter activity.
pubmed:language
chi
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1009-2137
pubmed:author
pubmed:issnType
Print
pubmed:volume
17
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1482-6
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
[Influence of AML1 and AML1-ETO on transcriptional regulation of nucb2 gene].
pubmed:affiliation
National Key Laboratory of Medical Genomics, Ruijin Hospital, Shanghai Jiaotong University Medical College, Shanghai 200025, China.
pubmed:publicationType
Journal Article, English Abstract, Research Support, Non-U.S. Gov't