Ignet

Gene Information

Gene symbol: IRF1

Gene name: interferon regulatory factor 1

HGNC ID: 6116

Synonyms: MAR

Related Genes

#	Gene Symbol	Number of hits
1	B2M	1 hits
2	C19orf10	1 hits
3	CASP1	1 hits
4	CCL5	1 hits
5	CCR5	1 hits
6	CCR9	1 hits
7	CD4	1 hits
8	CD44	1 hits
9	CD55	1 hits
10	CIITA	1 hits
11	CSF2	1 hits
12	CXCL10	1 hits
13	CXCR3	1 hits
14	HLX	1 hits
15	IFN1	1 hits
16	IFNG	1 hits
17	IFNGR1	1 hits
18	IFNGR2	1 hits
19	IL10	1 hits
20	IL10RA	1 hits
21	IL12A	1 hits
22	IL12B	1 hits
23	IL12RB1	1 hits
24	IL12RB2	1 hits
25	IL27RA	1 hits
26	IL6	1 hits
27	IL8	1 hits
28	INDO	1 hits
29	IRF2	1 hits
30	IRF6	1 hits
31	IRF7	1 hits
32	IRF9	1 hits
33	ISG15	1 hits
34	JAK1	1 hits
35	JAK2	1 hits
36	JUNB	1 hits
37	MAP2K4	1 hits
38	MYD88	1 hits
39	NFKB1	1 hits
40	NFKBIA	1 hits
41	NLRP3	1 hits
42	NOS2A	1 hits
43	PARP9	1 hits
44	PTPRC	1 hits
45	RPL32	1 hits
46	SLA	1 hits
47	SLC11A1	1 hits
48	SOCS1	1 hits
49	STAT1	1 hits
50	STAT3	1 hits
51	TBX21	1 hits
52	TGFBR1	1 hits
53	TNF	1 hits
54	TNFRSF1A	1 hits
55	TYK2	1 hits

Related Sentences

#	PMID	Sentence
1	28453771	The requirements for inflammation were examined in mice deficient in genes required (Ifng, Il6) or not required (Casp1) for mHgIA.
2	28453771	The requirements for inflammation were examined in mice deficient in genes required (Ifng, Il6) or not required (Casp1) for mHgIA.
3	28453771	Additionally, lack of IFN-γ or IL-6 impacted expression of genes regulated by either IFN-γ or type I IFN.
4	28453771	Additionally, lack of IFN-γ or IL-6 impacted expression of genes regulated by either IFN-γ or type I IFN.
5	28453771	Significantly, both IFN-γ and IL-6 were required for increased expression of IRF-1 which regulates IFN stimulated genes and is required for mHgIA.
6	28453771	Significantly, both IFN-γ and IL-6 were required for increased expression of IRF-1 which regulates IFN stimulated genes and is required for mHgIA.
7	28453771	Thus IRF-1 may be at the nexus of the interplay between IFN-γ and IL-6 in exacerbating a xenobiotic-induced inflammatory response, regulation of interferon responsive genes and autoimmunity.
8	28453771	Thus IRF-1 may be at the nexus of the interplay between IFN-γ and IL-6 in exacerbating a xenobiotic-induced inflammatory response, regulation of interferon responsive genes and autoimmunity.
9	28316372	The expression of genes, including IL10, JAK1, STAT3, SOCS3, IP10, ICAM1, IFNA, IFNG, STAT1, and IRF1, was investigated by RT-qPCR.
10	28316372	Patients with dyslipidemia demonstrated statistically higher expression of the IL10 and IFNA genes, while IFNG, IP10, IRF1, JAK1, and STAT3 were lower in comparison with nondyslipidemic patients.
11	27441275	We identified a number of uncharacterized genes (ZNF300, NUP1333, KLK1 and others) and confirmed previous studies demonstrating specific genes/genesets that are important mediators of host immune responses and that displayed associations with antibody response to influenza A/H1N1 vaccine.
12	27441275	These included interferon-regulatory transcription factors (IRF1/IRF2/IRF6/IRF7/IRF9), chemokine/chemokine receptors (CCR5/CCR9/CCL5), cytokine/cytokine receptors (IFNG/IL10RA/TNFRSF1A), protein kinases (MAP2K4/MAPK3), growth factor receptor (TGFBR1).
13	27276061	In addition to pathogen associated lipopolysaccharides (LPS), iNOS gene expression is dependent on numerous proinflammatory cytokines in the cellular microenvironment of the macrophage, two of which include interferon gamma (IFN-γ) and tumor necrosis factor alpha (TNF-α).
14	27276061	Results from our theoretical studies indicated that IFN-γ and subsequent activation of IRF1 are essential in consequential production of iNOS upon LPS stimulation.
15	26242990	Genetic variants were identified by sequencing the promoter regions and all exons of IFNG, IFNGR1, IFNGR2, IRF1, IL12A, IL12B, IL12RB1, IL12RB2, IL23A, IL23R, IL27, EBI3, IL27RA, IL6ST, SOCS1, STAT1, STAT4, JAK2, TYK2 and TBX21 in 69 DNA samples from Ghana.
16	26175298	The levels of p-STAT1, interferon regulatory factor 1, and class II transactivator exhibited similar phenomena.
17	24200694	JUNB/AP-1 controls IFN-γ during inflammatory liver disease.
18	24200694	In hepatocytes, the dimeric transcription factor c-JUN/AP-1 is a major mediator of cell survival during hepatitis, although functions for other JUN proteins in liver disease are less defined.
19	24200694	The absence of JUNB in immune cells decreased IFN-γ expression and secretion from NK and NKT cells, leading to reduced STAT1 pathway activation.
20	24200694	Systemic IFN-γ treatment or adenovirus-based IRF1 delivery to Junb-deficient mice restored hepatotoxicity, and we demonstrate that Ifng is a direct transcriptional target of JUNB.
21	24200694	These findings demonstrate that JUNB/AP-1 promotes cell death during acute hepatitis by regulating IFN-γ production in NK and NKT cells and thus functionally antagonizes the hepatoprotective function of c-JUN/AP-1 in hepatocytes.
22	23487038	BAL1/ARTD9 represses the anti-proliferative and pro-apoptotic IFNγ-STAT1-IRF1-p53 axis in diffuse large B-cell lymphoma.
23	23487038	BAL1/ARTD9 represses the anti-proliferative and pro-apoptotic IFNγ-STAT1-IRF1-p53 axis in diffuse large B-cell lymphoma.
24	23487038	BAL1/ARTD9 represses the anti-proliferative and pro-apoptotic IFNγ-STAT1-IRF1-p53 axis in diffuse large B-cell lymphoma.
25	23487038	Here we identify BAL1 as a novel oncogenic survival factor in DLBCL and show that constitutive overexpression of BAL1 in DLBCL tightly associates with intrinsic interferon-gamma (IFNγ) signaling and constitutive activity of signal transducer and activator of transcription (STAT)-1.
26	23487038	Here we identify BAL1 as a novel oncogenic survival factor in DLBCL and show that constitutive overexpression of BAL1 in DLBCL tightly associates with intrinsic interferon-gamma (IFNγ) signaling and constitutive activity of signal transducer and activator of transcription (STAT)-1.
27	23487038	Here we identify BAL1 as a novel oncogenic survival factor in DLBCL and show that constitutive overexpression of BAL1 in DLBCL tightly associates with intrinsic interferon-gamma (IFNγ) signaling and constitutive activity of signal transducer and activator of transcription (STAT)-1.
28	23487038	Remarkably, BAL1 stimulates the phosphorylation of both STAT1 isoforms, STAT1α and STAT1β, on Y701 and thereby promotes the nuclear accumulation of the antagonistically acting and transcriptionally repressive isoform STAT1β.
29	23487038	Remarkably, BAL1 stimulates the phosphorylation of both STAT1 isoforms, STAT1α and STAT1β, on Y701 and thereby promotes the nuclear accumulation of the antagonistically acting and transcriptionally repressive isoform STAT1β.
30	23487038	Remarkably, BAL1 stimulates the phosphorylation of both STAT1 isoforms, STAT1α and STAT1β, on Y701 and thereby promotes the nuclear accumulation of the antagonistically acting and transcriptionally repressive isoform STAT1β.
31	23487038	BAL1 directly inhibits, together with STAT1β, the expression of tumor suppressor and interferon response factor (IRF)-1.
32	23487038	BAL1 directly inhibits, together with STAT1β, the expression of tumor suppressor and interferon response factor (IRF)-1.
33	23487038	BAL1 directly inhibits, together with STAT1β, the expression of tumor suppressor and interferon response factor (IRF)-1.
34	23487038	Conversely, BAL1 enhances the expression of the proto-oncogenes IRF2 and B-cell CLL/lymphoma (BCL)-6 in DLBCL.
35	23487038	Conversely, BAL1 enhances the expression of the proto-oncogenes IRF2 and B-cell CLL/lymphoma (BCL)-6 in DLBCL.
36	23487038	Conversely, BAL1 enhances the expression of the proto-oncogenes IRF2 and B-cell CLL/lymphoma (BCL)-6 in DLBCL.
37	23487038	Our results show for the first time that BAL1 represses the anti-proliferative and pro-apoptotic IFNγ-STAT1-IRF1-p53 axis and mediates proliferation, survival and chemo-resistance in DLBCL.
38	23487038	Our results show for the first time that BAL1 represses the anti-proliferative and pro-apoptotic IFNγ-STAT1-IRF1-p53 axis and mediates proliferation, survival and chemo-resistance in DLBCL.
39	23487038	Our results show for the first time that BAL1 represses the anti-proliferative and pro-apoptotic IFNγ-STAT1-IRF1-p53 axis and mediates proliferation, survival and chemo-resistance in DLBCL.
40	23487038	Our results suggest that BAL1 may induce an switch in STAT1 from a tumor suppressor to an oncogene in high-risk DLBCL.
41	23487038	Our results suggest that BAL1 may induce an switch in STAT1 from a tumor suppressor to an oncogene in high-risk DLBCL.
42	23487038	Our results suggest that BAL1 may induce an switch in STAT1 from a tumor suppressor to an oncogene in high-risk DLBCL.
43	23271704	Moreover, IFN-γ enhanced STAT1 phosphorylation and expression of IRF-1.
44	23271704	Moreover, IFN-γ enhanced STAT1 phosphorylation and expression of IRF-1.
45	23271704	Collectively, these results suggest that IFN-γ induces BAFF expression in human intestinal epithelial cells through JAK/STAT signaling pathways that might activate the GAS and IRF-1-binding element in the BAFF promoter.
46	23271704	Collectively, these results suggest that IFN-γ induces BAFF expression in human intestinal epithelial cells through JAK/STAT signaling pathways that might activate the GAS and IRF-1-binding element in the BAFF promoter.
47	22578563	To test this hypothesis, mice deficient in genes regulating IFN-γ expression (Casp1, Nlrp3, Il12a, Il12b, Stat4) or function (Ifngr1, Irf1) were examined for mHgIA susceptibility.
48	22578563	To test this hypothesis, mice deficient in genes regulating IFN-γ expression (Casp1, Nlrp3, Il12a, Il12b, Stat4) or function (Ifngr1, Irf1) were examined for mHgIA susceptibility.
49	22578563	To test this hypothesis, mice deficient in genes regulating IFN-γ expression (Casp1, Nlrp3, Il12a, Il12b, Stat4) or function (Ifngr1, Irf1) were examined for mHgIA susceptibility.
50	22578563	Absence of either Ifngr1 or Irf1 resulted in a striking reduction of disease, while deficiency of genes promoting IFN-γ expression had modest to no effect.
51	22578563	Absence of either Ifngr1 or Irf1 resulted in a striking reduction of disease, while deficiency of genes promoting IFN-γ expression had modest to no effect.
52	22578563	Absence of either Ifngr1 or Irf1 resulted in a striking reduction of disease, while deficiency of genes promoting IFN-γ expression had modest to no effect.
53	22578563	Furthermore, both Irf1- and Ifng-deficiency only modestly reduced the expansion of CD44(hi) and CD44(hi)CD55(lo) CD4(+) T cells, indicating that they are not absolutely required for T cell activation.
54	22578563	Furthermore, both Irf1- and Ifng-deficiency only modestly reduced the expansion of CD44(hi) and CD44(hi)CD55(lo) CD4(+) T cells, indicating that they are not absolutely required for T cell activation.
55	22578563	Furthermore, both Irf1- and Ifng-deficiency only modestly reduced the expansion of CD44(hi) and CD44(hi)CD55(lo) CD4(+) T cells, indicating that they are not absolutely required for T cell activation.
56	19848299	By Day 12 of pregnancy, estrogens increase the expression of multiple genes in the uterine luminal epithelium including SPP1, STC1, IRF2 and STAT1 that likely have roles for implantation.
57	19848299	By Day 15 of pregnancy, IFNs upregulate a large array of IFN responsive genes in the underlying stroma and glandular epithelium including ISG15, IRF1, STAT1, SLAs and B2M that likely have roles in uterine remodeling to support placentation.
58	18296866	The CLENDOs were also exposed to cytokines to assess differences in activation of nuclear factor kappa B signaling (NF-kappaB), induction of the transcription factor interferon regulatory factor 1 (IRF1), cytokine production, and cytokine-induced cell death.
59	18296866	The CLENDOs were also exposed to cytokines to assess differences in activation of nuclear factor kappa B signaling (NF-kappaB), induction of the transcription factor interferon regulatory factor 1 (IRF1), cytokine production, and cytokine-induced cell death.
60	18296866	In response to TNF, for instance, both types of CLENDOs exhibited a rapid, 5-fold decrease in NF-kappaB inhibitor alpha (NFKBIA) protein expression (P<0.05), and a 4-fold increase in IRF1 expression (P<0.05), that did not differ with phenotype (P>0.05).
61	18296866	In response to TNF, for instance, both types of CLENDOs exhibited a rapid, 5-fold decrease in NF-kappaB inhibitor alpha (NFKBIA) protein expression (P<0.05), and a 4-fold increase in IRF1 expression (P<0.05), that did not differ with phenotype (P>0.05).
62	18296866	Similarly, both types of CLENDOs produced tumor necrosis factor alpha and chemokine ligand 2 in response to IFNG stimulation (P<0.05) that did not differ with phenotype (P>0.05).
63	18296866	Similarly, both types of CLENDOs produced tumor necrosis factor alpha and chemokine ligand 2 in response to IFNG stimulation (P<0.05) that did not differ with phenotype (P>0.05).
64	17337057	Seven genes identified by suppression subtractive hybridization as up-regulated in the mesenteric lymph nodes at 24h (h) post-inoculation (p.i.) in serovar Choleraesuis-infected pigs (ARPC2, CCT7, HSPH1, LCP1, PTMA, SDCBP, VCP) and three genes in serovar Typhimurium-infected pigs (CD47/IAP, CXCL10, SCARB2) were analyzed by real-time PCR at 8h, 24 h, 48 h, 7 days (d) and 21 d p.i.
65	17337057	(IFNG, IL12A, IL4, IL8, CSF2) coincided with extended transcriptional activation throughout the 21 d infection (IFNG, INDO, SOCS1, STAT1, IL1B, IL6, IL8, SLC11A1).
66	17337057	The serovar Typhimurium-infected swine presented a more transient induction of immune-related genes (IFNG, INDO, IRF1, SOCS1, STAT1, IL1B, IL8, SLC11A1) early in the infection (24-48 h) followed by a significant repression of IL12A, IL12B, IL4, IL8 and CSF2.
67	16728393	There was no functional difference in the signal transducers and activators of transcription (STAT) pathways between progenitors and mature oligodendrocytes as determined by induction of IRF1 mRNA in response to IFNG.
68	16728393	Therefore, we concluded that simultaneous activation of the STAT pathway by IFNG and of the ERK pathway by exogenous trophic factors played a role in the stage-specific IFNG-induced cytotoxicity in oligodendroglial progenitors.
69	15183000	This publication describes the cloning of full or partial length sequences for pig TBX21 (T-bet), MYD88, ICSBP1, CD8A (CD8alpha), CD8B (CD8beta), and CD28 cDNAs.
70	15183000	This publication describes the cloning of full or partial length sequences for pig TBX21 (T-bet), MYD88, ICSBP1, CD8A (CD8alpha), CD8B (CD8beta), and CD28 cDNAs.
71	15183000	This publication describes the cloning of full or partial length sequences for pig TBX21 (T-bet), MYD88, ICSBP1, CD8A (CD8alpha), CD8B (CD8beta), and CD28 cDNAs.
72	15183000	Real-time PCR assays have been developed for the relative quantitation of these products as well as previously characterized transcripts that encode exon A-containing CD45, HLX1, IRF1, STAT1 and RPL32.
73	15183000	Real-time PCR assays have been developed for the relative quantitation of these products as well as previously characterized transcripts that encode exon A-containing CD45, HLX1, IRF1, STAT1 and RPL32.
74	15183000	Real-time PCR assays have been developed for the relative quantitation of these products as well as previously characterized transcripts that encode exon A-containing CD45, HLX1, IRF1, STAT1 and RPL32.
75	15183000	When used for examining temporal immune gene expression in the liver of Toxoplasma gondii infected pigs, the positive regulators of Th1 responses, IRF1, MYD88, and STAT1, were found to be expressed prior to the simultaneous upregulation of interferon gamma (IFNG), HLX1 and TBX21 gene expression.
76	15183000	When used for examining temporal immune gene expression in the liver of Toxoplasma gondii infected pigs, the positive regulators of Th1 responses, IRF1, MYD88, and STAT1, were found to be expressed prior to the simultaneous upregulation of interferon gamma (IFNG), HLX1 and TBX21 gene expression.
77	15183000	When used for examining temporal immune gene expression in the liver of Toxoplasma gondii infected pigs, the positive regulators of Th1 responses, IRF1, MYD88, and STAT1, were found to be expressed prior to the simultaneous upregulation of interferon gamma (IFNG), HLX1 and TBX21 gene expression.
78	15183000	In contrast, in the mesenteric lymph node (MLN), only expression of IRF1 and IFNG was significantly upregulated.
79	15183000	In contrast, in the mesenteric lymph node (MLN), only expression of IRF1 and IFNG was significantly upregulated.
80	15183000	In contrast, in the mesenteric lymph node (MLN), only expression of IRF1 and IFNG was significantly upregulated.