HCSGD entry for IFNA1
1. General information
Official gene symbol | IFNA1 |
---|---|
Entrez ID | 3439 |
Gene full name | interferon, alpha 1 |
Other gene symbols | IFL IFN IFN-ALPHA IFN-alphaD IFNA13 IFNA@ |
Links to Entrez Gene | Links to Entrez Gene |
2. Neighbors in the network

3. Gene ontology annotation
GO ID | GO term | Evidence | Category |
---|---|---|---|
GO:0002250 | Adaptive immune response | IBA | biological_process |
GO:0002286 | T cell activation involved in immune response | IBA | biological_process |
GO:0002323 | Natural killer cell activation involved in immune response | IBA | biological_process |
GO:0005125 | Cytokine activity | IBA | molecular_function |
GO:0005132 | Type I interferon receptor binding | IBA | molecular_function |
GO:0005576 | Extracellular region | TAS | cellular_component |
GO:0005615 | Extracellular space | IBA | cellular_component |
GO:0006959 | Humoral immune response | IBA | biological_process |
GO:0007596 | Blood coagulation | TAS | biological_process |
GO:0019221 | Cytokine-mediated signaling pathway | IBA TAS | biological_process |
GO:0030183 | B cell differentiation | IBA | biological_process |
GO:0033141 | Positive regulation of peptidyl-serine phosphorylation of STAT protein | IBA | biological_process |
GO:0042100 | B cell proliferation | IBA | biological_process |
GO:0043330 | Response to exogenous dsRNA | IBA | biological_process |
GO:0045087 | Innate immune response | IBA TAS | biological_process |
GO:0045343 | Regulation of MHC class I biosynthetic process | IBA | biological_process |
GO:0051607 | Defense response to virus | IEA | biological_process |
GO:0060337 | Type I interferon signaling pathway | TAS | biological_process |
GO:0060338 | Regulation of type I interferon-mediated signaling pathway | TAS | biological_process |
Entries Per Page
Displaying Page of
4. Expression levels in datasets
- Meta-analysis result
p-value up | p-value down | FDR up | FDR down |
---|---|---|---|
0.0829352228 | 0.9692137723 | 0.6072150209 | 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 | Up | 0.1912824611 |
GSE13712_SHEAR | Down | -0.0144970657 |
GSE13712_STATIC | Down | -0.1632667987 |
GSE19018 | Up | 0.0719335319 |
GSE19899_A1 | Down | 0.0000000000 |
GSE19899_A2 | Down | -0.2260921786 |
PubMed_21979375_A1 | Down | -0.0165708812 |
PubMed_21979375_A2 | Down | -0.2449280424 |
GSE35957 | Up | 0.1986228773 |
GSE36640 | Up | 0.6468259595 |
GSE54402 | Up | 1.8346085478 |
GSE9593 | Up | 0.0958083208 |
GSE43922 | - | - |
GSE24585 | - | - |
GSE37065 | - | - |
GSE28863_A1 | - | - |
GSE28863_A2 | - | - |
GSE28863_A3 | - | - |
GSE28863_A4 | - | - |
GSE48662 | - | - |
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-122-5p | MIMAT0000421 | MIRT023373 | Microarray | Functional MTI (Weak) | 17612493 |
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: 20 abstracts the gene occurs.
PubMed ID of the article | Sentenece the gene occurs |
---|---|
27052162 | IFN signaling-deficient melanocytes expressing activated Braf do not exhibit senescence and develop aggressive melanomas |
27052162 | Restoration of IFN signaling in IFN-deficient melanoma cells induces senescence and suppresses melanoma progression |
27052162 | Additional data from human melanoma patients and mouse transplanted tumor models suggest the importance of non-cell-autonomous IFN signaling |
27052162 | Inactivation of the IFN pathway is mediated by the IFN receptor IFNAR1 downregulation that invariably occurs during melanoma development |
27052162 | These results suggest that IFN signaling is an important tumor-suppressive pathway that inhibits melanoma development and progression and argue for targeting IFNAR1 downregulation to prevent metastatic disease and improve the efficacy of molecularly target and immune-targeted melanoma therapies |
26046815 | Furthermore, recent studies demonstrated that IFN also restrict proliferation of damaged cells by inducing cell senescence |
26046815 | Here we investigated the subsequent role of IFN in elimination of the senescent cells |
26046815 | Our studies demonstrate that endogenous IFN produced by already senescent cells contribute to increased expression of the natural killer (NK) receptor ligands, including MIC-A and ULBP2 |
26046815 | Furthermore, neutralization of endogenous IFN or genetic ablation of its receptor chain IFNAR1 compromises the recognition of senescent cells and their clearance in vitro and in vivo |
26046815 | We discuss the role of IFN in protecting the multi-cellular host from accumulation of damaged senescent cells and potential significance of this mechanism in human cancers |
24445253 | Mutations in SAMHD1 cause Aicardi-Goutieres syndrome (AGS), an inflammatory disorder that shares phenotypic similarity with systemic lupus erythematosus, including activation of antiviral type 1 interferon (IFN) |
24445253 | Knockdown of SAMHD1 by RNA interference recapitulates activation of DNA damage signalling and type 1 IFN activation |
23966171 | There is growing evidence that many host proteins involved in innate and intrinsic immunity are regulated by SUMOylation, and that SUMO contributes to the regulatory process that governs the initiation of the type I interferon (IFN) response |
23966171 | The tumor suppressor p53 is a modulator of the IFN response that plays a role in virus-induced apoptosis and in IFN-induced senescence |
23966171 | Here we demonstrate that IFN treatment increases the levels of SUMOylated p53 and induces cellular senescence through a process that is partially dependent upon SUMOylation of p53 |
23966171 | Thus, our study provides evidence that IFN signaling induces p53 SUMOylation, which results in the activation of a cellular senescence program and contributes to the antiviral functions of interferon |
23864729 | Given that human prostatic infections are associated with chronic inflammation, the development of BPH is associated with an accumulation of senescent cells with a proinflammatory phenotype, and the development of prostate cancer is associated with the loss of IFN signaling, the role of AIM2 in mediating the formation of prostatic diseases was investigated |
22615843 | Taken together, these studies suggest that signaling through the IFN pathway might play an important role in cellular senescence |
22615843 | This additional understanding of IFN antitumor action and mechanisms influencing tumor responsiveness or resistance appears useful in aiding further promising development of biomolecular strategies in the IFN therapy of cancer |
21471287 | Accordingly, increased constitutive levels of IFI16 and AIM2 proteins in ataxia telangiectasia mutated (ATM) HDFs were associated with the activation of the IFN signaling and increased levels of IL-1beta |
21471287 | Interestingly, the knockdown of AIM2 expression in HDFs increased the basal levels of IFI16 protein and activated the IFN signaling |
21471287 | In contrast, the knockdown of the IFI16 expression in HDFs decreased the basal and dsDNA-induced activation of the IFN signaling |
21198351 | Several pathways have been implicated in the establishment of antiviral state in response to interferon (IFN), one of which implicates the promyelocytic leukemia (PML) protein |
21198351 | PML is induced by IFN, leading to a marked increase of expression of PML isoforms and the number of PML nuclear bodies (NBs) |
20016203 | Senescence and decreased NO production were observed in cells and several signaling pathways - such as IFN/STAT, IGF, TGF-beta, cytoskeleton rearrangement and lipid metabolism - were altered at P4, as judged from the microarray analysis |
18505922 | By gene expression profiling, we have found that genes in the interferon (IFN) pathway were dysregulated during the spontaneous cellular immortalization of fibroblasts from Li-Fraumeni syndrome (LFS) patients with germ-line mutations in p53 |
18505922 | IFN signaling pathway genes were down-regulated by epigenetic silencing during immortalization, and some of these same IFN-regulated genes were activated during replicative senescence |
18505922 | Bisulfite sequencing of the promoter regions of two IFN regulatory transcription factors (IRF5 and IRF7) revealed that IRF7, but not IRF5, was epigenetically silenced by methylation of CpG islands in immortal LFS cells |
18505922 | We conclude that the epigenetic inactivation of the IFN pathway plays a critical role in cellular immortalization, and the reactivation of IFN-regulated genes by transcription factors IRF5 and/or IRF7 is sufficient to induce cellular senescence |
18505922 | The IFN pathway may provide valuable molecular targets for therapeutic interventions at early stages of cancer development |
17981205 | Superimposed on this basic scheme are a shift in the CD8(+) T cell response to type I and II interferon (IFN) from anti- to pro-proliferative and transcriptional control of replicative senescence by Bmi-1, Blimp-1, and BCL6/BCL6b |
16426144 | We found that multiple interferon (IFN) signaling pathway genes were regulated by epigenetic silencing |
16426144 | We concluded that factor(s) additional to Stat1 (whether IFN dependent or not) are required for the immortalization of LFS fibroblasts |
15208661 | Defects in interferon (IFN) signaling that result in loss of expression of IFN-inducible proteins are associated with cellular immortalization, an important early event in the development of human cancer |
14563561 | Analysis of hPNPase(old-35) expression in cell lines defective in various IFN signaling molecules confirms that hPNPase(old-35) expression is dependent upon the Janus activated kinase (JAK)/signal transducers and activators of transcription (STAT) pathway |
14563561 | Induction of hPNPase(old-35) by IFN treatment as well as during differentiation and senescence suggest that this gene may play a significant role in regulating cellular growth and that overlapping gene expression changes, also induced by IFN, may contribute to these important physiological processes |
12473748 | This approach involved screening of a subtracted cDNA library prepared from human melanoma cells induced to terminally differentiate by treatment with fibroblast IFN and mezerein with mRNA derived from senescent human progeria cells |
12473748 | Identification of hPNPase(old-35), an IFN-inducible 3'-5' RNA exonuclease, provides additional support for a relationship between IFN action and RNA processing and suggests an important role for this gene in growth control associated with terminal differentiation and cellular senescence |
10049783 | Furthermore, the expression of mRNAs for p21/Waf1/Cip1/Sdi1, IRF-1 and IFN inducible 6-16 was higher in the telomere-reduced cells than in the parental cells |
9144735 | Using the highest mouse IFN-beta-producing sublines, the mode of IFN secretion was examined |
8376318 | Tumor necrosis factor-alpha (TNF) and various interferons (IFN) have potent cytostatic or cytotoxic effects on a variety of human tumor-derived cell lines |
2483689 | Interferons (IFN) are a family of glycoproteins well known for their antiviral activity and their ability to inhibit growth and alter the behavior of various normal and transformed cell types, both in vitro and in vivo |
2483689 | Extracts from healthy, non-virally infected keratinocyte cultures contained IFN activity as determined by viral plaque inhibition assays |
2483689 | Further, we have demonstrated that IFN inhibits the growth of the human keratinocyte in a non-cytotoxic, reversible manner and that the keratinocytes harvested from older adult donors are significantly more sensitive to the growth inhibitory effects of IFN than are the keratinocytes of young donors |
6193247 | The presence of a low level of interferon (IFN) activity was demonstrated in aged culture medium of primary chick embryo (CE) cells |
6193247 | This increase was suppressed by addition of antiserum against chick IFN |
6193247 | In contrast, anti-chick IFN serum did not inhibit the ageing effect, i |
Entries Per Page
Displaying Page of