HCSGD entry for RELA
1. General information
Official gene symbol | RELA |
---|---|
Entrez ID | 5970 |
Gene full name | v-rel reticuloendotheliosis viral oncogene homolog A (avian) |
Other gene symbols | NFKB3 p65 |
Links to Entrez Gene | Links to Entrez Gene |
2. Neighbors in the network
3. Gene ontology annotation
GO ID | GO term | Evidence | Category |
---|---|---|---|
GO:0001889 | Liver development | IEA | biological_process |
GO:0001942 | Hair follicle development | IEA | biological_process |
GO:0002224 | Toll-like receptor signaling pathway | TAS | biological_process |
GO:0002755 | MyD88-dependent toll-like receptor signaling pathway | TAS | biological_process |
GO:0002756 | MyD88-independent toll-like receptor signaling pathway | TAS | biological_process |
GO:0003677 | DNA binding | IDA | molecular_function |
GO:0003682 | Chromatin binding | IDA IEA | molecular_function |
GO:0003700 | Sequence-specific DNA binding transcription factor activity | IDA IEA | molecular_function |
GO:0003705 | RNA polymerase II distal enhancer sequence-specific DNA binding transcription factor activity | IDA IEA | molecular_function |
GO:0005515 | Protein binding | IPI | molecular_function |
GO:0005634 | Nucleus | IDA IEA | cellular_component |
GO:0005654 | Nucleoplasm | TAS | cellular_component |
GO:0005667 | Transcription factor complex | IDA | cellular_component |
GO:0005737 | Cytoplasm | IDA | cellular_component |
GO:0005829 | Cytosol | IDA IEA TAS | cellular_component |
GO:0006117 | Acetaldehyde metabolic process | IEA | biological_process |
GO:0006366 | Transcription from RNA polymerase II promoter | IDA | biological_process |
GO:0006952 | Defense response | IEA | biological_process |
GO:0006954 | Inflammatory response | IDA | biological_process |
GO:0006968 | Cellular defense response | NAS | biological_process |
GO:0007568 | Aging | IEA | biological_process |
GO:0008134 | Transcription factor binding | IEA IPI | molecular_function |
GO:0008284 | Positive regulation of cell proliferation | IDA IEA | biological_process |
GO:0009612 | Response to mechanical stimulus | IEA | biological_process |
GO:0009887 | Organ morphogenesis | IEA | biological_process |
GO:0010033 | Response to organic substance | IDA | biological_process |
GO:0010224 | Response to UV-B | IDA | biological_process |
GO:0014040 | Positive regulation of Schwann cell differentiation | IEA | biological_process |
GO:0016032 | Viral process | IEA | biological_process |
GO:0019221 | Cytokine-mediated signaling pathway | IDA | biological_process |
GO:0019901 | Protein kinase binding | IEA IPI | molecular_function |
GO:0031293 | Membrane protein intracellular domain proteolysis | TAS | biological_process |
GO:0031625 | Ubiquitin protein ligase binding | IPI | molecular_function |
GO:0032332 | Positive regulation of chondrocyte differentiation | IEA | biological_process |
GO:0032403 | Protein complex binding | IEA | molecular_function |
GO:0032481 | Positive regulation of type I interferon production | TAS | biological_process |
GO:0032495 | Response to muramyl dipeptide | IEA | biological_process |
GO:0032570 | Response to progesterone | IEA | biological_process |
GO:0032868 | Response to insulin | IEA | biological_process |
GO:0033590 | Response to cobalamin | IEA | biological_process |
GO:0033613 | Activating transcription factor binding | IPI | molecular_function |
GO:0034097 | Response to cytokine | IEA | biological_process |
GO:0034134 | Toll-like receptor 2 signaling pathway | TAS | biological_process |
GO:0034138 | Toll-like receptor 3 signaling pathway | TAS | biological_process |
GO:0034142 | Toll-like receptor 4 signaling pathway | TAS | biological_process |
GO:0034146 | Toll-like receptor 5 signaling pathway | TAS | biological_process |
GO:0034162 | Toll-like receptor 9 signaling pathway | TAS | biological_process |
GO:0034166 | Toll-like receptor 10 signaling pathway | TAS | biological_process |
GO:0035666 | TRIF-dependent toll-like receptor signaling pathway | TAS | biological_process |
GO:0038095 | Fc-epsilon receptor signaling pathway | TAS | biological_process |
GO:0038123 | Toll-like receptor TLR1:TLR2 signaling pathway | TAS | biological_process |
GO:0038124 | Toll-like receptor TLR6:TLR2 signaling pathway | TAS | biological_process |
GO:0042177 | Negative regulation of protein catabolic process | IEA | biological_process |
GO:0042301 | Phosphate ion binding | IDA | molecular_function |
GO:0042493 | Response to drug | IEA | biological_process |
GO:0042542 | Response to hydrogen peroxide | IEA | biological_process |
GO:0042802 | Identical protein binding | IDA IPI | molecular_function |
GO:0043066 | Negative regulation of apoptotic process | IDA IEA TAS | biological_process |
GO:0043123 | Positive regulation of I-kappaB kinase/NF-kappaB signaling | IEA IEP | biological_process |
GO:0043200 | Response to amino acid | IEA | biological_process |
GO:0043234 | Protein complex | IEA | cellular_component |
GO:0043278 | Response to morphine | IEA | biological_process |
GO:0043565 | Sequence-specific DNA binding | IEA | molecular_function |
GO:0044212 | Transcription regulatory region DNA binding | IDA | molecular_function |
GO:0045084 | Positive regulation of interleukin-12 biosynthetic process | IEA | biological_process |
GO:0045087 | Innate immune response | TAS | biological_process |
GO:0045892 | Negative regulation of transcription, DNA-templated | IDA | biological_process |
GO:0045893 | Positive regulation of transcription, DNA-templated | IDA IEA | biological_process |
GO:0045944 | Positive regulation of transcription from RNA polymerase II promoter | IDA IMP | biological_process |
GO:0046627 | Negative regulation of insulin receptor signaling pathway | IEA | biological_process |
GO:0047485 | Protein N-terminus binding | IPI | molecular_function |
GO:0048011 | Neurotrophin TRK receptor signaling pathway | TAS | biological_process |
GO:0050727 | Regulation of inflammatory response | IEA ISS | biological_process |
GO:0050852 | T cell receptor signaling pathway | TAS | biological_process |
GO:0051059 | NF-kappaB binding | IPI | molecular_function |
GO:0051092 | Positive regulation of NF-kappaB transcription factor activity | IDA TAS | biological_process |
GO:0051591 | Response to cAMP | IEA | biological_process |
GO:0051607 | Defense response to virus | NAS | biological_process |
GO:0070301 | Cellular response to hydrogen peroxide | IDA | biological_process |
GO:0070431 | Nucleotide-binding oligomerization domain containing 2 signaling pathway | IDA | biological_process |
GO:0070491 | Repressing transcription factor binding | IPI | molecular_function |
GO:0070555 | Response to interleukin-1 | IGI | biological_process |
GO:0071222 | Cellular response to lipopolysaccharide | IEA | biological_process |
GO:0071347 | Cellular response to interleukin-1 | IDA | biological_process |
GO:0071356 | Cellular response to tumor necrosis factor | IDA | biological_process |
GO:0071532 | Ankyrin repeat binding | IEA | molecular_function |
GO:2001237 | Negative regulation of extrinsic apoptotic signaling pathway | IEA IMP | biological_process |
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4. Expression levels in datasets
- Meta-analysis result
p-value up | p-value down | FDR up | FDR down |
---|---|---|---|
0.0192641351 | 0.9836268303 | 0.3381279813 | 1.0000000000 |
- Individual experiment result
( "-" represent NA in the specific microarray platform )
( "-" represent NA in the specific microarray platform )
Data source | Up or down | Log fold change |
---|---|---|
GSE11954 | Down | -0.1636673471 |
GSE13712_SHEAR | Up | 0.3344953296 |
GSE13712_STATIC | Up | 0.0520330596 |
GSE19018 | Up | 0.2816868549 |
GSE19899_A1 | Up | 0.1389730366 |
GSE19899_A2 | Up | 0.6385307859 |
PubMed_21979375_A1 | Up | 0.6024966499 |
PubMed_21979375_A2 | Up | 0.4197663621 |
GSE35957 | Up | 0.2282530638 |
GSE36640 | Up | 0.2112096637 |
GSE54402 | Up | 0.2324989556 |
GSE9593 | Up | 0.2337936521 |
GSE43922 | Up | 0.2825570282 |
GSE24585 | Down | -0.2922061052 |
GSE37065 | Up | 0.1889913240 |
GSE28863_A1 | Up | 0.2876344713 |
GSE28863_A2 | Up | 0.6076873703 |
GSE28863_A3 | Up | 0.5205574381 |
GSE28863_A4 | Down | -0.0559603317 |
GSE48662 | Up | 0.1358768482 |
5. Regulation relationships with compounds/drugs/microRNAs
- Compounds
Not regulated by compounds
- Drugs
Not regulated by drugs
- MicroRNAs
- mirTarBase
- mirTarBase
MiRNA_name | mirBase ID | miRTarBase ID | Experiment | Support type | References (Pubmed ID) |
---|---|---|---|---|---|
hsa-miR-373-3p | MIMAT0000726 | MIRT002531 | Microarray//Microarray;Other | Functional MTI (Weak) | 15685193 |
hsa-miR-124-3p | MIMAT0000422 | MIRT002616 | Luciferase reporter assay//Microarray//Microarray;Other | Functional MTI | 15685193 |
hsa-miR-7-5p | MIMAT0000252 | MIRT025722 | Sequencing | Functional MTI (Weak) | 20371350 |
hsa-miR-7-5p | MIMAT0000252 | MIRT025722 | Microarray | Functional MTI (Weak) | 17612493 |
hsa-miR-7-5p | MIMAT0000252 | MIRT025722 | Microarray | Functional MTI (Weak) | 19073608 |
hsa-miR-96-5p | MIMAT0000095 | MIRT027888 | Sequencing | Functional MTI (Weak) | 20371350 |
hsa-miR-324-5p | MIMAT0000761 | MIRT043112 | CLASH | Functional MTI (Weak) | 23622248 |
hsa-miR-30e-5p | MIMAT0000692 | MIRT044156 | CLASH | Functional MTI (Weak) | 23622248 |
hsa-miR-320a | MIMAT0000510 | MIRT044799 | CLASH | Functional MTI (Weak) | 23622248 |
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- mirRecord
No target information from mirRecord
- 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 |
---|---|
27349869 | Additionally, Acrp30 stimulation suppresses NFkappaB p65, which induces abnormal expression of hBD-2 induced by H2O2 |
26824319 | This 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 |
26588041 | We 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 |
26588041 | RelA 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 |
25536232 | In addition, Western blotting demonstrated less translocation of p65 from cytoplasm to nucleus |
25255445 | The 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 |
23542362 | Furthermore, 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 |
22889746 | Stat3 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 |
22740410 | HTLV-1 tax-induced rapid senescence is driven by the transcriptional activity of NF-kappaB and depends on chronically activated IKKalpha and p65/RelA |
22740410 | The senescence checkpoint triggered by Tax is driven by the transcriptional activity of NF-kappaB, which depends on activated IKKalpha and p65/RelA |
22673730 | On 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 |
22390170 | Silencing of the DEK gene induces apoptosis and senescence in CaSki cervical carcinoma cells via the up-regulation of NF-kappaB p65 |
22390170 | The intracellular expression of NF-kappaB p65 protein was studied by cytochemistry |
22390170 | In addition, the NF-kappaB p65 DNA-binding activity was measured by ELISA |
22390170 | All of these effects may be related to the up-regulation of NF-kappaB p65 expression and its nuclear translocation |
21979375 | Through 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 |
21832251 | Indoxyl sulfate induced phosphorylation of NF-kappaB p65 on Ser-276, which was suppressed by N-acetylcysteine, an antioxidant |
21832251 | Furthermore, indoxyl sulfate induced NF-kappaB p65 expression |
21832251 | Inhibitors 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) |
21832251 | NF-kappaB inhibitors suppressed indoxyl sulfate-induced p21 expression, whereas NF-kappaB p65 siRNA enhanced its expression |
21738489 | The majority of genes bound by NF-kappaB subunit RelA recruit Sirt6, and dynamic Sirt6 relocalization is largely driven in a RelA-dependent manner |
21738489 | Integrative 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 |
21738489 | Genes under the direct joint control of Sirt6 and RelA include several with prominent roles in cell senescence and organismal aging |
21698300 | Compared 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 |
21552325 | Small 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 |
21536657 | CPEB 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 |
21471201 | SIRT1 phosphorylation caused concomitant increases in p65/RelA NF-kappaB acetylation and the expression of an anti-apoptotic Bfl-1/A1 |
19779484 | RelA/p65 functions to maintain cellular senescence by regulating genomic stability and DNA repair |
19779484 | Our findings show that RelA/p65(-/-) murine fibroblasts immortalize at considerably faster rates than RelA/p65(+/+) cells |
19779484 | The 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 |
19779484 | This increase in genomic instability is closely related to a compromised DNA repair that occurs in both murine RelA/p65(-/-) fibroblasts and tissues |
19135889 | In 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 |
19135889 | Moreover, haploinsufficiency of RelA rescues the early lethality and degenerative syndrome of Sirt6-deficient mice |
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