HCSGD entry for AFP


1. General information

Official gene symbolAFP
Entrez ID174
Gene full namealpha-fetoprotein
Other gene symbolsFETA HPAFP
Links to Entrez GeneLinks to Entrez Gene

2. Neighbors in the network

color bar
This gene isn't in PPI subnetwork.

3. Gene ontology annotation

GO ID

GO term

Evidence

Category

GO:0001542Ovulation from ovarian follicleIEAbiological_process
GO:0005615Extracellular spaceIEAcellular_component
GO:0005737CytoplasmIEAcellular_component
GO:0006810TransportIEAbiological_process
GO:0042448Progesterone metabolic processIEAbiological_process
GO:0046872Metal ion bindingIEAmolecular_function
GO:0060395SMAD protein signal transductionIEAbiological_process
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4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.32858858330.73106838270.99999024731.0000000000

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

Data sourceUp or downLog fold change
GSE11954Up0.2896668540
GSE13712_SHEARDown-0.0569655515
GSE13712_STATICUp0.3683919928
GSE19018Up0.1968255392
GSE19899_A1Up0.0716875963
GSE19899_A2Down-0.2414192439
PubMed_21979375_A1Down-0.3515400397
PubMed_21979375_A2Down-0.1210906372
GSE35957Up0.2637744710
GSE36640Up0.7234928458
GSE54402Down-0.1313948276
GSE9593Up0.4712283073
GSE43922Down-0.0334877720
GSE24585Down-0.1803426008
GSE37065Down-0.0531896874
GSE28863_A1Up0.0927282934
GSE28863_A2Up0.0403759768
GSE28863_A3Up0.1293524412
GSE28863_A4Down-0.0746937670
GSE48662Down-0.1639115410

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-106b-5pMIMAT0000680MIRT020427MicroarrayFunctional MTI (Weak)17242205
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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: 5 abstracts the gene occurs.


PubMed ID of the article

Sentenece the gene occurs

21562774The iPSC clones could differentiate to cells originated from all three germ-cell layers, as shown by RT-PCR, for messenger RNA (mRNA) expression of alpha-fetoprotein (endoderm), MSX1 (mesoderm) and microtubule-associated protein 2 (ectoderm), and by immunostaining for alpha-fetoprotein (endoderm), alpha-smooth muscle actin (mesoderm), and beta-III-tubulin (ectoderm)
19726080They showed gene expression of alpha-fetoprotein and albumin in a time-dependent manner of the hepatic differentiation process
14522900In this study, we found that a subset of ING family members strongly repressed human alpha-fetoprotein (AFP) promoter activity but stimulated the p21(WAF1) promoter in parallel experiments in the same cell type, similar to the effects of p53
14522900In this study, we found that a subset of ING family members strongly repressed human alpha-fetoprotein (AFP) promoter activity but stimulated the p21(WAF1) promoter in parallel experiments in the same cell type, similar to the effects of p53
14522900The p47(ING1a) isoform also repressed AFP promoter activity, but in contrast to other ING isoforms, it repressed the p21(WAF1) promoter
14522900Suppression of AFP gene transcription by ING was strongly dependent on AT-motifs that bind to the hepatocyte nuclear factor 1 (HNF1) transcription factor
14522900Both ING1 and p53 were able to suppress AFP transcription and cause p21 induction; hSIR2, a negative regulator of the p53 protein, showed the opposite effects on the AFP promoter and, like HDAC1, repressed p21 promoter activity
14522900Both ING1 and p53 were able to suppress AFP transcription and cause p21 induction; hSIR2, a negative regulator of the p53 protein, showed the opposite effects on the AFP promoter and, like HDAC1, repressed p21 promoter activity
14522900In addition, we found that p33(ING1b) physically interacts with hSIR2, reverses its ability to induce the AFP promoter, and induces acetylation of p53 residues at Lys(373) and/or Lys(382)
14522900These findings provide novel evidence that p33(ING1b) represses AFP transcription by at least two mechanisms, one of which includes p53
11237869When transfected into human HepG2 cells, both cDcoH and cDcoHalpha showed similar functional activity as measured by increased expression of a reporter gene, as well as alpha-fetoprotein and albumin genes that both contain HNF-1 binding elements in their promoters
7532927The inhibition of apoptosis by alpha-fetoprotein (AFP) and the role of AFP receptors in anti-cellular senescence
7532927The inhibition of apoptosis by alpha-fetoprotein (AFP) and the role of AFP receptors in anti-cellular senescence
7532927The inhibition of apoptosis by alpha-fetoprotein (AFP) and the role of AFP receptors in anti-cellular senescence
7532927The mechanism of paradoxical growth enhancement by alpha-fetoprotein (AFP), a nonmitogenic factor, was explored in HL-60 cells using novel AFP agonists, the 167H
7532927The mechanism of paradoxical growth enhancement by alpha-fetoprotein (AFP), a nonmitogenic factor, was explored in HL-60 cells using novel AFP agonists, the 167H
7532927The mechanism of paradoxical growth enhancement by alpha-fetoprotein (AFP), a nonmitogenic factor, was explored in HL-60 cells using novel AFP agonists, the 167H
75329274 monoclonal antibodies (MAbs) to AFP receptor (AFPr) isoforms
7532927The conditions underwhich AFP led to increases in thymidine incorporation were found to promote activation induced cell death (AICD) associated with adherence in 96 well plates
7532927Both AFP and the 167H
75329274 MAb blocked the induction of cell death under these conditions indicating apparent growth enhancement by AFP relates to the abrogation of cell death and not that AFP contains bona fide growth factor-like activity
75329274 MAb blocked the induction of cell death under these conditions indicating apparent growth enhancement by AFP relates to the abrogation of cell death and not that AFP contains bona fide growth factor-like activity
7532927Overall, our findings lend further support to the recent proposals that AFP by binding to AFP receptors may block cellular senescence and that there may be differential expression of AFPr isoforms related to commitment (167H
7532927Overall, our findings lend further support to the recent proposals that AFP by binding to AFP receptors may block cellular senescence and that there may be differential expression of AFPr isoforms related to commitment (167H
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