HCSGD entry for RELA

1. General information

Official gene symbolRELA
Entrez ID5970
Gene full namev-rel reticuloendotheliosis viral oncogene homolog A (avian)
Other gene symbolsNFKB3 p65
Links to Entrez GeneLinks to Entrez Gene

2. Neighbors in the network

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3. Gene ontology annotation

GO ID

GO term

Evidence

Category

GO:0001889Liver developmentIEAbiological_process
GO:0001942Hair follicle developmentIEAbiological_process
GO:0002224Toll-like receptor signaling pathwayTASbiological_process
GO:0002755MyD88-dependent toll-like receptor signaling pathwayTASbiological_process
GO:0002756MyD88-independent toll-like receptor signaling pathwayTASbiological_process
GO:0003677DNA bindingIDAmolecular_function
GO:0003682Chromatin bindingIDA IEAmolecular_function
GO:0003700Sequence-specific DNA binding transcription factor activityIDA IEAmolecular_function
GO:0003705RNA polymerase II distal enhancer sequence-specific DNA binding transcription factor activityIDA IEAmolecular_function
GO:0005515Protein bindingIPImolecular_function
GO:0005634NucleusIDA IEAcellular_component
GO:0005654NucleoplasmTAScellular_component
GO:0005667Transcription factor complexIDAcellular_component
GO:0005737CytoplasmIDAcellular_component
GO:0005829CytosolIDA IEA TAScellular_component
GO:0006117Acetaldehyde metabolic processIEAbiological_process
GO:0006366Transcription from RNA polymerase II promoterIDAbiological_process
GO:0006952Defense responseIEAbiological_process
GO:0006954Inflammatory responseIDAbiological_process
GO:0006968Cellular defense responseNASbiological_process
GO:0007568AgingIEAbiological_process
GO:0008134Transcription factor bindingIEA IPImolecular_function
GO:0008284Positive regulation of cell proliferationIDA IEAbiological_process
GO:0009612Response to mechanical stimulusIEAbiological_process
GO:0009887Organ morphogenesisIEAbiological_process
GO:0010033Response to organic substanceIDAbiological_process
GO:0010224Response to UV-BIDAbiological_process
GO:0014040Positive regulation of Schwann cell differentiationIEAbiological_process
GO:0016032Viral processIEAbiological_process
GO:0019221Cytokine-mediated signaling pathwayIDAbiological_process
GO:0019901Protein kinase bindingIEA IPImolecular_function
GO:0031293Membrane protein intracellular domain proteolysisTASbiological_process
GO:0031625Ubiquitin protein ligase bindingIPImolecular_function
GO:0032332Positive regulation of chondrocyte differentiationIEAbiological_process
GO:0032403Protein complex bindingIEAmolecular_function
GO:0032481Positive regulation of type I interferon productionTASbiological_process
GO:0032495Response to muramyl dipeptideIEAbiological_process
GO:0032570Response to progesteroneIEAbiological_process
GO:0032868Response to insulinIEAbiological_process
GO:0033590Response to cobalaminIEAbiological_process
GO:0033613Activating transcription factor bindingIPImolecular_function
GO:0034097Response to cytokineIEAbiological_process
GO:0034134Toll-like receptor 2 signaling pathwayTASbiological_process
GO:0034138Toll-like receptor 3 signaling pathwayTASbiological_process
GO:0034142Toll-like receptor 4 signaling pathwayTASbiological_process
GO:0034146Toll-like receptor 5 signaling pathwayTASbiological_process
GO:0034162Toll-like receptor 9 signaling pathwayTASbiological_process
GO:0034166Toll-like receptor 10 signaling pathwayTASbiological_process
GO:0035666TRIF-dependent toll-like receptor signaling pathwayTASbiological_process
GO:0038095Fc-epsilon receptor signaling pathwayTASbiological_process
GO:0038123Toll-like receptor TLR1:TLR2 signaling pathwayTASbiological_process
GO:0038124Toll-like receptor TLR6:TLR2 signaling pathwayTASbiological_process
GO:0042177Negative regulation of protein catabolic processIEAbiological_process
GO:0042301Phosphate ion bindingIDAmolecular_function
GO:0042493Response to drugIEAbiological_process
GO:0042542Response to hydrogen peroxideIEAbiological_process
GO:0042802Identical protein bindingIDA IPImolecular_function
GO:0043066Negative regulation of apoptotic processIDA IEA TASbiological_process
GO:0043123Positive regulation of I-kappaB kinase/NF-kappaB signalingIEA IEPbiological_process
GO:0043200Response to amino acidIEAbiological_process
GO:0043234Protein complexIEAcellular_component
GO:0043278Response to morphineIEAbiological_process
GO:0043565Sequence-specific DNA bindingIEAmolecular_function
GO:0044212Transcription regulatory region DNA bindingIDAmolecular_function
GO:0045084Positive regulation of interleukin-12 biosynthetic processIEAbiological_process
GO:0045087Innate immune responseTASbiological_process
GO:0045892Negative regulation of transcription, DNA-templatedIDAbiological_process
GO:0045893Positive regulation of transcription, DNA-templatedIDA IEAbiological_process
GO:0045944Positive regulation of transcription from RNA polymerase II promoterIDA IMPbiological_process
GO:0046627Negative regulation of insulin receptor signaling pathwayIEAbiological_process
GO:0047485Protein N-terminus bindingIPImolecular_function
GO:0048011Neurotrophin TRK receptor signaling pathwayTASbiological_process
GO:0050727Regulation of inflammatory responseIEA ISSbiological_process
GO:0050852T cell receptor signaling pathwayTASbiological_process
GO:0051059NF-kappaB bindingIPImolecular_function
GO:0051092Positive regulation of NF-kappaB transcription factor activityIDA TASbiological_process
GO:0051591Response to cAMPIEAbiological_process
GO:0051607Defense response to virusNASbiological_process
GO:0070301Cellular response to hydrogen peroxideIDAbiological_process
GO:0070431Nucleotide-binding oligomerization domain containing 2 signaling pathwayIDAbiological_process
GO:0070491Repressing transcription factor bindingIPImolecular_function
GO:0070555Response to interleukin-1IGIbiological_process
GO:0071222Cellular response to lipopolysaccharideIEAbiological_process
GO:0071347Cellular response to interleukin-1IDAbiological_process
GO:0071356Cellular response to tumor necrosis factorIDAbiological_process
GO:0071532Ankyrin repeat bindingIEAmolecular_function
GO:2001237Negative regulation of extrinsic apoptotic signaling pathwayIEA IMPbiological_process
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4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.01926413510.98362683030.33812798131.0000000000

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

Data sourceUp or downLog fold change
GSE11954Down-0.1636673471
GSE13712_SHEARUp0.3344953296
GSE13712_STATICUp0.0520330596
GSE19018Up0.2816868549
GSE19899_A1Up0.1389730366
GSE19899_A2Up0.6385307859
PubMed_21979375_A1Up0.6024966499
PubMed_21979375_A2Up0.4197663621
GSE35957Up0.2282530638
GSE36640Up0.2112096637
GSE54402Up0.2324989556
GSE9593Up0.2337936521
GSE43922Up0.2825570282
GSE24585Down-0.2922061052
GSE37065Up0.1889913240
GSE28863_A1Up0.2876344713
GSE28863_A2Up0.6076873703
GSE28863_A3Up0.5205574381
GSE28863_A4Down-0.0559603317
GSE48662Up0.1358768482

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-373-3pMIMAT0000726MIRT002531Microarray//Microarray;OtherFunctional MTI (Weak)15685193
hsa-miR-124-3pMIMAT0000422MIRT002616Luciferase reporter assay//Microarray//Microarray;OtherFunctional MTI15685193
hsa-miR-7-5pMIMAT0000252MIRT025722SequencingFunctional MTI (Weak)20371350
hsa-miR-7-5pMIMAT0000252MIRT025722MicroarrayFunctional MTI (Weak)17612493
hsa-miR-7-5pMIMAT0000252MIRT025722MicroarrayFunctional MTI (Weak)19073608
hsa-miR-96-5pMIMAT0000095MIRT027888SequencingFunctional MTI (Weak)20371350
hsa-miR-324-5pMIMAT0000761MIRT043112CLASHFunctional MTI (Weak)23622248
hsa-miR-30e-5pMIMAT0000692MIRT044156CLASHFunctional MTI (Weak)23622248
hsa-miR-320aMIMAT0000510MIRT044799CLASHFunctional 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: 19 abstracts the gene occurs.


PubMed ID of the article

Sentenece the gene occurs

27349869Additionally, Acrp30 stimulation suppresses NFkappaB p65, which induces abnormal expression of hBD-2 induced by H2O2
26824319This is neither dependent on p65/NF-kappaB signaling nor RAF/MEK/ERK pathway activity as inhibition of MEK by GSK1120212 (trametinib) and induction of ERK1/2 activity by parthenolide itself do not interfere with parthenolide-triggered depletion of MITF-M in both wild-type BRAF and BRAF(V600E) melanoma populations
26588041We found higher RelA binding at the NF-kappaB1/RelA target gene promoters as well as upregulation of several pro-inflammatory cytokines in cells cultured at 21% O2
26588041RelA knockdown prevented the upregulation of the pro-inflammatory cytokines at 21% O2, suggesting NF-kappaB1/RelA as a major mediator of inflammatory response in cells cultured at 21% O2
25536232In addition, Western blotting demonstrated less translocation of p65 from cytoplasm to nucleus
25255445The classical (or canonical) pathway typically leads to the induction of RelA or c-Rel containing complexes, and involves the degradation of IkappaBalpha in a manner dependent on IkappaB kinase (IKK) beta and the IKK regulatory subunit NEMO
23542362Furthermore, oxidant/carbonyl stress-mediated reduction of SIRT1 leads to the loss of its control on acetylation of target proteins including p53, RelA/p65, and FOXO3, thereby enhancing the inflammatory, prosenescent, and apoptotic responses, as well as endothelial dysfunction
22889746Stat3 small interfering RNA suppressed indoxyl sulfate-induced expression of an inflammation marker gene (monocyte chemotactic protein-1), fibrosis marker genes (TGF-beta(1), alpha-smooth muscle actin) and a subunit of nuclear factor-kB (p65), and attenuated a cellular senescence marker, senescence-associated beta-galactosidase activity
22740410HTLV-1 tax-induced rapid senescence is driven by the transcriptional activity of NF-kappaB and depends on chronically activated IKKalpha and p65/RelA
22740410The senescence checkpoint triggered by Tax is driven by the transcriptional activity of NF-kappaB, which depends on activated IKKalpha and p65/RelA
22673730On the other hand, the aging process was accompanied by elevated amounts and binding activities of NF-kappaB (p65 and p50 subunits), together with an increased number of senescent cells
22390170Silencing of the DEK gene induces apoptosis and senescence in CaSki cervical carcinoma cells via the up-regulation of NF-kappaB p65
22390170The intracellular expression of NF-kappaB p65 protein was studied by cytochemistry
22390170In addition, the NF-kappaB p65 DNA-binding activity was measured by ELISA
22390170All of these effects may be related to the up-regulation of NF-kappaB p65 expression and its nuclear translocation
21979375Through a proteomics analysis of senescent chromatin, we identified the nuclear factor-kappaB (NF-kappaB) subunit p65 as a major transcription factor that accumulates on chromatin of senescent cells
21832251Indoxyl sulfate induced phosphorylation of NF-kappaB p65 on Ser-276, which was suppressed by N-acetylcysteine, an antioxidant
21832251Furthermore, indoxyl sulfate induced NF-kappaB p65 expression
21832251Inhibitors of NF-kappaB (pyrrolidine dithiocarbamate and isohelenin) and NF-kappaB p65 small interfering RNA (siRNA) suppressed indoxyl sulfate-induced senescence-associated beta-galactosidase activity and expression of p53, transforming growth factor (TGF)-beta1, and alpha-smoothe muscle actin (SMA)
21832251NF-kappaB inhibitors suppressed indoxyl sulfate-induced p21 expression, whereas NF-kappaB p65 siRNA enhanced its expression
21738489The majority of genes bound by NF-kappaB subunit RelA recruit Sirt6, and dynamic Sirt6 relocalization is largely driven in a RelA-dependent manner
21738489Integrative analysis with global gene expression patterns in wild-type, Sirt6-/-, and double Sirt6-/- RelA-/- cells reveals the epistatic relationships between Sirt6 and RelA in shaping diverse temporal patterns of gene expression
21738489Genes under the direct joint control of Sirt6 and RelA include several with prominent roles in cell senescence and organismal aging
21698300Compared to early cultures, late passage HUVECs also exhibited nuclear translocation of NF-kappaB (p65) and reciprocal shifts in BAX and BCL2 protein content resulting in almost 2-fold increase in BAX/BCL2 ratio and 3-fold increase in apoptotic response to TNFalpha exposure (p<0
21552325Small hairpin RNA-mediated knockdown indicates that RelA induces this senescence program by acting upstream of the anaphase promoting complex and RelB to stabilize p27(KIP1) protein and p21(CIP1/WAF1) mRNA respectively
21536657CPEB regulates the production of IL-6 at both the translational and transcriptional levels; in CPEB-depleted cells, aberrant IL-6 transcription is mediated by improper NF-kappaB p65 phosphorylation and nuclear localization
21471201SIRT1 phosphorylation caused concomitant increases in p65/RelA NF-kappaB acetylation and the expression of an anti-apoptotic Bfl-1/A1
19779484RelA/p65 functions to maintain cellular senescence by regulating genomic stability and DNA repair
19779484Our findings show that RelA/p65(-/-) murine fibroblasts immortalize at considerably faster rates than RelA/p65(+/+) cells
19779484The ability of RelA/p65(-/-) fibroblasts to escape senescence earlier is due to their genomic instability, characterized by high frequencies of DNA mutations, gene deletions and gross chromosomal translocations
19779484This increase in genomic instability is closely related to a compromised DNA repair that occurs in both murine RelA/p65(-/-) fibroblasts and tissues
19135889In SIRT6-deficient cells, hyperacetylation of H3K9 at these target promoters is associated with increased RELA promoter occupancy and enhanced NF-kappaB-dependent modulation of gene expression, apoptosis, and cellular senescence
19135889Moreover, haploinsufficiency of RelA rescues the early lethality and degenerative syndrome of Sirt6-deficient mice
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