HCSGD entry for TNFSF10

1. General information

Official gene symbolTNFSF10
Entrez ID8743
Gene full nametumor necrosis factor (ligand) superfamily, member 10
Other gene symbolsAPO2L Apo-2L CD253 TL2 TRAIL
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:0005102Receptor bindingTASmolecular_function
GO:0005125Cytokine activityIEAmolecular_function
GO:0005164Tumor necrosis factor receptor bindingIEAmolecular_function
GO:0005515Protein bindingIPImolecular_function
GO:0005576Extracellular regionTAScellular_component
GO:0005615Extracellular spaceIEAcellular_component
GO:0005887Integral component of plasma membraneTAScellular_component
GO:0006915Apoptotic processTASbiological_process
GO:0006919Activation of cysteine-type endopeptidase activity involved in apoptotic processTASbiological_process
GO:0006955Immune responseIEAbiological_process
GO:0007165Signal transductionTASbiological_process
GO:0007267Cell-cell signalingTASbiological_process
GO:0008584Male gonad developmentIEAbiological_process
GO:0032868Response to insulinIEAbiological_process
GO:0043065Positive regulation of apoptotic processIDAbiological_process
GO:0043123Positive regulation of I-kappaB kinase/NF-kappaB signalingIEPbiological_process
GO:0043280Positive regulation of cysteine-type endopeptidase activity involved in apoptotic processIDAbiological_process
GO:0046872Metal ion bindingIEAmolecular_function
GO:0090200Positive regulation of release of cytochrome c from mitochondriaIDAbiological_process
GO:0097190Apoptotic signaling pathwayTASbiological_process
GO:2001238Positive regulation of extrinsic apoptotic signaling pathwayIDAbiological_process
GO:2001239Regulation of extrinsic apoptotic signaling pathway in absence of ligandTASbiological_process
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4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.04249794840.05675757000.46051197040.4474859707

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

Data sourceUp or downLog fold change
GSE11954Up0.0032330246
GSE13712_SHEARDown-1.8071736113
GSE13712_STATICDown-1.0842762281
GSE19018Up0.0662645468
GSE19899_A1Up0.0757783053
GSE19899_A2Down-0.0300549109
PubMed_21979375_A1Down-0.1177185704
PubMed_21979375_A2Down-0.0400032795
GSE35957Down-1.1024466599
GSE36640Up0.5750288708
GSE54402Down-0.6656585014
GSE9593Down-0.2879664393
GSE43922Down-0.6353529445
GSE24585Up0.5754058543
GSE37065Up1.6067344708
GSE28863_A1Up1.3918420040
GSE28863_A2Up1.6405216494
GSE28863_A3Up0.0992457842
GSE28863_A4Down-0.0359319090
GSE48662Up0.1379779893

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-222-3pMIMAT0000279MIRT003756Western blotFunctional MTI18246122
hsa-miR-221-3pMIMAT0000278MIRT003757Western blotFunctional MTI18246122
hsa-miR-98-5pMIMAT0000096MIRT027770MicroarrayFunctional MTI (Weak)19088304
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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

26152738EXPERIMENTAL DESIGN: We combined treatment with an aurora kinase A inhibitor, MLN8237, with agents that activate death receptors (Apo2L/TRAIL or death receptor 5 agonists) and monitored the ability of this treatment to induce tumor apoptosis and melanoma tumor regression using human cell lines and patient-derived xenograft (PDX) mouse models
26152738Mechanistic analysis showed that the induction of tumor cell senescence in response to the AURKA inhibitor resulted in a decreased display of Apo2L/TRAIL decoy receptors and increased display of one Apo2L/TRAIL receptor (death receptor 5), resulting in enhanced response to death receptor ligand/agonists
26152738Senescent tumor cells exhibited BID-mediated mitochondrial depolarization in response to Apo2L/TRAIL treatment
12473065Apo2Ligand/tumor necrosis factor-related apoptosis-inducing ligand (Apo2L/TRAIL) has been observed to preferentially induce cytopathic effects on transformed/malignant cell types compared with their non-neoplastic counterparts
12473065In this report, two different biologically active preparations of Apo2L/TRAIL, a non-tagged version, NT-Apo2L/TRAIL, and a leucine zipper fusion protein, LZ-Apo2L/TRAIL, were examined for their ability to trigger apoptosis in normal human keratinocytes, and in an immortalized cell line (HaCaT cells)
12473065Similarities between preparations included: an enhanced ability for both Apo2L/TRAIL preparations to kill a greater relative percentage of HaCaT cells compared with keratinocytes; enhanced cytotoxicity towards keratinocytes that had their NF-B activity inhibited; a dependence of both Apo2L/TRAIL preparations on FADD and caspase activation; triggering of the same caspase cascades including caspase 8 and 3; and an ability to induce apoptosis even when HaCaT cells and keratinocytes were transduced to overexpress either Bcl-2 or Bcl-x(L) (survival factors that reduce susceptibility to UV-light-induced apoptosis)
12473065These results indicate that while both preparations of Apo2L/TRAIL possess biological activity, there are important differences as regards their ability to induce apoptosis in normal and immortalized keratinocytes
12473065In addition, it may be possible to utilize these Apo2L/TRAIL preparations for the treatment of various sun-induced skin cancers as they can differentially trigger apoptosis of transformed keratinocytes, or keratinocytes with abnormal NF-kappaB signaling, while sparing adjacent normal keratinocytes
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