| + |
IFNG | up-regulates quantity by expression 
transcriptional regulation
|
HLA-B |
0.338 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251926 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 2507660 |
HLA-B (class I) and C13 gene expression was transcriptionally activated by IFN-gamma and IFN-alpha 2 |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
IFNG | down-regulates activity 
|
NfKb-p65/p50 |
0.442 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255937 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 23667107 |
Early inhibition of IL-1β expression by IFN-γ is mediated by impaired binding of NF-κB to the IL-1β promoter but is independent of nitric oxide. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Macrophage polarization, Multiple sclerosis, SARS-CoV CYTOKINE STORM |
| + |
IFNG | up-regulates
|
Immune_response |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261024 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 32283152 |
High levels of expression of IL-1B, IFN-γ, IP-10, and monocyte chemoattractant protein 1 (MCP-1) have been detected in patients with COVID-19. These inflammatory cytokines may activate the T-helper type 1 (Th1) cell response. Th1 activation is a key event in the activation of specific immunity. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Multiple sclerosis, SARS-CoV CYTOKINE STORM |
| + |
IFNG | up-regulates quantity by expression
transcriptional regulation
|
GCH1 |
0.254 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252223 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20525234 |
Pro-inflammatory cytokines like interferon-γ (IFN-γ) induce expression of GTP-cyclohydrolase I in various brain cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Tissue: |
Brain |
| + |
IFNG | up-regulates quantity by expression
transcriptional regulation
|
NOD2 |
0.397 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252408 |
|
|
Homo sapiens |
BEAS-2B/BBM Cell |
| pmid |
sentence |
| 18647246 |
NOD2, toll-like receptor 4 (TLR4) and the adapter protein receptor-interacting protein 2 (RIP2) are induced by tumor-necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma) in the bronchial epithelial cell line BEAS-2B. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
IL18 | up-regulates quantity by expression
transcriptional regulation
|
IFNG |
0.48 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260858 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 10653850 |
IL-18, originally described as IFN-γ-inducing factor, is secreted from activated macrophages and Kupffer cells (1–3). The major activity associated with this cytokine is induction of IFN-γ production from CD4+ Th1 cells, T cells, B cells and NK cells, especially in collaboration with IL-12. IL-12 and IL-18 acted in a synergistic manner for the development of T cells into IFN-γ-producing cells without their TCR engagement. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260860 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 10653850 |
IL-18, originally described as IFN-γ-inducing factor, is secreted from activated macrophages and Kupffer cells (1–3). The major activity associated with this cytokine is induction of IFN-γ production from CD4+ Th1 cells, T cells, B cells and NK cells, especially in collaboration with IL-12. IL-12 and IL-18 acted in a synergistic manner for the development of T cells into IFN-γ-producing cells without their TCR engagement. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| Pathways: | SARS-CoV CYTOKINE STORM |
| + |
HMBOX1 | down-regulates quantity by repression 
transcriptional regulation
|
IFNG |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261625 |
|
|
Homo sapiens |
Natural Killer Cell Line |
| pmid |
sentence |
| 21839858 |
Additionally, by luciferase reporter assay, HMBOX1 displayed suppressive effect on the transcription activity of IFN-γ promoter. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
IFNG | down-regulates quantity by repression
transcriptional regulation
|
DIO |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-267810 |
|
|
Rattus norvegicus |
|
| pmid |
sentence |
| 9397972 |
From the results in Figs. 1-3, it is clear that several cytokines reduce the expression of 5’-DI mRNA and enzymatic activity in FRTL-5 cells grown in TSH-containing medium. These include TNF-a, IL-lb and INF-g but not TGF-b. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-270238 |
|
|
Rattus norvegicus |
|
| pmid |
sentence |
| 9397972 |
From the results in Figs. 1-3, it is clear that several cytokines reduce the expression of 5’-DI mRNA and enzymatic activity in FRTL-5 cells. These include TNF-a, IL-lb and INF-y. |
|
| Publications: |
2 |
Organism: |
Rattus Norvegicus |
| + |
PROX1 | down-regulates quantity by repression
transcriptional regulation
|
IFNG |
0.262 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254506 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20064070 |
Human PROX1 is involved in biologic functions closely tied to HIV infection, most notably as a negative regulator of interferon (IFN) gamma expression in T cells |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
T_cell_activation | up-regulates quantity
|
IFNG |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260967 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 10653850 |
IL-12 Synergizes With IL-18 or IL-1beta for IFN-gamma Production From Human T Cells. IL-12 and IL-18 acted in a synergistic manner for the development of T cells into IFN-γ-producing cells without their TCR. Here we show that IL-12 and IL-1beta synergistically induce T cells to proliferate and produce IFN-gamma without their TCR engagement. IL-12 stimulation induced an increase in the proportion of T cells positive for IL-18R engagement. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-263818 |
|
|
Homo sapiens |
Helper T-lymphocyte |
| pmid |
sentence |
| 32454942 |
interferon gamma- (IFNγ-) and interleukin-17- (IL-17-) secreting CD4+ T cells are believed to be the pathogenic initiators of MS [22], and in MS patients, the increased production of either IFNγ or IL-17 is associated with pathology |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| Pathways: | Multiple sclerosis, SARS-CoV CYTOKINE STORM |
| + |
IFNG | up-regulates 
binding
|
IFNGR1 |
0.882 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-95626 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 12438563 |
Ifn-g Binds to the ifn-g Receptor binding subunit (ifn-gR1;receptor chain 1), a species-specific cell surface transmembrane receptor chain (41, 42). A second transmembrane protein (ifn-gR2) (4345) is required for signal transduction |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-81804 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 10986460 |
Molecular interactions among cytokines and cytokine receptors form the basis of many cell-signaling pathways relevant to immune function. Interferon-g (ifng) signals through a multimeric receptor complex consistingof two different but structurally related transmembrane chains: the high-affinityreceptor-binding subunit (ifn-gra) and a species-specific accessory factor (af-1 or ifn-grb). |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
IL12A | up-regulates quantity by expression
transcriptional regulation
|
IFNG |
0.374 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260859 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 10653850 |
IL-18, originally described as IFN-γ-inducing factor, is secreted from activated macrophages and Kupffer cells (1–3). The major activity associated with this cytokine is induction of IFN-γ production from CD4+ Th1 cells, T cells, B cells and NK cells, especially in collaboration with IL-12 |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260861 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 10653850 |
IL-18, originally described as IFN-γ-inducing factor, is secreted from activated macrophages and Kupffer cells (1–3). The major activity associated with this cytokine is induction of IFN-γ production from CD4+ Th1 cells, T cells, B cells and NK cells, especially in collaboration with IL-12 |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| Pathways: | SARS-CoV CYTOKINE STORM |
| + |
IFNG | up-regulates quantity by expression
transcriptional regulation
|
RIPK2 |
0.286 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252410 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 18647246 |
NOD2, toll-like receptor 4 (TLR4) and the adapter protein receptor-interacting protein 2 (RIP2) are induced by tumor-necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma) in the bronchial epithelial cell line BEAS-2B. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
IFNG | up-regulates activity
binding
|
IFNGR1 |
0.882 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249484 |
|
|
Homo sapiens |
Macrophage |
| pmid |
sentence |
| 23898330 |
In the classical model of IFNgamma signaling, dimeric IFNgamma cross-links the IFNGR1 receptor subunit that results in allosteric changes in receptor cytoplasmic domain. This results in movement of JAK2 from receptor subunit IFNGR2 to IFNGR1. The JAKs autophosphorylate and then phosphorylate IFNGR1 cytoplasmic domain. This results in binding, phosphorylation, and dimer formation of STAT1_. The dimeric STAT1_ dissociates from receptor and undergoes nuclear translocation via an intrinsic NLS for specific gene activation |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
IFNG | up-regulates activity
|
RFX5 |
0.287 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-241368 |
|
|
Homo sapiens |
HeLa Cell |
| pmid |
sentence |
| 9177217 |
Transcriptional Activation by the RFX5 Activation Domain Is IFN-_-Inducible in HeLa Cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SOCS1 | down-regulates
|
IFNG |
0.538 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249571 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21628332 |
SOCS1 inhibits macrophage responses to IFN-g, and SOCS1-deficient mice develop symptoms of severe systemic autoimmune and inflammatory disease. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Macrophage polarization |
| + |
IFNG | down-regulates quantity by repression
transcriptional regulation
|
LPL |
0.364 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251848 |
|
|
Homo sapiens |
Macrophage |
| pmid |
sentence |
| 2114181 |
Interferon-gamma inhibits lipoprotein lipase in human monocyte-derived macrophages. The data indicate that IFN-gamma is inhibiting macrophage LPL at least in part via a reduction of LPL synthesis |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251854 |
|
|
Mus musculus |
J774.2 Cell |
| pmid |
sentence |
| 10909770 |
The suppression of lipoprotein lipase expression in J774.2 macrophages by IFN-gamma and TNF-alpha is mediated at the transcriptional level. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens, Mus Musculus |
| + |
IFNG | up-regulates
|
Demyelination |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-263833 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 24507514 |
Beside its wellknown antiviral and proinflammatory action, overexpression of IFN-g in the CNS could participate in demyelination. Transgenic overexpression of IFN-g in the mouse by CNS oligodendrocytes led to chronic demyelination that may be severe |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Tissue: |
Central Nervous System |
| Pathways: | Multiple sclerosis |
| + |
IFNG | up-regulates
binding
|
IFNGR2 |
0.634 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-31013 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 7673114 |
Ifn-g Binds to the ifn-g Receptor binding subunit (ifn-gR1;receptor chain 1), a species-specific cell surface transmembrane receptor chain (41, 42). A second transmembrane protein (ifn-gR2) (43 45) is required for signal transduction |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
IFNG | up-regulates quantity by expression
transcriptional regulation
|
SOCS1 |
0.538 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-236809 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19482358 |
IFN-_ induces socs1 gene expression through an inducible factor |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Macrophage polarization |
| + |
IFNG | up-regulates
|
Inflammation |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260259 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 18231581 |
Induction and over-production of proinflammatory cytokines and chemokines, such as IL-6, IL-8, TNF-a and INF-c, were considered to be main mediators in the pathogenesis of SARS |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Multiple sclerosis, SARS-CoV CYTOKINE STORM |
| + |
IFNG | up-regulates
|
ARDS |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261033 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 32446778 |
Taken together, these data clearly indicate that, in SARS-CoV in-fection, ARDS is the ultimate result of a cytokine storm. In this scenario,the release by immune effector cells of large amounts of pro-in-flammatory cytokines (IFNα, IFNγ, IL-1β, IL-6, IL-12, IL-18, IL-33,TNFα, TGFβ) and chemokines (CXCL10, CXCL8, CXCL9, CCL2, CCL3,CCL5) precipitates and sustains the aberrant systemic inflammatoryresponse. The cytokine storm is readily followed by theimmune system “attacking” the body, which in turn will cause ARDSand multiple organ failure, the final result being death, at least in themost severe cases of SARS-CoV-2 infection |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | SARS-CoV CYTOKINE STORM |
| + |
IFNG | up-regulates quantity by expression
transcriptional regulation
|
S100A10 |
0.27 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255236 |
|
|
Homo sapiens |
HeLa Cell, BEAS-2B Cell |
| pmid |
sentence |
| 12645529 |
The effect of interferon (IFN)-gamma on p11 expression was studied in two human epithelial cell lines (BEAS-2B and HeLa). Treatment with IFN-gamma resulted in increased steady-state levels of p11 mRNA and protein expression, with a time-dependent and dose-dependent effect. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TBX21 | up-regulates quantity by expression
transcriptional regulation
|
IFNG |
0.49 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254508 |
|
|
|
|
| pmid |
sentence |
| 17541280 |
T-bet is crucially implicated in Th1 differentiation due to its strong promoting activity for IFN-gamma gene transcription |
|
| Publications: |
1 |
| + |
IFNG | up-regulates
|
SLC11A1 |
0.356 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254038 |
|
|
Homo sapiens |
Macrophage |
| pmid |
sentence |
| 11909746 |
Functional studies in Nramp1 transfected macrophages have demonstrated that the Nramp1 protein plays a vital role in early macrophage activation [10,29,30]. Nramp1 is constitutively expressed in macrophage cell lines of the myeloid lineage (isolated peritoneal, splenic, and liver resident macrophages), and can be induced by treatment of macrophages with IFN-γ, or IFN-γ plus lipopolysaccharide (LPS) |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
M1_polarization | up-regulates
|
IFNG |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-263827 |
|
|
Homo sapiens |
Macrophage |
| pmid |
sentence |
| 32454942 |
Macrophages and microglia show a high plasticity and have been arbitrarily classified into “M1” (proinflammatory) and “M2” (prorepair, anti-inflammatory) phenotypes depending on their activation state, although it is now widely accepted that this classification is hugely oversimplified, particularly for microglia, and only partially reflects the real situation. According to the M1/M2 model, M1 polarized cells are characterized by the release of proinflammatory mediators, such as TNF, IL-1β, and IFNγ |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Macrophage polarization, Multiple sclerosis |
| + |
TBX21 | up-regulates quantity by expression
transcriptional regulation
|
IFNG |
0.49 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-266234 |
|
|
Mus musculus |
EL-4 Cell |
| pmid |
sentence |
| 10761931 |
T-bet Transactivates the IFNγ Gene and Represses the IL-2 Gene in EL4 Cells |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
IFNG | down-regulates
|
MYOD1 |
0.295 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-82467 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11009425 |
In contrast, in differentiated myotubes, tnf plus interferon-gamma (ifn-gamma) signaling was required for nf-kappab-dependent down-regulation of myod and dysfunction of skeletal myofibers. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Tissue: |
Myotube |
| + |
IFNG | down-regulates quantity by repression
transcriptional regulation
|
DIO1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-267487 |
|
|
Rattus norvegicus |
|
| pmid |
sentence |
| 9397972 |
From the results in Figs. 1-3, it is clear that several cytokines reduce the expression of 5’-DI mRNA and enzymatic activity in FRTL-5 cells. These include TNF-a, IL-lb and INF-y. |
|
| Publications: |
1 |
Organism: |
Rattus Norvegicus |
| Pathways: | Thyroid Hormone Metabolism |
| + |
IFNG | up-regulates activity
binding
|
IFNGR2/INFGR1 |
0.758 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249487 |
|
|
Homo sapiens |
Macrophage |
| pmid |
sentence |
| 23898330 |
In the classical model of IFNgamma signaling, dimeric IFNgamma cross-links the IFNGR1 receptor subunit that results in allosteric changes in receptor cytoplasmic domain. This results in movement of JAK2 from receptor subunit IFNGR2 to IFNGR1. The JAKs autophosphorylate and then phosphorylate IFNGR1 cytoplasmic domain. This results in binding, phosphorylation, and dimer formation of STAT1_. The dimeric STAT1_ dissociates from receptor and undergoes nuclear translocation via an intrinsic NLS for specific gene activation |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Macrophage polarization, SARS-CoV CYTOKINE STORM |
3.0
IFNG
- 
- 