HCSGD entry for C2orf40


1. General information

Official gene symbolC2orf40
Entrez ID84417
Gene full namechromosome 2 open reading frame 40
Other gene symbolsECRG4
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:0005615Extracellular spaceIEAcellular_component
GO:0008054Cyclin catabolic processIEAbiological_process
GO:0030133Transport vesicleIEAcellular_component
GO:0070314G1 to G0 transitionIEAbiological_process
GO:0090398Cellular senescenceIEAbiological_process
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4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.51961476770.89111903800.99999024731.0000000000

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

Data sourceUp or downLog fold change
GSE11954Up0.0724302196
GSE13712_SHEARDown-0.0456281737
GSE13712_STATICDown-0.1405911431
GSE19018Up0.0032828851
GSE19899_A1Up0.1849693224
GSE19899_A2Up0.1705794667
PubMed_21979375_A1Down-0.0523675604
PubMed_21979375_A2Up0.1562757612
GSE35957Down-0.1622645742
GSE36640Down-0.0025226477
GSE54402Up0.1501296274
GSE9593Down-0.0645210869
GSE43922Up0.0157161683
GSE24585Up0.2252483596
GSE37065Up0.0654070366
GSE28863_A1Down-0.1513238219
GSE28863_A2Up0.0327311576
GSE28863_A3Up0.1141104619
GSE28863_A4Up0.0590719354
GSE48662Up0.1125670460

5. Regulation relationships with compounds/drugs/microRNAs

  • Compounds

Not regulated by compounds

  • Drugs

Not regulated by drugs

  • MicroRNAs

  • mirTarBase
No target information from mirTarBase
  • mirRecord
No target information from mirRecord

6. Text-mining results about the gene

Gene occurances in abstracts of cellular senescence-associated articles: 2 abstracts the gene occurs.


PubMed ID of the article

Sentenece the gene occurs

22899245The candidate tumor suppressor gene Ecrg4 as a wound terminating factor in cutaneous injury
22899245The Esophageal cancer-related gene-4 (Ecrg4) is a candidate tumor suppressor gene whose secreted protein product has been implicated in the development and progression of epithelial cancers, neuroprogenitor cell activation after central nervous system injury, cell senescence in neurodegeneration, and the survival of hematopoietic stem cells
22899245Here, we investigated the temporal and spatial localization of Ecrg4 expression in healthy and injured mouse skin, and evaluated the biological activity of Ecrg4 using viral-mediated gene delivery in cutaneous wound healing models
22899245Using in situ hybridization and immunohistochemistry, we found both Ecrg4 mRNA and its protein product localized to the epidermis, dermis, and hair follicles of healthy mouse skin
22899245Upon cutaneous injury, Ecrg4 redistributed to the wound margins where gene microarray and quantitative RT-PCR showed an increased gene expression 5-10 days post-injury as a late phase injury response gene
22899245Ecrg4 over-expression inhibited the directional migration of fibroblasts in modified Boyden chambers in vitro, but had no effect on rates of fibroblast proliferation
22899245Ecrg4 over-expression in vivo at the wound margins delayed the rate of wound closure at 1 and 2 days after full-thickness punch injury
22899245These findings point to the candidate tumor suppressor gene Ecrg4 as a novel, biologically active, constituent of skin and skin injury
22899245The possibility that Ecrg4 serves as a wound termination factor during wound resolution is discussed
20404145Here, using a serum-induced mouse oligodendrocyte precursor cell (mOPC) senescence model, we identified esophageal cancer-related gene 4 (Ecrg4) as a senescence inducer with implications for the senescence-like state of postmitotic cells in the aging brain
20404145We show that Ecrg4 was up-regulated in the senescent OPCs, its overexpression in OPCs induced senescence by accelerating the proteasome-dependent degradation of cyclins D1 and D3, and that its knockdown by a specific short hairpin RNA prevented these phenotypes
20404145We also show that senescent OPCs secreted Ecrg4 and that recombinant Ecrg4 induced OPC senescence in culture
20404145Moreover, increased Ecrg4 expression was observed in the OPCs and neural precursor cells in the aged mouse brain; this was accompanied by the expression of senescence-associated beta-galactosidase activity, indicating the cells' entrance into senescence
20404145These results suggest that Ecrg4 is a factor linking neural-cell senescence and aging
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