HCSGD entry for ADI1


1. General information

Official gene symbolADI1
Entrez ID55256
Gene full nameacireductone dioxygenase 1
Other gene symbolsAPL1 ARD Fe-ARD MTCBP1 Ni-ARD SIPL mtnD
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:0000096Sulfur amino acid metabolic processTASbiological_process
GO:0005506Iron ion bindingIEAmolecular_function
GO:0005515Protein bindingIPImolecular_function
GO:0005634NucleusIDAcellular_component
GO:0005730NucleolusIDAcellular_component
GO:0005737CytoplasmIDAcellular_component
GO:0005794Golgi apparatusIDAcellular_component
GO:0005829CytosolTAScellular_component
GO:0005886Plasma membraneIDAcellular_component
GO:0006595Polyamine metabolic processTASbiological_process
GO:0010309Acireductone dioxygenase [iron(II)-requiring] activityIEA TASmolecular_function
GO:0016491Oxidoreductase activityIDAmolecular_function
GO:0019509L-methionine salvage from methylthioadenosineIDA IEA TASbiological_process
GO:0034641Cellular nitrogen compound metabolic processTASbiological_process
GO:0044281Small molecule metabolic processTASbiological_process
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4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.96376201510.02602064890.99999024730.3090656588

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

Data sourceUp or downLog fold change
GSE11954Up0.4839424487
GSE13712_SHEARDown-0.0133120693
GSE13712_STATICDown-0.3696953767
GSE19018Up0.1596298468
GSE19899_A1Down-1.1577880316
GSE19899_A2Down-0.4062837619
PubMed_21979375_A1Down-0.9249202141
PubMed_21979375_A2Down-0.5632431771
GSE35957Up0.2017777282
GSE36640Down-0.0386423640
GSE54402Down-0.3486111713
GSE9593Up0.0377317595
GSE43922Down-0.5356321653
GSE24585Down-0.1337986693
GSE37065Down-0.0793990178
GSE28863_A1Down-0.1024440711
GSE28863_A2Down-0.0120077293
GSE28863_A3Down-0.3895224562
GSE28863_A4Down-0.0463885818
GSE48662Down-0.3537238084

5. Regulation relationships with compounds/drugs/microRNAs

  • Compounds

Not regulated by compounds

  • Drugs

Name

Drug

Accession number

Isopropyl AlcoholDB02325 EXPT01912 | DB04402

  • MicroRNAs

  • mirTarBase

MiRNA_name

mirBase ID

miRTarBase ID

Experiment

Support type

References (Pubmed ID)

hsa-miR-193b-3pMIMAT0002819MIRT016389ProteomicsFunctional MTI (Weak)21512034
hsa-miR-26b-5pMIMAT0000083MIRT029129MicroarrayFunctional MTI (Weak)19088304
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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

26431329The identification of the functions of shuttled senescence-associated miRNAs is expected to shed light on the aging process and on how to delay ARD development
26414019BACKGROUND: Oral submucous fibrosis (OSMF) is a pre-malignant condition that is strongly associated with the areca nut alkaloids, arecoline (ARC) and arecaidine (ARD)
26414019METHODS: Two oral fibroblast lines were treated for 48h with ARC and ARD
26414019RESULTS: ARC (100 and 300 muM) and ARD (30 and 100 muM) significantly (P < 0
22797304Postmitotic neurons, such as photoreceptor cells in the retina and epithelial cells in the adjacent retinal pigmented epithelium, are especially susceptible to cellular senescence, which contributes to age-related retinal degeneration (ARD)
22797304The multigenic and complex etiology of ARD in humans is reflected by the relative paucity of effective compounds for its early prevention and treatment
22797304To understand the genetic differences that drive ARD pathogenesis, we studied A/J mice, which develop ARD more pronounced than that in other inbred mouse models
22797304Although our investigation of consomic strains failed to identify a chromosome associated with the observed retinal deterioration, pathway analysis of RNA-Seq data from young mice prior to retinal pathological changes revealed that increased vulnerability to ARD in A/J mice was due to initially high levels of inflammatory factors and low levels of homeostatic neuroprotective factors
22797304The genetic signatures of an uncompensated preinflammatory state and ARD progression identified here aid in understanding the susceptible genetic loci that underlie pathogenic mechanisms of age-associated disorders, including several human blinding diseases
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