HCSGD entry for ARID3A


1. General information

Official gene symbolARID3A
Entrez ID1820
Gene full nameAT rich interactive domain 3A (BRIGHT-like)
Other gene symbolsBRIGHT DRIL1 DRIL3 E2FBP1
Links to Entrez GeneLinks to Entrez Gene

2. Neighbors in the network

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This gene isn't in Literature mining network.

3. Gene ontology annotation

GO ID

GO term

Evidence

Category

GO:0003677DNA bindingIEAmolecular_function
GO:0003682Chromatin bindingIEAmolecular_function
GO:0003700Sequence-specific DNA binding transcription factor activityIEAmolecular_function
GO:0005515Protein bindingIPImolecular_function
GO:0005634NucleusIEAcellular_component
GO:0005737CytoplasmIEAcellular_component
GO:0006351Transcription, DNA-templatedIEAbiological_process
GO:0042803Protein homodimerization activityIEAmolecular_function
GO:0045121Membrane raftIDAcellular_component
GO:0045944Positive regulation of transcription from RNA polymerase II promoterIEAbiological_process
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4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.11637662700.88756275980.70016902371.0000000000

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

Data sourceUp or downLog fold change
GSE11954Down-0.1298671824
GSE13712_SHEARUp0.2065244889
GSE13712_STATICUp0.7000379341
GSE19018Up0.0199970773
GSE19899_A1Down-0.1733709275
GSE19899_A2Up0.5276112266
PubMed_21979375_A1Up0.5954073634
PubMed_21979375_A2Up0.6735966088
GSE35957Down-0.0904385316
GSE36640Down-0.3563243857
GSE54402Down-0.1010179675
GSE9593Down-0.0829345252
GSE43922Up0.0469164503
GSE24585Up0.2852509589
GSE37065Up0.0382629729
GSE28863_A1Up0.1469210684
GSE28863_A2Up0.1283572944
GSE28863_A3Up0.3155714867
GSE28863_A4Down-0.0239058714
GSE48662Up0.1391918824

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-let-7b-5pMIMAT0000063MIRT005059MicroarrayFunctional MTI (Weak)17699775
hsa-miR-30b-5pMIMAT0000420MIRT023439SequencingFunctional MTI (Weak)20371350
hsa-miR-98-5pMIMAT0000096MIRT027857MicroarrayFunctional MTI (Weak)19088304
hsa-let-7d-5pMIMAT0000065MIRT032173SequencingFunctional MTI (Weak)20371350
hsa-miR-484MIMAT0002174MIRT041956CLASHFunctional MTI (Weak)23622248
hsa-miR-425-3pMIMAT0001343MIRT042421CLASHFunctional 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

25931205Further analysis has provided data supporting this model, implicating Arid3a as a key transcription factor in mediating fetal-type B cell development
22010578E2FBP1 antagonizes the p16(INK4A)-Rb tumor suppressor machinery for growth suppression and cellular senescence by regulating promyelocytic leukemia protein stability
22010578E2F-binding protein 1 (E2FBP1), a transcription regulator for E2F, induces PML reduction and suppresses the formation of PML-nuclear bodies, whereas the down-regulation of E2FBP1 provokes the PML-dependent premature senescence in human normal fibroblasts
22010578Here we report that the depletion of E2FBP1 induces the accumulation of PML through the Ras-dependent activation of MAP kinase signaling
22010578The cellular levels of p16(INK4A) and p53 are elevated during premature senescence induced by depletion of E2FBP1, and the depletion of p16(INK4A), but not p53 rescued senescent cells from growth arrest
22010578Similar to human normal fibroblasts, the growth inhibition induced by E2FBP1 depletion is also observed in human tumor cells with intact p16(INK4A) and Rb
22010578These results suggest that E2FBP1 functions as a critical antagonist to the p16(INK4A)-Rb tumor suppressor machinery by regulating PML stability
19436740SUMOylation of DRIL1 directs its transcriptional activity towards leukocyte lineage-specific genes
19436740DRIL1 is an ARID family transcription factor that can immortalize primary mouse fibroblasts, bypass RAS(V12)-induced cellular senescence and collaborate with RAS(V12) or MYC in mediating oncogenic transformation
19436740Little, however, is known about the regulation of DRIL1 activity
19436740Recently, DRIL1 was found to interact with the SUMO-conjugating enzyme Ubc9, but the functional relevance of this association has not been assessed
19436740Here, we show that DRIL1 is sumoylated both in vitro and in vivo at lysine 398
19436740Moreover, we provide evidence that PIASy functions as a specific SUMO E3-ligase for DRIL1 and promotes its sumoylation both in vitro and in vivo
19436740Furthermore, consistent with the subnuclear localization of PIASy in the Matrix-Associated Region (MAR), SUMO-modified DRIL1 species are found exclusively in the MAR fraction
19436740In contrast, DRIL1 sumoylation impairs its interaction with E2F1 in vitro and modifies its transcriptional activity in vivo, driving transcription of subset of genes regulating leukocyte fate
19436740Taken together, these results identify sumoylation as a novel post-translational modification of DRIL1 that represents an important mechanism for targeting and modulating DRIL1 transcriptional activity
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