HCSGD entry for FADD


1. General information

Official gene symbolFADD
Entrez ID8772
Gene full nameFas (TNFRSF6)-associated via death domain
Other gene symbolsMORT1
Links to Entrez GeneLinks to Entrez Gene

2. Neighbors in the network

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This gene isn't in PPI subnetwork.

3. Gene ontology annotation

GO ID

GO term

Evidence

Category

GO:0001916Positive regulation of T cell mediated cytotoxicityISSbiological_process
GO:0002020Protease bindingIPImolecular_function
GO:0002224Toll-like receptor signaling pathwayTASbiological_process
GO:0002756MyD88-independent toll-like receptor signaling pathwayTASbiological_process
GO:0002821Positive regulation of adaptive immune responseISSbiological_process
GO:0005123Death receptor bindingTASmolecular_function
GO:0005164Tumor necrosis factor receptor bindingIEAmolecular_function
GO:0005515Protein bindingIPImolecular_function
GO:0005829CytosolTAScellular_component
GO:0006915Apoptotic processIMP TASbiological_process
GO:0006919Activation of cysteine-type endopeptidase activity involved in apoptotic processTASbiological_process
GO:0008625Extrinsic apoptotic signaling pathway via death domain receptorsTASbiological_process
GO:0016032Viral processIEAbiological_process
GO:0031264Death-inducing signaling complexIDA TAScellular_component
GO:0031265CD95 death-inducing signaling complexIDAcellular_component
GO:0032729Positive regulation of interferon-gamma productionISSbiological_process
GO:0032757Positive regulation of interleukin-8 productionIDAbiological_process
GO:0032760Positive regulation of tumor necrosis factor productionIDAbiological_process
GO:0032813Tumor necrosis factor receptor superfamily bindingIPImolecular_function
GO:0033077T cell differentiation in thymusISSbiological_process
GO:0034138Toll-like receptor 3 signaling pathwayTASbiological_process
GO:0034142Toll-like receptor 4 signaling pathwayTASbiological_process
GO:0035666TRIF-dependent toll-like receptor signaling pathwayTASbiological_process
GO:0042104Positive regulation of activated T cell proliferationISSbiological_process
GO:0042802Identical protein bindingIPImolecular_function
GO:0043005Neuron projectionIEAcellular_component
GO:0043029T cell homeostasisISSbiological_process
GO:0043065Positive regulation of apoptotic processIMPbiological_process
GO:0043123Positive regulation of I-kappaB kinase/NF-kappaB signalingIEPbiological_process
GO:0044297Cell bodyIEAcellular_component
GO:0045087Innate immune responseTASbiological_process
GO:0045121Membrane raftIEAcellular_component
GO:0045651Positive regulation of macrophage differentiationIMPbiological_process
GO:0045862Positive regulation of proteolysisIDAbiological_process
GO:0045944Positive regulation of transcription from RNA polymerase II promoterIDAbiological_process
GO:0048535Lymph node developmentISSbiological_process
GO:0048536Spleen developmentISSbiological_process
GO:0048538Thymus developmentISSbiological_process
GO:0051291Protein heterooligomerizationIEAbiological_process
GO:0051607Defense response to virusIMPbiological_process
GO:0060340Positive regulation of type I interferon-mediated signaling pathwayIMPbiological_process
GO:0070236Negative regulation of activation-induced cell death of T cellsISSbiological_process
GO:0070265Necrotic cell deathIMPbiological_process
GO:0071260Cellular response to mechanical stimulusIEPbiological_process
GO:0097049Motor neuron apoptotic processIEAbiological_process
GO:0097190Apoptotic signaling pathwayIDA TASbiological_process
GO:0097191Extrinsic apoptotic signaling pathwayIDA IMP TASbiological_process
GO:0097192Extrinsic apoptotic signaling pathway in absence of ligandIEAbiological_process
GO:0097202Activation of cysteine-type endopeptidase activityIDAbiological_process
GO:0097342RipoptosomeIDAcellular_component
GO:1902043Positive regulation of extrinsic apoptotic signaling pathway via death domain receptorsIEAbiological_process
GO:2000454Positive regulation of CD8-positive, alpha-beta cytotoxic T cell extravasationISSbiological_process
GO:2001238Positive regulation of extrinsic apoptotic signaling pathwayIMPbiological_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
0.73020379160.18554191330.99999024730.8350972469

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

Data sourceUp or downLog fold change
GSE11954Up0.4997052212
GSE13712_SHEARDown-0.0819369212
GSE13712_STATICDown-0.0425071479
GSE19018Down-0.4206796900
GSE19899_A1Down-0.1419943844
GSE19899_A2Up0.3371545244
PubMed_21979375_A1Up0.9975027991
PubMed_21979375_A2Down-0.2438549612
GSE35957Down-0.1514194969
GSE36640Down-0.3944381987
GSE54402Up0.2084671812
GSE9593Down-0.1333278304
GSE43922Up0.0596709721
GSE24585Down-0.3223224520
GSE37065Down-0.2499195242
GSE28863_A1Down-0.1696483175
GSE28863_A2Down-0.1038627805
GSE28863_A3Down-0.4436767982
GSE28863_A4Up0.0699104309
GSE48662Up0.1262025446

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-146a-5pMIMAT0000449MIRT000638Luciferase reporter assayFunctional MTI19965651
hsa-miR-1MIMAT0000416MIRT023826MicroarrayFunctional MTI (Weak)18668037
hsa-miR-7-5pMIMAT0000252MIRT025869SequencingFunctional MTI (Weak)20371350
hsa-miR-15b-5pMIMAT0000417MIRT046456CLASHFunctional MTI (Weak)23622248
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    • mirRecord

MicroRNA name

mirBase ID

Target site number

MiRNA mature ID

Test method inter

MiRNA regulation site

Reporter target site

Pubmed ID

hsa-miR-146a-5pMIMAT0000449NAhsa-miR-146a{Western blot}{overexpression by miRNA mimics tranfection}19965651
hsa-miR-155-5pMIMAT0000646NAhsa-miR-155{Western blot}{overexpression by miRNA mimics tranfection}19650740
hsa-miR-27a-3pMIMAT0000084NAhsa-miR-27a{Western blot}{overexpression}19513126
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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

24295239RESULTS: We have reported that Fas-associated protein with death domain (FADD) phosphorylation abolishes the recruitment of phosphatase type 2A C subunit (PP2Ac) to protein kinase C (PKC)betaII, which specifically regulates mitochondrial ROS generation by p66shc
24295239Here, we have studied the role of FADD phosphorylation in an FADD constitutive-phosphorylation mutation (FADD-D) mouse model
24295239In FADD-D mice, the constitutive FADD phosphorylation led to ROS accumulation (hydrogen peroxide [H(2)O(2)]), in a process that was dependent on PKCbeta and accompanied by increased PKCbeta and p66shc phosphorylation, impaired mitochondrial integrity, and enhanced sensitivity to oxidative stress-mediated apoptosis
24295239In addition, we demonstrate that FADD phosphorylation and the recruitment of PP2A and FADD to PKCbeta are induced responses to oxidative stress, and that the extent of FADD phosphorylation in wild-type mice was augmented during aging, accompanied by impairment of the interaction between PKCbeta and PP2A
24295239INNOVATION: The present study first addresses the role of FADD phosphorylation in aging through controlling mitochondrial ROS specifically generated by PKCbeta
24295239CONCLUSION: These data identify that FADD phosphorylation is critical for the PKCbeta-p66shc signaling route to generate H(2)O(2) and to implicate enhanced FADD phosphorylation as a primary cause of ROS accumulation during aging
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)
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