HCSGD entry for CBX1


1. General information

Official gene symbolCBX1
Entrez ID10951
Gene full namechromobox homolog 1
Other gene symbolsCBX HP1-BETA HP1Hs-beta HP1Hsbeta M31 MOD1 p25beta
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:0000775Chromosome, centromeric regionIDAcellular_component
GO:0000785ChromatinIDAcellular_component
GO:0001939Female pronucleusIEAcellular_component
GO:0001940Male pronucleusIEAcellular_component
GO:0003682Chromatin bindingTASmolecular_function
GO:0005515Protein bindingIPImolecular_function
GO:0005634NucleusIEAcellular_component
GO:0005654NucleoplasmTAScellular_component
GO:0005720Nuclear heterochromatinTAScellular_component
GO:0005721Centromeric heterochromatinIEAcellular_component
GO:0005819SpindleIDAcellular_component
GO:0010369ChromocenterIEAcellular_component
GO:0019899Enzyme bindingIPImolecular_function
GO:0042802Identical protein bindingIEAmolecular_function
GO:0045892Negative regulation of transcription, DNA-templatedIEAbiological_process
GO:1990226Histone methyltransferase bindingIPImolecular_function
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4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.98870746170.00817674480.99999024730.1805537752

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

Data sourceUp or downLog fold change
GSE11954Down-0.3397877289
GSE13712_SHEARDown-0.1457022212
GSE13712_STATICDown-0.1248097439
GSE19018Down-0.0865854607
GSE19899_A1Down-0.7662639481
GSE19899_A2Down-1.3773886814
PubMed_21979375_A1Down-1.1903811533
PubMed_21979375_A2Down-1.2216721943
GSE35957Down-0.5691036109
GSE36640Down-0.4854642731
GSE54402Down-0.2477592434
GSE9593Down-0.4335455070
GSE43922Down-0.4804316193
GSE24585Up0.3294712905
GSE37065Down-0.2423583802
GSE28863_A1Up0.0183823351
GSE28863_A2Down-0.2796165773
GSE28863_A3Up0.0640010037
GSE28863_A4Up0.1603996293
GSE48662Up0.1316323891

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-210-3pMIMAT0000267MIRT003170immunoprecipitaion//Microarray//qRT-PCRFunctional MTI (Weak)19826008
hsa-miR-590-3pMIMAT0004801MIRT016166SequencingFunctional MTI (Weak)20371350
hsa-miR-193b-3pMIMAT0002819MIRT016475MicroarrayFunctional MTI (Weak)20304954
hsa-miR-186-5pMIMAT0000456MIRT021150SequencingFunctional MTI (Weak)20371350
hsa-miR-877-3pMIMAT0004950MIRT037076CLASHFunctional MTI (Weak)23622248
hsa-miR-342-3pMIMAT0000753MIRT043713CLASHFunctional 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: 4 abstracts the gene occurs.


PubMed ID of the article

Sentenece the gene occurs

25548483RESULTS: Senescent hepatocytes induced classical markers of senescence (p21, heterochromatin protein 1beta, and senescence-associated-beta-galactosidase activity); and downregulated the proliferation marker, Ki67
24763337Epigenome rejuvenation: HP1beta mobility as a measure of pluripotent and senescent chromatin ground states
24763337We measured the dynamics of an essential epigenetic modifier, HP1beta, in human cells at different stages of differentiation using Fluorescence Recovery After Photobleaching (FRAP)
24763337We found that HP1beta mobility is similar in human embryonic stem cells (hES) and iPS cells where it is more mobile compared to fibroblasts; HP1beta is less mobile in senescent fibroblasts than in young (dividing) fibroblasts
24763337Introduction of "reprogramming factors", Oct4, Sox2, Klf4, cMyc and Lin28, into senescent fibroblasts and measuring the changes in HP1beta mobility as reprogramming proceeds shows that the mobility of HP1beta in senescent cells increases and by day 9 is the same as that found in young fibroblasts
21677876Here we show that androgen deprivation therapy (ADT), a widely used treatment for advanced prostate cancer, induces a senescence-associated secretory phenotype in prostate cancer epithelial cells, indicated by increases in senescence-associated beta-galactosidase activity, heterochromatin protein 1beta foci, and expression of cathepsin B and insulin-like growth factor binding protein 3
17242207In cells entering senescence, HP1gamma, but not the related proteins HP1alpha and HP1beta, becomes phosphorylated on serine 93
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