HCSGD entry for NPY

1. General information

Official gene symbolNPY
Entrez ID4852
Gene full nameneuropeptide Y
Other gene symbolsPYY4
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:0001664G-protein coupled receptor bindingIEAmolecular_function
GO:0004930G-protein coupled receptor activityTASmolecular_function
GO:0005102Receptor bindingTASmolecular_function
GO:0005184Neuropeptide hormone activityTASmolecular_function
GO:0005246Calcium channel regulator activityTASmolecular_function
GO:0005576Extracellular regionTAScellular_component
GO:0005615Extracellular spaceISScellular_component
GO:0005623CellTAScellular_component
GO:0006816Calcium ion transportTASbiological_process
GO:0006928Cellular component movementTASbiological_process
GO:0007187G-protein coupled receptor signaling pathway, coupled to cyclic nucleotide second messengerTASbiological_process
GO:0007218Neuropeptide signaling pathwayIEAbiological_process
GO:0007268Synaptic transmissionTASbiological_process
GO:0007586DigestionNASbiological_process
GO:0007610BehaviorTASbiological_process
GO:0007631Feeding behaviorTASbiological_process
GO:0008015Blood circulationNASbiological_process
GO:0008217Regulation of blood pressureIEAbiological_process
GO:0008283Cell proliferationTASbiological_process
GO:0008343Adult feeding behaviorISSbiological_process
GO:0021954Central nervous system neuron developmentIEPbiological_process
GO:0021987Cerebral cortex developmentIEPbiological_process
GO:0031175Neuron projection developmentIEPbiological_process
GO:0032100Positive regulation of appetiteISSbiological_process
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4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.39595040840.83373317500.99999024731.0000000000

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

Data sourceUp or downLog fold change
GSE11954Down-0.1716337574
GSE13712_SHEARDown-0.1922536798
GSE13712_STATICDown-0.0112081759
GSE19018Up0.0167938781
GSE19899_A1Down-0.1268913498
GSE19899_A2Up0.0305512592
PubMed_21979375_A1Up0.3105546120
PubMed_21979375_A2Up0.0414532456
GSE35957Up0.2007546678
GSE36640Up0.0609395148
GSE54402Up0.0114912144
GSE9593Up0.1398682631
GSE43922Up0.1222877480
GSE24585Up0.4821140937
GSE37065Up0.0136220208
GSE28863_A1Up0.0579363893
GSE28863_A2Up0.0259659159
GSE28863_A3Up0.2643046098
GSE28863_A4Up0.0192004112
GSE48662Down-0.1143877091

5. Regulation relationships with compounds/drugs/microRNAs

  • Compounds

Not regulated by compounds

  • Drugs

Name

Drug

Accession number

Alpha-Aminoisobutyric AcidDB02952 EXPT00471
L-TyrosinamideDB03380 EXPT03135

  • MicroRNAs

  • mirTarBase

MiRNA_name

mirBase ID

miRTarBase ID

Experiment

Support type

References (Pubmed ID)

hsa-miR-335-5pMIMAT0000765MIRT016709MicroarrayFunctional 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: 2 abstracts the gene occurs.


PubMed ID of the article

Sentenece the gene occurs

26549884Neuropeptide Y: An Anti-Aging Player
26549884Accumulating evidence suggests that neuropeptide Y (NPY) has a role in aging and lifespan determination
26549884In this review, we critically discuss age-related changes in NPY levels in the brain, together with recent findings concerning the contribution of NPY to, and impact on, six hallmarks of aging, specifically: loss of proteostasis, stem cell exhaustion, altered intercellular communication, deregulated nutrient sensing, cellular senescence, and mitochondrial dysfunction
26549884Understanding how NPY contributes to, and counteracts, these hallmarks of aging will open new avenues of research on limiting damage related to aging
26047956Analysis of gene expression during aging of CGNs in culture: implication of SLIT2 and NPY in senescence
26047956Our results showed that the two genes neuropeptide Y (Npy) and Slit homolog 2 (Drosophila) (Slit2) gradually increase during aging, and upon suppression of these two genes, there was gradual increase in cell viability along with restoration of the expression of Topo IIbeta and potential repair proteins
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