HCSGD entry for CD226


1. General information

Official gene symbolCD226
Entrez ID10666
Gene full nameCD226 molecule
Other gene symbolsDNAM-1 DNAM1 PTA1 TLiSA1
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:0001816Cytokine productionIEAbiological_process
GO:0002860Positive regulation of natural killer cell mediated cytotoxicity directed against tumor cell targetIMPbiological_process
GO:0002891Positive regulation of immunoglobulin mediated immune responseIDAbiological_process
GO:0005178Integrin bindingIPImolecular_function
GO:0005515Protein bindingIPImolecular_function
GO:0005886Plasma membraneTAScellular_component
GO:0005887Integral component of plasma membraneTAScellular_component
GO:0007155Cell adhesionIEAbiological_process
GO:0007165Signal transductionTASbiological_process
GO:0008037Cell recognitionTASbiological_process
GO:0009897External side of plasma membraneIEAcellular_component
GO:0009986Cell surfaceIDAcellular_component
GO:0019901Protein kinase bindingIPImolecular_function
GO:0033005Positive regulation of mast cell activationIDAbiological_process
GO:0045121Membrane raftTAScellular_component
GO:0045954Positive regulation of natural killer cell mediated cytotoxicityIMPbiological_process
GO:0050776Regulation of immune responseTASbiological_process
GO:0050839Cell adhesion molecule bindingIPImolecular_function
GO:0060369Positive regulation of Fc receptor mediated stimulatory signaling pathwayIDAbiological_process
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4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.83216106910.24203118800.99999024730.9477526778

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

Data sourceUp or downLog fold change
GSE11954Up0.1583795345
GSE13712_SHEARDown-0.3965420813
GSE13712_STATICDown-0.0561959750
GSE19018Down-0.1363448688
GSE19899_A1Down-0.0935512768
GSE19899_A2Down-0.1774636289
PubMed_21979375_A1Up0.0825061949
PubMed_21979375_A2Up0.2450328896
GSE35957Down-0.0888409036
GSE36640Up0.4110008290
GSE54402Up0.0269529938
GSE9593Up0.0521959180
GSE43922Up0.0147879319
GSE24585Down-0.2144068071
GSE37065Up0.2837665909
GSE28863_A1Down-0.2012262966
GSE28863_A2Down-0.6452257121
GSE28863_A3Up0.0936644638
GSE28863_A4Down-0.0864260954
GSE48662Down-0.0048518116

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-335-5pMIMAT0000765MIRT018110MicroarrayFunctional MTI (Weak)18185580
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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

27853638Melphalan treatment was able to enhance the surface expression of the stress-induced NKG2D ligands RAE-1 and MULT-1, and of the DNAM-1 ligand PVR (CD155) on MM cells, leading to better tumor cell recognition and killing by NK cells, as highlighted by NK cell increased degranulation triggered by melphalan-treated tumor cells
24913980In this article, we identify the signaling events underlying chemotherapy-induced NKG2D and DNAM-1 ligand expression on multiple myeloma (MM) cells
19098271ATM-ATR-dependent up-regulation of DNAM-1 and NKG2D ligands on multiple myeloma cells by therapeutic agents results in enhanced NK-cell susceptibility and is associated with a senescent phenotype
19098271Induction of DNA damage response has been recently shown capable of enhancing NKG2D ligand (NKG2DL) expression, but nothing is known about DNAM-1 ligand (DNAM-1L) regulation
19098271In this study, we show that myeloma cells treated with low doses of therapeutic agents commonly used in the management of patients with MM, such as doxorubicin, melphalan, and bortezomib, up-regulate DNAM-1 and NKG2D ligands
19098271Accordingly, therapeutic drug treatment of MM cells increases NK-cell degranulation, the NKG2D and DNAM-1 receptors being the major triggering molecules
19098271Drug-induced DNAM-1 and NKG2D ligand expression was abolished after treatment with the ATM (ataxia telangiectasia mutated) and ATR (ATM- and RAD3-related) pharmacologic inhibitors caffeine and KU-55933, and was preferentially associated with senescent cells arrested in the G2 phase of the cell cycle
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