HCSGD entry for CD2AP


1. General information

Official gene symbolCD2AP
Entrez ID23607
Gene full nameCD2-associated protein
Other gene symbolsCMS
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:0001726RuffleIDAcellular_component
GO:0005172Vascular endothelial growth factor receptor bindingIEAmolecular_function
GO:0005200Structural constituent of cytoskeletonTASmolecular_function
GO:0005515Protein bindingIPImolecular_function
GO:0005730NucleolusIDAcellular_component
GO:0005737CytoplasmIDAcellular_component
GO:0005886Plasma membraneIDAcellular_component
GO:0006461Protein complex assemblyTASbiological_process
GO:0006930Substrate-dependent cell migration, cell extensionTASbiological_process
GO:0007067MitosisIEAbiological_process
GO:0007165Signal transductionNASbiological_process
GO:0008013Beta-catenin bindingIEAmolecular_function
GO:0008022Protein C-terminus bindingIEAmolecular_function
GO:0015629Actin cytoskeletonTAScellular_component
GO:0016050Vesicle organizationIEAbiological_process
GO:0016337Cell-cell adhesionIEAbiological_process
GO:0017124SH3 domain bindingIPImolecular_function
GO:0030139Endocytic vesicleIEAcellular_component
GO:0031941Filamentous actinIDAcellular_component
GO:0032403Protein complex bindingIEAmolecular_function
GO:0043161Proteasome-mediated ubiquitin-dependent protein catabolic processIEAbiological_process
GO:0045296Cadherin bindingIEAmolecular_function
GO:0048259Regulation of receptor-mediated endocytosisIEAbiological_process
GO:0048471Perinuclear region of cytoplasmIEAcellular_component
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4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.44358821850.72182994950.99999024731.0000000000

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

Data sourceUp or downLog fold change
GSE11954Down-0.1540492626
GSE13712_SHEARUp0.2898580717
GSE13712_STATICUp0.1658221420
GSE19018Up0.3741036660
GSE19899_A1Down-0.0224665776
GSE19899_A2Up0.0869632081
PubMed_21979375_A1Up0.3383321158
PubMed_21979375_A2Up0.0638070403
GSE35957Up0.0787244328
GSE36640Up0.0726582278
GSE54402Up0.0919470394
GSE9593Up0.0516457017
GSE43922Down-0.0131297048
GSE24585Up0.0619091603
GSE37065Up0.1131209164
GSE28863_A1Down-0.0120129463
GSE28863_A2Up0.2733395448
GSE28863_A3Down-0.1389883894
GSE28863_A4Down-0.3604862399
GSE48662Down-0.1624373768

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-130b-3pMIMAT0000691MIRT020288SequencingFunctional MTI (Weak)20371350
hsa-miR-128-3pMIMAT0000424MIRT022095SequencingFunctional MTI (Weak)20371350
hsa-miR-124-3pMIMAT0000422MIRT022891MicroarrayFunctional MTI (Weak)18668037
hsa-miR-30b-5pMIMAT0000420MIRT023443SequencingFunctional MTI (Weak)20371350
hsa-miR-1MIMAT0000416MIRT023930Proteomics;MicroarrayFunctional MTI (Weak)18668037
hsa-miR-19b-3pMIMAT0000074MIRT031227SequencingFunctional MTI (Weak)20371350
hsa-miR-484MIMAT0002174MIRT041730CLASHFunctional MTI (Weak)23622248
hsa-miR-186-5pMIMAT0000456MIRT045208CLASHFunctional MTI (Weak)23622248
hsa-miR-92a-3pMIMAT0000092MIRT049274CLASHFunctional MTI (Weak)23622248
hsa-let-7a-5pMIMAT0000062MIRT052456CLASHFunctional 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

24589226We found that conditioned media from several types of senescent cells (CMS) efficiently sensitized pretransformed cells to TRAIL, while the same was not observed with normal or immortalized cells
24589226Notably, CMS dose-dependent sensitization to TRAIL was observed with TRAIL-insensitive cancer cells and confirmed in co-culture experiments
24589226Dissection and characterization of TRAIL-sensitizing CMS factors and the associated signaling pathway(s) will not only provide a mechanistic insight into the acquisition of TRAIL sensitivity but may lead to novel concepts for apoptogenic therapies of premalignant and TRAIL-resistant tumors
24581241All CMs were found to inhibit overall collagen synthesis both in early passage and in senescent fibroblasts
24581241The LCC-derived CM was found to be more potent than fibroblast-derived CMs and, furthermore, to inhibit alpha-smooth muscle actin expression
22843416In this study, we used hPSC-derived CMs as an in vitro aging model
22843416We generated cardiomyocytes from hPSCs and demonstrated the process of aging in both human embryonic stem cell (hESC)- and induced pluripotent stem cell (hiPSC)-derived CMs
22843416Aging in hESC-derived CMs correlated with reduced membrane potential in mitochondria, the accumulation of lipofuscin, a slower beating pattern, and the downregulation of human telomerase RNA (hTR) and cell cycle regulating genes
22843416Interestingly, the expression of hTR in hiPSC-derived CMs was not significantly downregulated, unlike in hESC-derived CMs
22843416In order to delay aging, vitamin C was added to the cultured CMs
22843416Taken together, these results suggest that hPSC-derived CMs can be used as a unique human cardiomyocyte aging model in vitro and that vitamin C shows anti-aging effects in this model
22683798Cardiomyocytes (CMs) and mesenchymal stem cells (MSCs) are important cell types for cardiac repair post myocardial infarction
22683798Here we proved that both CMs and MSCs can be simultaneously generated from human induced pluripotent stem cells (hiPSCs) via a pro-mesoderm differentiation strategy
22683798In summary, we generated a large number of homogenous MSCs in conjunction with CMs in a low-cost and efficient one step manner
22683798Functionally competent CMs and MSCs co-generated from hiPSCs may be useful for autologous cardiac repair
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