HCSGD entry for ASF1A


1. General information

Official gene symbolASF1A
Entrez ID25842
Gene full nameanti-silencing function 1A histone chaperone
Other gene symbolsCGI-98 CIA HSPC146
Links to Entrez GeneLinks to Entrez Gene

2. Neighbors in the network

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3. Gene ontology annotation

GO ID

GO term

Evidence

Category

GO:0001649Osteoblast differentiationIEAbiological_process
GO:0003682Chromatin bindingNASmolecular_function
GO:0005515Protein bindingIPImolecular_function
GO:0005634NucleusIDA NAScellular_component
GO:0006281DNA repairIDAbiological_process
GO:0006334Nucleosome assemblyIDAbiological_process
GO:0006351Transcription, DNA-templatedIEAbiological_process
GO:0016568Chromatin modificationIEAbiological_process
GO:0031936Negative regulation of chromatin silencingNASbiological_process
GO:0042393Histone bindingIDAmolecular_function
GO:0042692Muscle cell differentiationIEAbiological_process
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4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.95170414500.02310308120.99999024730.2923539423

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

Data sourceUp or downLog fold change
GSE11954Up0.6324484996
GSE13712_SHEARUp0.0119017545
GSE13712_STATICUp0.0003714534
GSE19018Up0.1689573021
GSE19899_A1Down-0.2157817973
GSE19899_A2Down-0.8029648081
PubMed_21979375_A1Down-0.2788903435
PubMed_21979375_A2Down-0.6512047431
GSE35957Down-0.4519886412
GSE36640Down-0.6619230683
GSE54402Up0.0399193503
GSE9593Down-0.4701772641
GSE43922Up0.0005602597
GSE24585Down-0.3678021397
GSE37065Up0.0633998536
GSE28863_A1Down-0.1649390869
GSE28863_A2Up0.1315869334
GSE28863_A3Down-0.6900835728
GSE28863_A4Down-0.1900691947
GSE48662Down-0.5816218973

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-340-5pMIMAT0004692MIRT019628SequencingFunctional MTI (Weak)20371350
hsa-miR-130b-3pMIMAT0000691MIRT020266SequencingFunctional MTI (Weak)20371350
hsa-miR-93-5pMIMAT0000093MIRT028099SequencingFunctional MTI (Weak)20371350
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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: 6 abstracts the gene occurs.


PubMed ID of the article

Sentenece the gene occurs

19029251Formation of SAHF in human cells is driven by a complex of histone chaperones, namely, HIRA and ASF1a
17643369Formation of SAHF is driven by a complex of histone chaperones, HIRA and ASF1a, and depends upon prior localization of HIRA to PML nuclear bodies
17242207Previously, we showed that a complex of histone chaperones, histone repressor A (HIRA) and antisilencing function 1a (ASF1a), plays a key role in the formation of SAHF
17242207Chromosome condensation depends on the ability of ASF1a to physically interact with its deposition substrate, histone H3, in addition to its cochaperone, HIRA
17242198HIRA bound to another histone chaperone, ASF1a, drives formation of SAHF
16980972The HIRA B domain forms an antiparallel beta-hairpin that binds perpendicular to the strands of the beta-sandwich of ASF1a, via beta-sheet, salt bridge and van der Waals contacts
16980972The N- and C-terminal regions of ASF1a and ASF1b determine the different affinities of these two proteins for HIRA, by contacting regions outside the HIRA B domain
15621527Formation of MacroH2A-containing senescence-associated heterochromatin foci and senescence driven by ASF1a and HIRA
15621527A physical complex containing HIRA and another chromatin regulator, ASF1a, is rate limiting for formation of SAHF and onset of senescence, and ASF1a is required for formation of SAHF and efficient senescence-associated cell cycle exit
15621527These data indicate that HIRA and ASF1a drive formation of macroH2A-containing SAHF and senescence-associated cell cycle exit, via a pathway that appears to depend on flux of heterochromatic proteins through PML bodies
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