HCSGD entry for RUNX1T1


1. General information

Official gene symbolRUNX1T1
Entrez ID862
Gene full namerunt-related transcription factor 1; translocated to, 1 (cyclin D-related)
Other gene symbolsAML1T1 CBFA2T1 CDR ETO MTG8 ZMYND2
Links to Entrez GeneLinks to Entrez Gene

2. Neighbors in the network

color bar
This gene isn't in PPI subnetwork.

3. Gene ontology annotation

GO ID

GO term

Evidence

Category

GO:0003677DNA bindingIEAmolecular_function
GO:0003700Sequence-specific DNA binding transcription factor activityIEAmolecular_function
GO:0005515Protein bindingIPImolecular_function
GO:0005634NucleusIEAcellular_component
GO:0006091Generation of precursor metabolites and energyTASbiological_process
GO:0006351Transcription, DNA-templatedIEAbiological_process
GO:0006355Regulation of transcription, DNA-templatedIEAbiological_process
GO:0016363Nuclear matrixIDAcellular_component
GO:0042802Identical protein bindingIPImolecular_function
GO:0042803Protein homodimerization activityIEAmolecular_function
GO:0045444Fat cell differentiationIEAbiological_process
GO:0046872Metal ion bindingIEAmolecular_function
GO:0051101Regulation of DNA bindingIEAbiological_process
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4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.78504550360.00202808020.99999024730.0859176000

  • Individual experiment result
    ( "-" represent NA in the specific microarray platform )

Data sourceUp or downLog fold change
GSE11954Down-0.0193831106
GSE13712_SHEARDown-2.1831614065
GSE13712_STATICDown-1.5476383119
GSE19018Down-0.4935235462
GSE19899_A1Down-0.1251371323
GSE19899_A2Down-1.2812933165
PubMed_21979375_A1Down-0.2195948075
PubMed_21979375_A2Down-0.8835229959
GSE35957Up0.3284693076
GSE36640Down-0.7196750069
GSE54402Down-0.6385500932
GSE9593Up0.3041146143
GSE43922Down-0.4412777766
GSE24585Down-1.3100011406
GSE37065Down-0.3826347491
GSE28863_A1Up1.2180467892
GSE28863_A2Up0.5656104600
GSE28863_A3Down-0.1162905339
GSE28863_A4Down-0.0355335951
GSE48662Down-0.0103617330

5. Regulation relationships with compounds/drugs/microRNAs

  • Compounds

Not regulated by compounds

  • Drugs

Not regulated by drugs

  • MicroRNAs

    • mirTarBase

MiRNA_name

mirBase ID

miRTarBase ID

Experiment

Support type

References (Pubmed ID)

hsa-miR-106b-5pMIMAT0000680MIRT020443MicroarrayFunctional MTI (Weak)17242205
hsa-miR-103a-3pMIMAT0000101MIRT027124SequencingFunctional MTI (Weak)20371350
hsa-miR-16-5pMIMAT0000069MIRT031791SequencingFunctional MTI (Weak)20371350
hsa-let-7e-5pMIMAT0000066MIRT051459CLASHFunctional MTI (Weak)23622248
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    • mirRecord
No target information from mirRecord

6. Text-mining results about the gene

Gene occurances in abstracts of cellular senescence-associated articles: 3 abstracts the gene occurs.


PubMed ID of the article

Sentenece the gene occurs

26690546The antitumor drug etoposide (ETO) is widely used in treating several cancers, including adrenocortical tumor (ACT)
26690546Here, we checked the effect of sublethal dose of ETO in ACT cells
26690546Sublethal dose of ETO treatment did not induce cell death but arrested the ACT cells in G2/M phase
26690546In addition, autophagy was activated by ETO and was required for ACT cell survival
26690546Chloroquine alleviated CDK2 and ERK, but not Chk2, activation and thus inhibited centrosome amplification in either ETO- or hydroxyurea-treated ACT cells
26690546In addition, chloroquine also inhibited centrosome amplification in osteosarcoma U2OS cell lines when treated with ETO or hydroxyurea
26102294Previously, we showed that following etoposide (ETO) treatment embryonal carcinoma PA-1 cells undergo a p53-dependent upregulation of OCT4A and p21Cip1 (governing self-renewal and regulating cell cycle inhibition and senescence, respectively)
26102294PA-1 cells treated with ETO display highly heterogeneous increases in OCT4A and p21Cip1 indicative of dis-adaptation catastrophe
26102294SOX2 and NANOG expression did not change following ETO treatment suggesting a dissociation of OCT4A from its pluripotency function
12091906The t(8;21) fusion protein, AML1 ETO, specifically represses the transcription of the p14(ARF) tumor suppressor in acute myeloid leukemia
12091906This translocation creates a fusion protein consisting of the acute myeloid leukemia-1 transcription factor and the eight-twenty-one corepressor (AML1 ETO), which represses transcription through AML1 (RUNX1) DNA binding sites and immortalizes hematopoietic progenitor cells
12091906We have identified the p14(ARF) tumor suppressor, a mediator of the p53 oncogene checkpoint, as a direct transcriptional target of AML1 ETO
12091906AML1 ETO repressed the p14(ARF) promoter and reduced endogenous levels of p14(ARF) expression in multiple cell types
12091906Chromatin immunoprecipitation assays demonstrated that AML1 ETO was specifically bound to the p14(ARF) promoter
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