HCSGD entry for COL8A2


1. General information

Official gene symbolCOL8A2
Entrez ID1296
Gene full namecollagen, type VIII, alpha 2
Other gene symbolsFECD FECD1 PPCD PPCD2
Links to Entrez GeneLinks to Entrez Gene

2. Neighbors in the network

color bar

3. Gene ontology annotation

GO ID

GO term

Evidence

Category

GO:0001525AngiogenesisIEAbiological_process
GO:0005201Extracellular matrix structural constituentNASmolecular_function
GO:0005576Extracellular regionTAScellular_component
GO:0005578Proteinaceous extracellular matrixNAScellular_component
GO:0005581CollagenIEAcellular_component
GO:0005604Basement membraneNAScellular_component
GO:0005788Endoplasmic reticulum lumenTAScellular_component
GO:0016337Cell-cell adhesionNASbiological_process
GO:0022617Extracellular matrix disassemblyTASbiological_process
GO:0030198Extracellular matrix organizationNAS TASbiological_process
GO:0030574Collagen catabolic processTASbiological_process
GO:0030674Protein binding, bridgingNASmolecular_function
GO:0031012Extracellular matrixIDAcellular_component
GO:0048593Camera-type eye morphogenesisIEAbiological_process
GO:0050673Epithelial cell proliferationIEAbiological_process
Entries Per Page
Displaying Page of

4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.85140289880.05127426770.99999024730.4260069444

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

Data sourceUp or downLog fold change
GSE11954Down-0.3895492665
GSE13712_SHEARDown-0.6071360333
GSE13712_STATICDown-0.3412177828
GSE19018Up0.0346358064
GSE19899_A1Up0.0274041837
GSE19899_A2Down-0.2472490281
PubMed_21979375_A1Down-0.5661668083
PubMed_21979375_A2Down-0.2632130162
GSE35957Down-0.3500677960
GSE36640Up0.0551442719
GSE54402Down-0.2475036817
GSE9593Down-0.1885193372
GSE43922Up0.1158325373
GSE24585Up0.0837066511
GSE37065Down-0.1371754806
GSE28863_A1Down-0.3078293722
GSE28863_A2Up0.0295073467
GSE28863_A3Up0.0424756126
GSE28863_A4Down-0.1761563626
GSE48662Up1.1977383039

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-335-5pMIMAT0000765MIRT017982MicroarrayFunctional MTI (Weak)18185580
hsa-miR-124-3pMIMAT0000422MIRT022679MicroarrayFunctional MTI (Weak)18668037
Entries Per Page
Displaying Page of
  • 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

25311168Fuchs endothelial corneal dystrophy (FECD) is a genetically heterogeneous disease
25311168Hypothesizing that cellular senescence may be relevant in FECD pathogenesis, genetically undifferentiated late-onset FECD endothelial samples were analyzed to identify common changes of specific senescence-related transcripts
25311168Total RNA was extracted from 21 FECD endothelial samples retrieved from patients undergoing lamellar keratoplasty due to clinically diagnosed end-stage FECD and from 12 endothelial samples retrieved from normal autopsy eyes
25311168Markedly elevated mRNA-levels of the constitutively active and reactive oxygen species-generating enzyme NOX4 were found in all evaluable FECD samples
25311168In addition, increased expression of CDKN2A and its transcriptional activators ETS1 and ARHGAP18 (SENEX) along with decreased expression of CDKN2A inhibitor ID1 were detected in FECD samples
25311168Consistent over-expression of NOX4 in FECD endothelial samples suggests a role as pathogenic factor and as a potential new treatment target in FECD
25311168Transcriptional up-regulation of the CDKN2A-pathway provides further evidence for increased cellular senescence in FECD endothelium
23132454PURPOSE: To investigate the novel application of tissue microarray (TMA) technology to corneal disease and to report altered protein expression of senescence-associated cyclin-dependent kinase inhibitors p21 and p16 in Fuchs endothelial corneal dystrophy (FECD)
23132454METHODS: A TMA including 208 cores was generated from paraffin-embedded tissues, including corneal buttons of 50 FECD and 5 keratoconus patients retrieved after penetrating keratoplasty, 10 autopsy globes with nonpathologic corneas, and nonocular control specimens
23132454Corneal endothelial p21 and p16 expression levels in FECD specimens compared with controls served as main outcome measures
23132454RESULTS: TMA immunohistochemical analysis disclosed increased endothelial expression levels of nuclear p21 in FECD specimens (P < 0
23132454It demonstrates p21 and p16 overexpression in the corneal endothelium of genetically undifferentiated FECD patients supporting a role of cellular senescence in the pathogenesis of FECD
Entries Per Page
Displaying Page of