HCSGD entry for PCSK7


1. General information

Official gene symbolPCSK7
Entrez ID9159
Gene full nameproprotein convertase subtilisin/kexin type 7
Other gene symbolsLPC PC7 PC8 SPC7
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:0004252Serine-type endopeptidase activityIBA IEAmolecular_function
GO:0006508ProteolysisIEAbiological_process
GO:0016486Peptide hormone processingNASbiological_process
GO:0030173Integral component of Golgi membraneIDAcellular_component
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4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.84687527070.01592008280.99999024730.2461419355

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

Data sourceUp or downLog fold change
GSE11954Up0.1327571806
GSE13712_SHEARUp0.5066095875
GSE13712_STATICUp0.3010753648
GSE19018Down-0.6432394235
GSE19899_A1Down-0.2685260371
GSE19899_A2Down-0.3515984257
PubMed_21979375_A1Down-0.8502472224
PubMed_21979375_A2Up0.4642123463
GSE35957Down-0.2710762287
GSE36640Up0.7952505592
GSE54402Up0.1278568782
GSE9593Down-0.3325107835
GSE43922Down-0.2725107305
GSE24585Up0.0574708799
GSE37065Down-0.3458455117
GSE28863_A1Down-0.7112731307
GSE28863_A2Down-1.2762701426
GSE28863_A3Down-0.2327993691
GSE28863_A4Down-0.0908251345
GSE48662Down-0.1871903443

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-652-3pMIMAT0003322MIRT039521CLASHFunctional 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: 2 abstracts the gene occurs.


PubMed ID of the article

Sentenece the gene occurs

25921542In these diseases, biliary lysophosphatidylcholine (LPC) level is reportedly increased
25921542This study investigated the influence of LPC on cholangiocytes focusing on cellular senescence and its potential contribution to carcinogenesis
25921542METHODS: Cultured MMNK-1, an immortalized human cholangiocyte was treated with LPC in vitro and its effect was evaluated
25921542Accordingly, LPC provoked oxidative DNA injury, whereas the gene expressions of DNA repair enzyme (OGG1, MUTYH, MTH1) remained unchanged
25921542Interestingly, LPC caused global DNA hypomethylation, which is frequently observed in cancer tissues
25921542Microarray analysis identified differentially regulated genes in response to LPC, which included the components of senescence-associated secretory phenotype (SASP) including interleukin-8 (IL-8), IL-6, transforming growth factor-beta and plasminogen activator inhibitor-1
25921542In addition to upregulation of p21 gene expression, senescence-associated beta-galactosidase activity, a widely used marker of cellular senescence was significantly induced by the treatment of LPC
25921542CONCLUSIONS: Based on these data, cholangiocyte senescence and SASP caused by LPC are potential pathogenic mechanisms in the development of biliary tract cancer
24498988We used structural analysis with representative standards and spectrum patterns with different collision energies to distinctly identify eight metabolites with altered expression during senescence as types of lysophosphatidylcholine (LPC) and lysophosphatidylethanolamine (LPE), such as LPC 16:0 and LPE 22:4
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