HCSGD entry for NDN


1. General information

Official gene symbolNDN
Entrez ID4692
Gene full namenecdin, melanoma antigen (MAGE) family member
Other gene symbolsHsT16328 PWCR
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:0001764Neuron migrationIEAbiological_process
GO:0003016Respiratory system processIEAbiological_process
GO:0003677DNA bindingIEAmolecular_function
GO:0005634NucleusIEAcellular_component
GO:0005813CentrosomeIEAcellular_component
GO:0005829CytosolIEAcellular_component
GO:0006351Transcription, DNA-templatedIEAbiological_process
GO:0006355Regulation of transcription, DNA-templatedIEAbiological_process
GO:0007399Nervous system developmentTASbiological_process
GO:0007413Axonal fasciculationIEAbiological_process
GO:0007417Central nervous system developmentIEAbiological_process
GO:0008285Negative regulation of cell proliferationTASbiological_process
GO:0008347Glial cell migrationIEAbiological_process
GO:0009791Post-embryonic developmentIEAbiological_process
GO:0019233Sensory perception of painIEAbiological_process
GO:0040008Regulation of growthIEAbiological_process
GO:0042995Cell projectionIEAcellular_component
GO:0043015Gamma-tubulin bindingIEAmolecular_function
GO:0043204PerikaryonIEAcellular_component
GO:0048011Neurotrophin TRK receptor signaling pathwayIEAbiological_process
GO:0048675Axon extensionIEAbiological_process
GO:0048871Multicellular organismal homeostasisIEAbiological_process
GO:0071514Genetic imprintingIEAbiological_process
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4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.93409994300.00155664300.99999024730.0760460111

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

Data sourceUp or downLog fold change
GSE11954Up0.0960716985
GSE13712_SHEARDown-6.0038163984
GSE13712_STATICDown-5.4924787687
GSE19018Down-0.0504809041
GSE19899_A1Down-1.5058749603
GSE19899_A2Up0.0181618018
PubMed_21979375_A1Down-0.4123161979
PubMed_21979375_A2Down-0.4927984714
GSE35957Down-0.6620633050
GSE36640Down-0.0385361646
GSE54402Down-0.0976112192
GSE9593Down-0.0630177810
GSE43922Down-0.0328921919
GSE24585Down-0.0562638587
GSE37065Down-0.0448637062
GSE28863_A1Up0.1017709314
GSE28863_A2Down-0.6611677588
GSE28863_A3Down-0.0515437997
GSE28863_A4Up0.0558609813
GSE48662Up0.3911564891

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-148b-3pMIMAT0000759MIRT019333MicroarrayFunctional MTI (Weak)17612493
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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: 1 abstracts the gene occurs.


PubMed ID of the article

Sentenece the gene occurs

22691188Necdin modulates proliferative cell survival of human cells in response to radiation-induced genotoxic stress
22691188Necdin interacts with p53 and is also a p53 target gene, although the importance of Necdin in the p53 response is not clearly understood
22691188METHODS: In this study, we first investigated Necdin protein expression during replicative senescence and premature senescence induced by gamma irradiation and by the overexpression of oncogenic RasV12
22691188Gain and loss of function experiments were used to evaluate the contribution of Necdin during the senescence process
22691188RESULTS: Necdin expression declined during replicative aging of IMR90 primary human fibroblasts or following induction of premature senescence
22691188Decrease in Necdin expression seemed to be a consequence of the establishment of senescence since the depletion of Necdin in human cells did not induce a senescence-like growth arrest nor a flat morphology or SA-beta-galactosidase activity normally associated with senescence
22691188Similarly, overexpression of Necdin did not affect the life span of IMR90 cells
22691188However, we demonstrate that in normal human cells, Necdin expression mimicked the effect of p53 inactivation by increasing radioresistance
22691188CONCLUSION: This result suggests that Necdin potentially attenuate p53 signaling in response to genotoxic stress in human cells and supports similar results describing an inhibitory function of Necdin over p53-dependent growth arrest in mice
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