HCSGD entry for IFNG

1. General information

Official gene symbolIFNG
Entrez ID3458
Gene full nameinterferon, gamma
Other gene symbolsIFG IFI
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:0000060Protein import into nucleus, translocationIDAbiological_process
GO:0000122Negative regulation of transcription from RNA polymerase II promoterISSbiological_process
GO:0001781Neutrophil apoptotic processIEAbiological_process
GO:0002026Regulation of the force of heart contractionIEAbiological_process
GO:0002053Positive regulation of mesenchymal cell proliferationISSbiological_process
GO:0002250Adaptive immune responseIEAbiological_process
GO:0002302CD8-positive, alpha-beta T cell differentiation involved in immune responseIEAbiological_process
GO:0003340Negative regulation of mesenchymal to epithelial transition involved in metanephros morphogenesisISSbiological_process
GO:0005125Cytokine activityIEAmolecular_function
GO:0005133Interferon-gamma receptor bindingIEAmolecular_function
GO:0005576Extracellular regionIDA TAScellular_component
GO:0005615Extracellular spaceIEAcellular_component
GO:0006915Apoptotic processIGIbiological_process
GO:0006928Cellular component movementTASbiological_process
GO:0006959Humoral immune responseIEAbiological_process
GO:0007050Cell cycle arrestIDAbiological_process
GO:0007166Cell surface receptor signaling pathwayTASbiological_process
GO:0009615Response to virusIDAbiological_process
GO:0009897External side of plasma membraneIEAcellular_component
GO:0019221Cytokine-mediated signaling pathwayTASbiological_process
GO:0019882Antigen processing and presentationIEAbiological_process
GO:0030593Neutrophil chemotaxisIEAbiological_process
GO:0030968Endoplasmic reticulum unfolded protein responseIEAbiological_process
GO:0031642Negative regulation of myelinationIEAbiological_process
GO:0032224Positive regulation of synaptic transmission, cholinergicIEAbiological_process
GO:0032700Negative regulation of interleukin-17 productionIDAbiological_process
GO:0032735Positive regulation of interleukin-12 productionIDAbiological_process
GO:0032747Positive regulation of interleukin-23 productionIDAbiological_process
GO:0032760Positive regulation of tumor necrosis factor productionIEAbiological_process
GO:0033141Positive regulation of peptidyl-serine phosphorylation of STAT proteinIDA NASbiological_process
GO:0034393Positive regulation of smooth muscle cell apoptotic processIDAbiological_process
GO:0042102Positive regulation of T cell proliferationIEAbiological_process
GO:0042493Response to drugIEAbiological_process
GO:0042511Positive regulation of tyrosine phosphorylation of Stat1 proteinIDAbiological_process
GO:0042742Defense response to bacteriumIEAbiological_process
GO:0042832Defense response to protozoanIEAbiological_process
GO:0044130Negative regulation of growth of symbiont in hostIEAbiological_process
GO:0045080Positive regulation of chemokine biosynthetic processIEAbiological_process
GO:0045084Positive regulation of interleukin-12 biosynthetic processIEAbiological_process
GO:0045348Positive regulation of MHC class II biosynthetic processIEAbiological_process
GO:0045410Positive regulation of interleukin-6 biosynthetic processIEAbiological_process
GO:0045429Positive regulation of nitric oxide biosynthetic processIDAbiological_process
GO:0045666Positive regulation of neuron differentiationIEAbiological_process
GO:0045672Positive regulation of osteoclast differentiationIDAbiological_process
GO:0045785Positive regulation of cell adhesionIEAbiological_process
GO:0045944Positive regulation of transcription from RNA polymerase II promoterIEAbiological_process
GO:0048304Positive regulation of isotype switching to IgG isotypesIEAbiological_process
GO:0048662Negative regulation of smooth muscle cell proliferationIDAbiological_process
GO:0050718Positive regulation of interleukin-1 beta secretionIEAbiological_process
GO:0050796Regulation of insulin secretionIDAbiological_process
GO:0051044Positive regulation of membrane protein ectodomain proteolysisIDAbiological_process
GO:0051607Defense response to virusIEAbiological_process
GO:0051712Positive regulation of killing of cells of other organismIDAbiological_process
GO:0060333Interferon-gamma-mediated signaling pathwayTASbiological_process
GO:0060334Regulation of interferon-gamma-mediated signaling pathwayTASbiological_process
GO:0060550Positive regulation of fructose 1,6-bisphosphate 1-phosphatase activityIDAbiological_process
GO:0060552Positive regulation of fructose 1,6-bisphosphate metabolic processIDAbiological_process
GO:0060557Positive regulation of vitamin D biosynthetic processIDAbiological_process
GO:0060559Positive regulation of calcidiol 1-monooxygenase activityIDAbiological_process
GO:0071222Cellular response to lipopolysaccharideIEAbiological_process
GO:0071351Cellular response to interleukin-18IEAbiological_process
GO:0072308Negative regulation of metanephric nephron tubule epithelial cell differentiationISSbiological_process
GO:0097191Extrinsic apoptotic signaling pathwayIDAbiological_process
GO:2000309Positive regulation of tumor necrosis factor (ligand) superfamily member 11 productionIDAbiological_process
Entries Per Page
Displaying Page of

4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.59078152430.86153851680.99999024731.0000000000

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

Data sourceUp or downLog fold change
GSE11954Up0.0030504673
GSE13712_SHEARDown-0.0137904376
GSE13712_STATICDown-0.0545452400
GSE19018Up0.1957471772
GSE19899_A1Up0.1387856168
GSE19899_A2Down-0.1222068486
PubMed_21979375_A1Down-0.1221754007
PubMed_21979375_A2Up0.1315956083
GSE35957Up0.2015139452
GSE36640Up0.0917672323
GSE54402Up0.0718213961
GSE9593Up0.0387847530
GSE43922Up0.0191952488
GSE24585Down-0.0004313336
GSE37065Down-0.0079895288
GSE28863_A1Down-0.0526527110
GSE28863_A2Down-0.0886107063
GSE28863_A3Up0.1252205643
GSE28863_A4Up0.0960698491
GSE48662Up0.0150412912

5. Regulation relationships with compounds/drugs/microRNAs

  • Compounds

Not regulated by compounds

  • Drugs

Name

Drug

Accession number

OlsalazineDB01250 -
GlucosamineDB01296 EXPT01563
VIR201DB05110 -
FontolizumabDB05111 -
ApremilastDB05676 -

  • MicroRNAs

    • mirTarBase

MiRNA_name

mirBase ID

miRTarBase ID

Experiment

Support type

References (Pubmed ID)

hsa-miR-16-5pMIMAT0000069MIRT006912Luciferase reporter assay//qRT-PCRFunctional MTI22379033
hsa-miR-15a-5pMIMAT0000068MIRT006913Luciferase reporter assay//qRT-PCRFunctional MTI22379033
hsa-miR-15b-5pMIMAT0000417MIRT006914Luciferase reporter assay//qRT-PCRFunctional MTI22379033
hsa-miR-29b-3pMIMAT0000100MIRT007034Luciferase reporter assayFunctional MTI22772450
hsa-miR-409-3pMIMAT0001639MIRT007285Luciferase reporter assayFunctional MTI23360331
hsa-miR-26b-5pMIMAT0000083MIRT029122MicroarrayFunctional MTI (Weak)19088304
Entries Per Page
Displaying Page of
    • mirRecord
No target information from mirRecord

6. Text-mining results about the gene

Gene occurances in abstracts of cellular senescence-associated articles: 29 abstracts the gene occurs.


PubMed ID of the article

Sentenece the gene occurs

27173733IFN-gamma(-/-) NOD
27057461As a part of cellular pathogen defense, IFNgamma triggers induction of NADPH oxidase NOX2, which produces superoxide into phagosomes of immune cells
27057461IFNgamma is capable of inducing expression of constitutively active NADPH oxidase NOX4 in tumor cells leading to generation of reactive oxygen species (ROS) damaging DNA, activation of DNA damage response and cell cycle arrest/premature cellular senescence
27039820We here aimed to investigate cellular senescence in immortalized cholangiocyte and cholangiocarcinoma cell lines using five different inducing agents: 5-aza-2'deoxycytidine, bromodeoxyuridine, interferons (IFNbeta and IFNgamma), and hydrogen peroxide
26857736Human CCR7(low)CD45RA(high) effector memory CD8(+) T cells (terminally differentiated TEMRA) are reportedly a functionally compromised population with characteristics of cellular senescence when examined ex vivo Although their frequencies are increased in elderly subjects in association with declined immune competence, however, it remains unclear whether their impaired functions can be reversed so that they contribute to immune responses in vivo Here, I show that, in contrast to TCR stimulation, stimulation of TEMRA with IL-15 induced a unique transcriptional signature, promoted IFN-gamma production and cell cycle entry, and reduced chemotaxis toward sphingosine-1-phosphate (S1P)
26802028XAF1 induction with interferon-gamma (IFN-gamma) treatment was abrogated by BRD7 knockdown, which resulted in blocking interferon-induced senescence
26802028In lung cancer cells, XAF1 tumor suppressor activity was decreased by BRD7 knockdown, and inhibition of tumor growth by IFN-gamma did not appear in BRD7-depleted xenograft tumors
25982278IFNgamma induces oxidative stress, DNA damage and tumor cell senescence via TGFbeta/SMAD signaling-dependent induction of Nox4 and suppression of ANT2
25982278While cytokines such as tumor necrosis factor-alpha (TNFalpha) and interferon gamma (IFNgamma) are important components of senescence-associated secretome and induce senescence in, for example, mouse pancreatic beta-cancer cell model, their downstream signaling pathway(s) and links with oxidative stress and DDR are mechanistically unclear
25982278Using human and mouse normal and cancer cell models, we now show that TNFalpha and IFNgamma induce NADPH oxidases Nox4 and Nox1, reactive oxygen species (ROS), DDR signaling and premature senescence
25982278Unlike mouse tumor cells that required concomitant presence of IFNgamma and TNFalpha, short exposure to IFNgamma alone was sufficient to induce Nox4, Nox1 and DDR in human cells
25982278Furthermore, the expression of adenine nucleotide translocase 2 (ANT2) was suppressed by IFNgamma contributing to elevation of ROS and DNA damage
25090227Among the anti-inflammatory cytokines, the production of prostaglandin E2 (PGE2) and the expression of its primary enzyme, cyclooxygenase-2 (COX-2), were profoundly increased by pre-stimulation with interferon gamma (IFN-gamma) and tumor necrosis factor alpha (TNF-alpha), and this response was significantly decreased with consecutive passages
25083993Despite their apparent senescent state, we determined that these cells secreted high levels of both TNF-alpha and IFN-gamma and showed potent cytotoxic activity
24913980Finally, in accordance with much evidence indicating that DDR and oxidative stress are major determinants of cellular senescence, we found that redox-dependent DDR activation upon chemotherapeutic treatment is critical for MM cell entry in premature senescence and is required for the preferential ligand upregulation on senescent cells, which are preferentially killed by NK cells and trigger potent IFN-gamma production
24175851IFN-gamma plays an indirect anti-cancer role through the immune system but may have direct negative effects on cancer cells
24175851We exposed AGS, HGC-27 and GES-1 gastric cancer cell lines to IFN-gamma and found significantly reduced colony formation ability
24175851Flow cytometry revealed no effect of IFN-gamma on apoptosis of cell lines and no effect on cell aging as assessed by beta-gal staining
24175851Microarray assay revealed that IFN-gamma changed the mRNA expression of genes related to the cell cycle and cell proliferation and migration, as well as chemokines and chemokine receptors, and immunity-related genes
24175851Finally, flow cytometry revealed that IFN-gamma arrested the cells in the G1/S phase
24175851IFN-gamma may slow proliferation of some gastric cancer cells by affecting the cell cycle to play a negative role in the development of gastric cancer
22182806Memory T-cells were assessed by interferon (IFN)-gamma ELISpot assay and flow cytometrically via IFN-gamma or IL-2
22182806Proportions of CD57(bright)CD28(null) CD4+ T-cells correlated with IFN-gamma responses to CMV (p =0
22182806Proportions of CD57(bright)CD28(null) CD8+T-cells and CD8+ T-cell IFN-gamma responses to CMV peptides correlated in controls but not HIV patients
22182806IL-2 was predominantly produced by CD28+T-cells from all donors, whereas IFN-gamma was mostly produced by CD57+ T-cells
22182806The findings provide evidence of an accumulation of immunosenescent T-cells able to make IFN-gamma
21764762Coculture of wild-type p53-induced human tumor cells with primary human NK cells enhanced NKG2D-dependent degranulation and IFN-gamma production by NK cells
21635686Moreover, pretreatment of CD4+CD28(null) T cells with IL-15 displayed a synergistic effect on the IFN-gamma production in CMV-specific responses, which was not observed in CD4+CD28+ T cells
20100671No impairment in IFN-gamma production by CD57+ T cells from the genital tract was observed
19885868Inducible activation of IFI 16 results in suppression of telomerase activity, growth suppression and induction of cellular senescence
19885868Expression of the human HIN-200 family member IFI 16 has been reported to suppress cell growth and contribute to the onset of cellular senescence
19885868Moreover, IFI 16 and hTERT co-localised within the nucleus and these two proteins physically interacted in vivo and in vitro
19885868Together, these data suggest that IFI 16 may act as an endogenous regulator of telomerase activity and, through its interaction with hTERT, contributes to the inhibition of proliferation and induces a senescence-like state
19802007JAK1/STAT-activating ligands, interleukin 10 (IL10), IL20, IL24, interferon gamma (IFNgamma), IFNbeta and IL6, were also expressed by senescent cells, supporting autocrine/paracrine activation of JAK1/STAT
19493573We show here that pre-treatment of trophoblast cells and certain cancer cells with agents that activate stress pathways (Ras oncogene, PMA or H2O2) and induce senescence can substantially enhance the induction of immune response genes (MHC class II, CD40, MICA, MICB) by HDACi and restore a vigorous IFN-gamma response in trophoblast cells and tumor cells
19133932The measurements of the alloimmune response-infiltrate, cytology, expression of perforin, granzyme B, IFN-gamma and MHC-were not increased in old allografts
19071156IFN-gamma treatment increased ROS production, and an antioxidant, N-acetylcysteine, inhibited IFN-gamma-induced cellular senescence
19071156Therefore, these results suggest that IFN-gamma might play an important role in cellular senescence through a p53-dependent DNA damage pathway and contribute to the pathogenesis of atherosclerosis via its pro-senescent activity
17416406Although CD57 expression on blood and BAL cells was associated with a reduced proliferative potential, examination of beryllium-specific CD4(+) T cells in blood and lung revealed no difference in CD57 expression on cells that produced IFN-gamma only versus IFN-gamma and IL-2
16821141In inflamed portal tracts of PBC, CD4+ T cells of Th1 type expressing IFN-gamma or CXCR3 are aggregated and more commonly detected around injured bile ducts than Th2-type CD4+ T cells expressing IL-4 or CCR4, indicating that Th1-dominant cellular immunity plays a more-prominent role in recruitment of memory T-cell subsets in PBC and may be responsible for the progressive bile duct damage
16806194However, the induction of immunosubunits by interferon-gamma (IFN-gamma) was lost in senescent cells
16806194In contrast, levels of the 11S proteasome regulator, PA28, were increased by IFN-gamma even in senescent cells, and both immunosubunits and PA28 increased with the reversible growth arrest in confluent cell cultures
16204645In CD8+ T cells and NK cells, the transcription factors T-bet and eomesodermin (Eomes) regulate maturation and effector functions, including IFN-gamma production
16204645As Eomes null mice are not viable, real-time polymerase chain reaction comparisons between C57Bl/6J (B6) and alymphoid (Rag2(0/0)gammac0/0) mice were used to assess uNK cell expression of T-bet, Eomes, and the target genes IFN-gamma, granzyme A, and perforin
16204645In uNK cells, transcripts for T-bet, Eomes, and IFN-gamma were most abundant in mature stage cells, and transcripts for granzyme A and perforin were lower at this stage than in immature or senescent cells
15208661Role of IFI 16 in cellular senescence of human fibroblasts
15208661Here we report that loss of IFN-inducible IFI 16 expression in human fibroblasts allows bypass of cellular senescence
15208661We found that levels of IFI 16 mRNA and protein were higher in human old versus young fibroblasts and immortalization of fibroblasts with telomerase resulted in decreased expression of IFI 16
15208661Moreover, overexpression of IFI 16 in immortalized fibroblasts strongly inhibited cell proliferation
15208661Interestingly, knockdown of IFI 16 expression in fibroblasts inhibited p53-mediated transcription, downregulated p21(WAF1) expression, and extended the proliferation potential
15208661Importantly, treatment of immortal cell lines with 5-aza-2'-deoxycytidine, an inhibitor of DNA methyltransferase, resulted in upregulation of IFI 16
15208661Our observations support the idea that increased levels of IFI 16 in older populations of human fibroblasts contribute to cellular senescence
12894224Role of IFI 16, a member of the interferon-inducible p200-protein family, in prostate epithelial cellular senescence
12894224Here we report that IFI 16, an interferon-inducible transcriptional modulator from the p200-protein family, contributes to cellular senescence of prostate epithelial cells
12894224Normal human prostate epithelial cells (PrEC) in culture expressed detectable levels of IFI 16, and the levels increased more than fourfold when cells approached cellular senescence
12894224Consistent with a role of IFI 16 in cellular senescence, human prostate cancer cell lines either did not express IFI 16 or expressed a variant form, which was primarily detected in the cytoplasm of prostate cancer cells and not in the nucleus
12894224Moreover, overexpression of functional IFI 16 in human prostate cancer cell lines inhibited colony formation
12894224Additionally, ectopic expression of IFI 16 in clonal prostate cancer cell lines was associated with a senescence-like phenotype, production of senescence-associated beta-galactosidase (a biochemical marker for cellular senescence), and reduction of S-phase cells in culture
12894224Importantly, upregulation of p21WAF1 and inhibition of E2F-stimulated transcription accompanied inhibition of cell growth by IFI 16 in prostate cancer cell lines
12894224Collectively, our observations support the idea that increased levels of IFI 16 in PrECs contribute to senescence-associated irreversible cell growth arrest
11872952In situ activated intestinal T cells expanded in vitro--without addition of antigen--produce IFN-gamma and IL-10 and preserve their function during growth
11872952OBJECTIVE: The balance between mucosal CD4+ T cells producing IFN-gamma or IL-10 is essential in the maintenance of intestinal homeostasis
11872952We aimed to investigate how in situ activated T cells were expanded in vitro according to a new cell culture protocol and if it selected for continuous clonal CD4+ T cells capable of producing mainly IFN-gamma or IL-10
11872952RESULTS: Cytokine production was increased in cultures from patients with Crohn's disease compared to controls (IFN-gamma, p = 0
7561522Rat and mouse fibroblasts were also found to produce nitric oxide when primed with IFN-gamma and simultaneously treated with IL-1, TNF-alpha, or LPS
7561522The doses of IFN-gamma effective in priming fibroblasts for nitric oxide production were as low as 1-10 U/ml
7561522Fibroblasts were also found to be distinct from macrophages in their sensitivity to the suppressive effects of transforming growth factor-beta, which in fibroblasts inhibited both IFN-gamma plus LPS- and IFN-gamma plus TNF-alpha-induced nitric oxide production
7561522At the stage of growth crisis, a dramatic increase in nitric oxide production was observed in rat fibroblasts in response to IFN-gamma or TNF-alpha that may be directly correlated with cellular senescence
8125178Most of these cells were treated with 200 to 1000 U recombinant bovine interferon-gamma (IFN-gamma) for 3 days
8125178Growth rate: In the absence of IFN-gamma, the growth rate was high for cell types 3 and 4, moderate for cell type 1, and low for cell types 2 and 5
8125178The presence of IFN-gamma caused anti-proliferative effects
8125178IFN-gamma could be cytotoxic on cell type 3
8513512Transfected T cells of both young and elderly subjects appear to display normal T cell function: they cease doubling upon removal of IL-2; in the presence of autologous adherent mononuclear cells they respond to mitogen stimulation and produce IL-2 and IFN-gamma during proliferation; and they express both IL-2 and transferrin receptors similar to those observed in mitogen-stimulated nontransfected T cells
Entries Per Page
Displaying Page of