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Gene Information
Gene symbol: IFNA1
Gene name: interferon, alpha 1
HGNC ID: 5417
Synonyms: IFNA@, IFL, IFN, IFN-ALPHA, IFNA13, IFN-alphaD
Related Genes
Related Sentences
| # | PMID | Sentence |
| 1 | 27071061 | HPAI H5N1 virus induced excessive expression of type I IFNs (IFNA and IFNG), cytokines (IL1B, IL18, IL22, IL13, and IL12B), chemokines (CCL4, CCL19, CCL10, and CX3CL1) and IFN stimulated genes (OASL, MX1, RSAD2, IFITM5, IFIT5, GBP 1, and EIF2AK) in lung tissues. |
| 2 | 26697438 | Compared to mock-inoculated PBMCs, WNV-stimulated PBMCs expressed high levels of interferon (IFN) alpha (IFNA), gamma (IFNG), IL6, IL12, IL22, CXCL10, and pentraxin 3 (PTX3) mRNA. |
| 3 | 26697438 | Compared to mock-inoculated PBMCs, WNV-stimulated PBMCs expressed high levels of interferon (IFN) alpha (IFNA), gamma (IFNG), IL6, IL12, IL22, CXCL10, and pentraxin 3 (PTX3) mRNA. |
| 4 | 26697438 | TLRs-signaling downstream genes (MyD88, STAT1, TRAF3, IRF7, and IRF9) subsequently became up-regulated. |
| 5 | 26697438 | TLRs-signaling downstream genes (MyD88, STAT1, TRAF3, IRF7, and IRF9) subsequently became up-regulated. |
| 6 | 26697438 | The high expression of IFNs, TLR3, TLR4, TRAF3, STAT1, IRF7, and IRF9 are in accordance with antiviral activities, while expression of TNFA, HO1, iNOS, caspase 3, and caspase 9 transcripts suggests the involvement of oxidative stress and apoptosis in WNV-stimulated rabbit PBMCs, respectively. |
| 7 | 26697438 | The high expression of IFNs, TLR3, TLR4, TRAF3, STAT1, IRF7, and IRF9 are in accordance with antiviral activities, while expression of TNFA, HO1, iNOS, caspase 3, and caspase 9 transcripts suggests the involvement of oxidative stress and apoptosis in WNV-stimulated rabbit PBMCs, respectively. |
| 8 | 26697438 | Higher expression of IFNA, IFN beta (IFNB), IFNG, TNFA, IL6, IL22, PTX3, TLR3 and TLR4, IRF7, IRF9, STST1, TRAF3, caspase 3, and caspase 9 were seen in PBMCs from WNV-infected rabbits on day 3 post-intradermal virus inoculation compared to PBMCs from uninfected control rabbits. |
| 9 | 26697438 | Higher expression of IFNA, IFN beta (IFNB), IFNG, TNFA, IL6, IL22, PTX3, TLR3 and TLR4, IRF7, IRF9, STST1, TRAF3, caspase 3, and caspase 9 were seen in PBMCs from WNV-infected rabbits on day 3 post-intradermal virus inoculation compared to PBMCs from uninfected control rabbits. |
| 10 | 26020282 | Type I IFNs (IFNA1, IFNB1), type II (IFNG), type III (IFNL1, IFNL2/3), IFNL4 and ISG hepatic expressions were measured by qPCR from in 65 chronic hepatitis C (CHC) patients whose IFNL4-associated rs368234815 and IFNL3-associated rs12989760 genotype were determined. |
| 11 | 26020282 | Levels of ISGs and IFNL2/3 mRNAs were lower in IFNL3 rs12979860 CC patients compared with non-CC patients, and in treatment responders, compared with nonresponders. |
| 12 | 26020282 | Hepatic levels of ISGs in CHC are associated with IFNL2/3 and IFNL4 expression, suggesting that IFNLs, not other types of IFNs, drive ISG expression. |
| 13 | 26020282 | Hepatic IFNL2/3 expression is functionally linked to IFNL4 and IFNL3 polymorphisms, potentially explaining the tight association among ISG expression and treatment response. |
| 14 | 25774455 | Genes that were significantly regulated between VRs and VNRs were CREB3L4, HIST1H3A, HIST1H3H, IFNA1, IFNA4, IFNA5, IFNA6, IFNA8, IFNA14, IFNG, IFNAR1, IL6, IRF9, MAPK4, MAPK5, MAPK14, NET1, and PIK3C2A in the IFN array. |
| 15 | 25774455 | In the TLR array, only LBP and MAPK8 were found to be differentially regulated. |
| 16 | 25774455 | In the antigen processing array, HLA-A, HLA-C, HLA-DMA, HLA-DMB, HLA-F, PSMA5, PSMB8, and PSMB9 were differentially downregulated. |
| 17 | 25445652 | Interferon-γ (IFNG) microsatellite repeat and single nucleotide polymorphism haplotypes of IFN-α receptor (IFNAR1) associated with enhanced malaria susceptibility in Indian populations. |
| 18 | 25445652 | One SNP each from the IFNA8 and IFNA17 of IFNA gene cluster had a protective effect in the non-endemic region but not in the endemic region. |
| 19 | 25346938 | Depression is a common side-effect of interferon (IFN)-alpha treatment of hepatitis C virus (HCV) infection and melanoma. |
| 20 | 25346938 | Depression is a common side-effect of interferon (IFN)-alpha treatment of hepatitis C virus (HCV) infection and melanoma. |
| 21 | 25346938 | Depression is a common side-effect of interferon (IFN)-alpha treatment of hepatitis C virus (HCV) infection and melanoma. |
| 22 | 25346938 | Depression is a common side-effect of interferon (IFN)-alpha treatment of hepatitis C virus (HCV) infection and melanoma. |
| 23 | 25346938 | Depression is a common side-effect of interferon (IFN)-alpha treatment of hepatitis C virus (HCV) infection and melanoma. |
| 24 | 25346938 | Disturbances of tryptophan (TRP) metabolism might contribute to development of IFN-alpha-associated depression due to IFN-alpha-induced activation of indoleamine 2,3-dioxygenase (IDO), a rate-limiting enzyme of TRP-kynurenine (KYN) metabolism. |
| 25 | 25346938 | Disturbances of tryptophan (TRP) metabolism might contribute to development of IFN-alpha-associated depression due to IFN-alpha-induced activation of indoleamine 2,3-dioxygenase (IDO), a rate-limiting enzyme of TRP-kynurenine (KYN) metabolism. |
| 26 | 25346938 | Disturbances of tryptophan (TRP) metabolism might contribute to development of IFN-alpha-associated depression due to IFN-alpha-induced activation of indoleamine 2,3-dioxygenase (IDO), a rate-limiting enzyme of TRP-kynurenine (KYN) metabolism. |
| 27 | 25346938 | Disturbances of tryptophan (TRP) metabolism might contribute to development of IFN-alpha-associated depression due to IFN-alpha-induced activation of indoleamine 2,3-dioxygenase (IDO), a rate-limiting enzyme of TRP-kynurenine (KYN) metabolism. |
| 28 | 25346938 | Disturbances of tryptophan (TRP) metabolism might contribute to development of IFN-alpha-associated depression due to IFN-alpha-induced activation of indoleamine 2,3-dioxygenase (IDO), a rate-limiting enzyme of TRP-kynurenine (KYN) metabolism. |
| 29 | 25346938 | The present study assessed KYN/TRP ratio (KTR) as a marker of IDO activity in American Caucasian HCV patients awaiting IFN-alpha treatment. |
| 30 | 25346938 | The present study assessed KYN/TRP ratio (KTR) as a marker of IDO activity in American Caucasian HCV patients awaiting IFN-alpha treatment. |
| 31 | 25346938 | The present study assessed KYN/TRP ratio (KTR) as a marker of IDO activity in American Caucasian HCV patients awaiting IFN-alpha treatment. |
| 32 | 25346938 | The present study assessed KYN/TRP ratio (KTR) as a marker of IDO activity in American Caucasian HCV patients awaiting IFN-alpha treatment. |
| 33 | 25346938 | The present study assessed KYN/TRP ratio (KTR) as a marker of IDO activity in American Caucasian HCV patients awaiting IFN-alpha treatment. |
| 34 | 25346938 | Up-regulation of IDO might be an additional risk factor of IFN-alpha-associated depression. |
| 35 | 25346938 | Up-regulation of IDO might be an additional risk factor of IFN-alpha-associated depression. |
| 36 | 25346938 | Up-regulation of IDO might be an additional risk factor of IFN-alpha-associated depression. |
| 37 | 25346938 | Up-regulation of IDO might be an additional risk factor of IFN-alpha-associated depression. |
| 38 | 25346938 | Up-regulation of IDO might be an additional risk factor of IFN-alpha-associated depression. |
| 39 | 25346938 | Future studies shall explore the causes of elevated serum TRP in relation to IFN-alpha-associated depression. |
| 40 | 25346938 | Future studies shall explore the causes of elevated serum TRP in relation to IFN-alpha-associated depression. |
| 41 | 25346938 | Future studies shall explore the causes of elevated serum TRP in relation to IFN-alpha-associated depression. |
| 42 | 25346938 | Future studies shall explore the causes of elevated serum TRP in relation to IFN-alpha-associated depression. |
| 43 | 25346938 | Future studies shall explore the causes of elevated serum TRP in relation to IFN-alpha-associated depression. |
| 44 | 22345648 | The production of M. tuberculosis and purified protein derivative-induced IFN-γ, TNF-α, IL-1β, and IL-6 was reduced in a DEP dose-dependent manner. |
| 45 | 22345648 | The production of M. tuberculosis and purified protein derivative-induced IFN-γ, TNF-α, IL-1β, and IL-6 was reduced in a DEP dose-dependent manner. |
| 46 | 22345648 | Furthermore, DEP stimulation prior to M. tuberculosis infection altered the expression of TLR3, -4, -7, and -10 mRNAs and of a subset of M. tuberculosis-induced host genes including inhibition of expression of many NF-κB (e.g., CSF3, IFNG, IFNA, IFNB, IL1A, IL6, and NFKBIA) and IFN regulatory factor (e.g., IFNG, IFNA1, IFNB1, and CXCL10) pathway target genes. |
| 47 | 22345648 | Furthermore, DEP stimulation prior to M. tuberculosis infection altered the expression of TLR3, -4, -7, and -10 mRNAs and of a subset of M. tuberculosis-induced host genes including inhibition of expression of many NF-κB (e.g., CSF3, IFNG, IFNA, IFNB, IL1A, IL6, and NFKBIA) and IFN regulatory factor (e.g., IFNG, IFNA1, IFNB1, and CXCL10) pathway target genes. |
| 48 | 22345648 | We propose that DEP downregulate M. tuberculosis-induced host gene expression via MyD88-dependent (IL6, IL1A, and PTGS2) as well as MyD88-independent (IFNA, IFNB) pathways. |
| 49 | 22345648 | We propose that DEP downregulate M. tuberculosis-induced host gene expression via MyD88-dependent (IL6, IL1A, and PTGS2) as well as MyD88-independent (IFNA, IFNB) pathways. |
| 50 | 21161299 | Interferon-gamma (+874) T/A genotypes and risk of IFN-alpha-induced depression. |
| 51 | 21161299 | Interferon-gamma (+874) T/A genotypes and risk of IFN-alpha-induced depression. |
| 52 | 21161299 | Interferon-gamma (+874) T/A genotypes and risk of IFN-alpha-induced depression. |
| 53 | 21161299 | Interferon-gamma (+874) T/A genotypes and risk of IFN-alpha-induced depression. |
| 54 | 21161299 | Interferon-gamma (+874) T/A genotypes and risk of IFN-alpha-induced depression. |
| 55 | 21161299 | Depression is a frequent side effect of interferon (IFN)-alpha therapy of hepatitis C (HCV) and is of great relevance with regard to adherence, compliance, and premature therapy discontinuation. |
| 56 | 21161299 | Depression is a frequent side effect of interferon (IFN)-alpha therapy of hepatitis C (HCV) and is of great relevance with regard to adherence, compliance, and premature therapy discontinuation. |
| 57 | 21161299 | Depression is a frequent side effect of interferon (IFN)-alpha therapy of hepatitis C (HCV) and is of great relevance with regard to adherence, compliance, and premature therapy discontinuation. |
| 58 | 21161299 | Depression is a frequent side effect of interferon (IFN)-alpha therapy of hepatitis C (HCV) and is of great relevance with regard to adherence, compliance, and premature therapy discontinuation. |
| 59 | 21161299 | Depression is a frequent side effect of interferon (IFN)-alpha therapy of hepatitis C (HCV) and is of great relevance with regard to adherence, compliance, and premature therapy discontinuation. |
| 60 | 21161299 | We retrospectively studied distribution of IFN-gamma (IFNG) (+874) T/A genotypes in 170 Caucasian HCV patients treated by IFN-alpha. |
| 61 | 21161299 | We retrospectively studied distribution of IFN-gamma (IFNG) (+874) T/A genotypes in 170 Caucasian HCV patients treated by IFN-alpha. |
| 62 | 21161299 | We retrospectively studied distribution of IFN-gamma (IFNG) (+874) T/A genotypes in 170 Caucasian HCV patients treated by IFN-alpha. |
| 63 | 21161299 | We retrospectively studied distribution of IFN-gamma (IFNG) (+874) T/A genotypes in 170 Caucasian HCV patients treated by IFN-alpha. |
| 64 | 21161299 | We retrospectively studied distribution of IFN-gamma (IFNG) (+874) T/A genotypes in 170 Caucasian HCV patients treated by IFN-alpha. |
| 65 | 21161299 | Assessment of IFNG (+874) genotypes might help to identify patients-at-risk for IFN-alpha-induced depression. |
| 66 | 21161299 | Assessment of IFNG (+874) genotypes might help to identify patients-at-risk for IFN-alpha-induced depression. |
| 67 | 21161299 | Assessment of IFNG (+874) genotypes might help to identify patients-at-risk for IFN-alpha-induced depression. |
| 68 | 21161299 | Assessment of IFNG (+874) genotypes might help to identify patients-at-risk for IFN-alpha-induced depression. |
| 69 | 21161299 | Assessment of IFNG (+874) genotypes might help to identify patients-at-risk for IFN-alpha-induced depression. |
| 70 | 21161299 | IFNG and IFN-alpha transcriptionally induce indoleamine-2,3-dioxygenase (IDO), the rate-limiting enzyme of the kynurenine (KYN) pathway of tryptophan (TRY) metabolism. |
| 71 | 21161299 | IFNG and IFN-alpha transcriptionally induce indoleamine-2,3-dioxygenase (IDO), the rate-limiting enzyme of the kynurenine (KYN) pathway of tryptophan (TRY) metabolism. |
| 72 | 21161299 | IFNG and IFN-alpha transcriptionally induce indoleamine-2,3-dioxygenase (IDO), the rate-limiting enzyme of the kynurenine (KYN) pathway of tryptophan (TRY) metabolism. |
| 73 | 21161299 | IFNG and IFN-alpha transcriptionally induce indoleamine-2,3-dioxygenase (IDO), the rate-limiting enzyme of the kynurenine (KYN) pathway of tryptophan (TRY) metabolism. |
| 74 | 21161299 | IFNG and IFN-alpha transcriptionally induce indoleamine-2,3-dioxygenase (IDO), the rate-limiting enzyme of the kynurenine (KYN) pathway of tryptophan (TRY) metabolism. |
| 75 | 20811799 | IFNG-inducible KYN/pteridines inflammation cascade is characterized by up-regulation of nitric oxide synthase (NOS) activity (induced by KYN) and decreased formation of NOS cofactor, BH4, that results in uncoupling of NOS that shifting arginine from NO to superoxide anion production. |
| 76 | 20811799 | IFNG-induced up-regulation of indoleamine 2,3-dioxygenase (IDO), rate-limiting enzyme of TRY-KYN pathway, decreases TRY conversion into serotonin (substrate of antidepressant effect) and increases production of KYN associated with diabetes [xanthurenic acid (XA)], anxiety (KYN), psychoses and cognitive impairment (kynurenic acid). |
| 77 | 20811799 | In addition to literature data on KYN/TRY ratio (IDO activity index), we observe neopterin levels (index of activity of rate-limiting enzyme of guanine-BH4 pathway) to be higher in carriers of high (T) than of low (A) producers alleles; and to correlate with AAMPD markers (e.g., insulin resistance, body mass index, mortality risk), and with IFN-alpha-induced depression in hepatitis C patients. |
| 78 | 20304822 | Activating transcription factor 3 is a positive regulator of human IFNG gene expression. |
| 79 | 20304822 | Activating transcription factor 3 is a positive regulator of human IFNG gene expression. |
| 80 | 20304822 | Activating transcription factor 3 is a positive regulator of human IFNG gene expression. |
| 81 | 20304822 | IL-12 and IL-18 are essential for Th1 differentiation, whereas the role of IFN-alpha in Th1 development is less understood. |
| 82 | 20304822 | IL-12 and IL-18 are essential for Th1 differentiation, whereas the role of IFN-alpha in Th1 development is less understood. |
| 83 | 20304822 | IL-12 and IL-18 are essential for Th1 differentiation, whereas the role of IFN-alpha in Th1 development is less understood. |
| 84 | 20304822 | In this microarray-based study, we searched for genes that are regulated by IFN-alpha, IL-12, or the combination of IL-12 plus IL-18 during the early differentiation of human umbilical cord blood CD4(+) Th cells. |
| 85 | 20304822 | In this microarray-based study, we searched for genes that are regulated by IFN-alpha, IL-12, or the combination of IL-12 plus IL-18 during the early differentiation of human umbilical cord blood CD4(+) Th cells. |
| 86 | 20304822 | In this microarray-based study, we searched for genes that are regulated by IFN-alpha, IL-12, or the combination of IL-12 plus IL-18 during the early differentiation of human umbilical cord blood CD4(+) Th cells. |
| 87 | 20304822 | Twenty-six genes were similarly regulated in response to treatment with IL-12, IFN-alpha, or the combination of IL-12 plus IL-18. |
| 88 | 20304822 | Twenty-six genes were similarly regulated in response to treatment with IL-12, IFN-alpha, or the combination of IL-12 plus IL-18. |
| 89 | 20304822 | Twenty-six genes were similarly regulated in response to treatment with IL-12, IFN-alpha, or the combination of IL-12 plus IL-18. |
| 90 | 20304822 | Ectopic expression of ATF3 in CD4(+) T cells enhanced the production of IFN-gamma, the hallmark cytokine of Th1 cells, whereas small interfering RNA knockdown of ATF3 reduced IFN-gamma production. |
| 91 | 20304822 | Ectopic expression of ATF3 in CD4(+) T cells enhanced the production of IFN-gamma, the hallmark cytokine of Th1 cells, whereas small interfering RNA knockdown of ATF3 reduced IFN-gamma production. |
| 92 | 20304822 | Ectopic expression of ATF3 in CD4(+) T cells enhanced the production of IFN-gamma, the hallmark cytokine of Th1 cells, whereas small interfering RNA knockdown of ATF3 reduced IFN-gamma production. |
| 93 | 20304822 | Furthermore, ATF3 formed an endogenous complex with JUN in CD4(+) T cells induced to Th1. |
| 94 | 20304822 | Furthermore, ATF3 formed an endogenous complex with JUN in CD4(+) T cells induced to Th1. |
| 95 | 20304822 | Furthermore, ATF3 formed an endogenous complex with JUN in CD4(+) T cells induced to Th1. |
| 96 | 20304822 | Chromatin immunoprecipitation and luciferase reporter assays showed that both ATF3 and JUN are recruited to and transactivate the IFNG promoter during early Th1 differentiation. |
| 97 | 20304822 | Chromatin immunoprecipitation and luciferase reporter assays showed that both ATF3 and JUN are recruited to and transactivate the IFNG promoter during early Th1 differentiation. |
| 98 | 20304822 | Chromatin immunoprecipitation and luciferase reporter assays showed that both ATF3 and JUN are recruited to and transactivate the IFNG promoter during early Th1 differentiation. |
| 99 | 16934001 | The previously reported L706S, like the novel Q463H and E320Q alleles, are intrinsically deleterious for both interferon gamma (IFNG)-induced gamma-activating factor-mediated immunity and interferon alpha (IFNA)-induced interferon-stimulated genes factor 3-mediated immunity, as shown in STAT1-deficient cells transfected with the corresponding alleles. |
| 100 | 16934001 | The previously reported L706S, like the novel Q463H and E320Q alleles, are intrinsically deleterious for both interferon gamma (IFNG)-induced gamma-activating factor-mediated immunity and interferon alpha (IFNA)-induced interferon-stimulated genes factor 3-mediated immunity, as shown in STAT1-deficient cells transfected with the corresponding alleles. |
| 101 | 16934001 | The previously reported L706S, like the novel Q463H and E320Q alleles, are intrinsically deleterious for both interferon gamma (IFNG)-induced gamma-activating factor-mediated immunity and interferon alpha (IFNA)-induced interferon-stimulated genes factor 3-mediated immunity, as shown in STAT1-deficient cells transfected with the corresponding alleles. |
| 102 | 16934001 | Indeed, IFNA-induced interferon-stimulated genes factor 3-mediated immunity is not affected, and these patients are not particularly susceptible to viral disease, unlike patients homozygous for other, equally deleterious STAT1 mutations recessive for both phenotypes. |
| 103 | 16934001 | Indeed, IFNA-induced interferon-stimulated genes factor 3-mediated immunity is not affected, and these patients are not particularly susceptible to viral disease, unlike patients homozygous for other, equally deleterious STAT1 mutations recessive for both phenotypes. |
| 104 | 16934001 | Indeed, IFNA-induced interferon-stimulated genes factor 3-mediated immunity is not affected, and these patients are not particularly susceptible to viral disease, unlike patients homozygous for other, equally deleterious STAT1 mutations recessive for both phenotypes. |
| 105 | 16934001 | The three STAT1 alleles are therefore dominant for IFNG-mediated antimycobacterial immunity but recessive for IFNA-mediated antiviral immunity at the cellular and clinical levels. |
| 106 | 16934001 | The three STAT1 alleles are therefore dominant for IFNG-mediated antimycobacterial immunity but recessive for IFNA-mediated antiviral immunity at the cellular and clinical levels. |
| 107 | 16934001 | The three STAT1 alleles are therefore dominant for IFNG-mediated antimycobacterial immunity but recessive for IFNA-mediated antiviral immunity at the cellular and clinical levels. |
| 108 | 15661146 | The most noteworthy changes in gene expression mainly affected the transcriptional network regulated by interferons (IFNs), including both IFN-alpha/beta-inducible genes (STAT1, STAT2, ISGF3G/IRF9, IFI27, G1P3, G1P2, OAS2, MX1) and IFN-gamma-inducible genes (CXCL9, CXCL10, CXCL11). |
| 109 | 15661146 | The most noteworthy changes in gene expression mainly affected the transcriptional network regulated by interferons (IFNs), including both IFN-alpha/beta-inducible genes (STAT1, STAT2, ISGF3G/IRF9, IFI27, G1P3, G1P2, OAS2, MX1) and IFN-gamma-inducible genes (CXCL9, CXCL10, CXCL11). |
| 110 | 15661146 | The most noteworthy changes in gene expression mainly affected the transcriptional network regulated by interferons (IFNs), including both IFN-alpha/beta-inducible genes (STAT1, STAT2, ISGF3G/IRF9, IFI27, G1P3, G1P2, OAS2, MX1) and IFN-gamma-inducible genes (CXCL9, CXCL10, CXCL11). |
| 111 | 15661146 | Interesting, upregulation of IFN-alpha/beta-inducible genes (but not IFN-gamma-inducible genes) was independent of histological scores (grade and stage of fibrosis) and HCV characteristics (hepatic HCV mRNA levels and the HCV genotype), and was specific to HCV (as compared to hepatitis B virus (HBV)). |
| 112 | 15661146 | Interesting, upregulation of IFN-alpha/beta-inducible genes (but not IFN-gamma-inducible genes) was independent of histological scores (grade and stage of fibrosis) and HCV characteristics (hepatic HCV mRNA levels and the HCV genotype), and was specific to HCV (as compared to hepatitis B virus (HBV)). |
| 113 | 15661146 | Interesting, upregulation of IFN-alpha/beta-inducible genes (but not IFN-gamma-inducible genes) was independent of histological scores (grade and stage of fibrosis) and HCV characteristics (hepatic HCV mRNA levels and the HCV genotype), and was specific to HCV (as compared to hepatitis B virus (HBV)). |
| 114 | 15661146 | Other genes dysregulated in F1-CH-C, albeit less markedly than IFN-alpha/beta- and IFN-gamma-inducible genes, were mainly involved in the activation of lymphocytes infiltrating the liver (IFNG, TNF, CXCL6, IL6, CCL8, CXCR3, CXCR4, CCR2), cell proliferation (p16/CDKN2A, MKI67, p14/ARF), extracellular matrix remodeling (MMP9, ITGA2), lymphangiogenesis (XLKD1/LYVE), oxidative stress (CYP2E1), and cytoskeleton microtubule organization (STMN2/SCG10). |
| 115 | 15661146 | Other genes dysregulated in F1-CH-C, albeit less markedly than IFN-alpha/beta- and IFN-gamma-inducible genes, were mainly involved in the activation of lymphocytes infiltrating the liver (IFNG, TNF, CXCL6, IL6, CCL8, CXCR3, CXCR4, CCR2), cell proliferation (p16/CDKN2A, MKI67, p14/ARF), extracellular matrix remodeling (MMP9, ITGA2), lymphangiogenesis (XLKD1/LYVE), oxidative stress (CYP2E1), and cytoskeleton microtubule organization (STMN2/SCG10). |
| 116 | 15661146 | Other genes dysregulated in F1-CH-C, albeit less markedly than IFN-alpha/beta- and IFN-gamma-inducible genes, were mainly involved in the activation of lymphocytes infiltrating the liver (IFNG, TNF, CXCL6, IL6, CCL8, CXCR3, CXCR4, CCR2), cell proliferation (p16/CDKN2A, MKI67, p14/ARF), extracellular matrix remodeling (MMP9, ITGA2), lymphangiogenesis (XLKD1/LYVE), oxidative stress (CYP2E1), and cytoskeleton microtubule organization (STMN2/SCG10). |
| 117 | 15187113 | We hypothesized that IL-12 pretreatments would result in endogenous IFN-gamma production, and that this, in turn, would up-regulate levels of Janus kinase-STAT signaling intermediates and lead to increased expression of genes regulated by IFN-alpha. |
| 118 | 15187113 | We hypothesized that IL-12 pretreatments would result in endogenous IFN-gamma production, and that this, in turn, would up-regulate levels of Janus kinase-STAT signaling intermediates and lead to increased expression of genes regulated by IFN-alpha. |
| 119 | 15187113 | We hypothesized that IL-12 pretreatments would result in endogenous IFN-gamma production, and that this, in turn, would up-regulate levels of Janus kinase-STAT signaling intermediates and lead to increased expression of genes regulated by IFN-alpha. |
| 120 | 15187113 | We hypothesized that IL-12 pretreatments would result in endogenous IFN-gamma production, and that this, in turn, would up-regulate levels of Janus kinase-STAT signaling intermediates and lead to increased expression of genes regulated by IFN-alpha. |
| 121 | 15187113 | We hypothesized that IL-12 pretreatments would result in endogenous IFN-gamma production, and that this, in turn, would up-regulate levels of Janus kinase-STAT signaling intermediates and lead to increased expression of genes regulated by IFN-alpha. |
| 122 | 15187113 | We hypothesized that IL-12 pretreatments would result in endogenous IFN-gamma production, and that this, in turn, would up-regulate levels of Janus kinase-STAT signaling intermediates and lead to increased expression of genes regulated by IFN-alpha. |
| 123 | 15187113 | Pretreatment of PBMCs and tumor cells with IFN-gamma-containing supernatants from IL-12-stimulated PBMCs led to up-regulation of STAT1, STAT2, and IFN regulatory factor 9 (IRF9) and potentiated IFN-alpha-induced STAT signaling within PBMCs and tumor cells. |
| 124 | 15187113 | Pretreatment of PBMCs and tumor cells with IFN-gamma-containing supernatants from IL-12-stimulated PBMCs led to up-regulation of STAT1, STAT2, and IFN regulatory factor 9 (IRF9) and potentiated IFN-alpha-induced STAT signaling within PBMCs and tumor cells. |
| 125 | 15187113 | Pretreatment of PBMCs and tumor cells with IFN-gamma-containing supernatants from IL-12-stimulated PBMCs led to up-regulation of STAT1, STAT2, and IFN regulatory factor 9 (IRF9) and potentiated IFN-alpha-induced STAT signaling within PBMCs and tumor cells. |
| 126 | 15187113 | Pretreatment of PBMCs and tumor cells with IFN-gamma-containing supernatants from IL-12-stimulated PBMCs led to up-regulation of STAT1, STAT2, and IFN regulatory factor 9 (IRF9) and potentiated IFN-alpha-induced STAT signaling within PBMCs and tumor cells. |
| 127 | 15187113 | Pretreatment of PBMCs and tumor cells with IFN-gamma-containing supernatants from IL-12-stimulated PBMCs led to up-regulation of STAT1, STAT2, and IFN regulatory factor 9 (IRF9) and potentiated IFN-alpha-induced STAT signaling within PBMCs and tumor cells. |
| 128 | 15187113 | Pretreatment of PBMCs and tumor cells with IFN-gamma-containing supernatants from IL-12-stimulated PBMCs led to up-regulation of STAT1, STAT2, and IFN regulatory factor 9 (IRF9) and potentiated IFN-alpha-induced STAT signaling within PBMCs and tumor cells. |
| 129 | 15187113 | Pretreatment of HT144 melanoma cells and PBMCs with IFN-gamma or IFN-gamma-containing supernatants enhanced the actions of IFN-alpha at the transcriptional level, as measured by real-time RT PCR analysis of the IFN-stimulated gene 15. |
| 130 | 15187113 | Pretreatment of HT144 melanoma cells and PBMCs with IFN-gamma or IFN-gamma-containing supernatants enhanced the actions of IFN-alpha at the transcriptional level, as measured by real-time RT PCR analysis of the IFN-stimulated gene 15. |
| 131 | 15187113 | Pretreatment of HT144 melanoma cells and PBMCs with IFN-gamma or IFN-gamma-containing supernatants enhanced the actions of IFN-alpha at the transcriptional level, as measured by real-time RT PCR analysis of the IFN-stimulated gene 15. |
| 132 | 15187113 | Pretreatment of HT144 melanoma cells and PBMCs with IFN-gamma or IFN-gamma-containing supernatants enhanced the actions of IFN-alpha at the transcriptional level, as measured by real-time RT PCR analysis of the IFN-stimulated gene 15. |
| 133 | 15187113 | Pretreatment of HT144 melanoma cells and PBMCs with IFN-gamma or IFN-gamma-containing supernatants enhanced the actions of IFN-alpha at the transcriptional level, as measured by real-time RT PCR analysis of the IFN-stimulated gene 15. |
| 134 | 15187113 | Pretreatment of HT144 melanoma cells and PBMCs with IFN-gamma or IFN-gamma-containing supernatants enhanced the actions of IFN-alpha at the transcriptional level, as measured by real-time RT PCR analysis of the IFN-stimulated gene 15. |
| 135 | 15187113 | Experiments in wild-type C57BL/6 and IFN-gamma receptor knockout (B6.129S7-Ifngr(tm1Agt)) mice demonstrated that a regimen of IL-12 pretreatment, followed by IFN-alpha, could cure mice of i.p. |
| 136 | 15187113 | Experiments in wild-type C57BL/6 and IFN-gamma receptor knockout (B6.129S7-Ifngr(tm1Agt)) mice demonstrated that a regimen of IL-12 pretreatment, followed by IFN-alpha, could cure mice of i.p. |
| 137 | 15187113 | Experiments in wild-type C57BL/6 and IFN-gamma receptor knockout (B6.129S7-Ifngr(tm1Agt)) mice demonstrated that a regimen of IL-12 pretreatment, followed by IFN-alpha, could cure mice of i.p. |
| 138 | 15187113 | Experiments in wild-type C57BL/6 and IFN-gamma receptor knockout (B6.129S7-Ifngr(tm1Agt)) mice demonstrated that a regimen of IL-12 pretreatment, followed by IFN-alpha, could cure mice of i.p. |
| 139 | 15187113 | Experiments in wild-type C57BL/6 and IFN-gamma receptor knockout (B6.129S7-Ifngr(tm1Agt)) mice demonstrated that a regimen of IL-12 pretreatment, followed by IFN-alpha, could cure mice of i.p. |
| 140 | 15187113 | Experiments in wild-type C57BL/6 and IFN-gamma receptor knockout (B6.129S7-Ifngr(tm1Agt)) mice demonstrated that a regimen of IL-12 pretreatment, followed by IFN-alpha, could cure mice of i.p. |
| 141 | 15187113 | However, this treatment regimen did not significantly prolong the survival of IFN-gamma-deficient (B6.129S7-Ifng(tm1Ts)) mice compared with mice treated with IFN-alpha alone. |
| 142 | 15187113 | However, this treatment regimen did not significantly prolong the survival of IFN-gamma-deficient (B6.129S7-Ifng(tm1Ts)) mice compared with mice treated with IFN-alpha alone. |
| 143 | 15187113 | However, this treatment regimen did not significantly prolong the survival of IFN-gamma-deficient (B6.129S7-Ifng(tm1Ts)) mice compared with mice treated with IFN-alpha alone. |
| 144 | 15187113 | However, this treatment regimen did not significantly prolong the survival of IFN-gamma-deficient (B6.129S7-Ifng(tm1Ts)) mice compared with mice treated with IFN-alpha alone. |
| 145 | 15187113 | However, this treatment regimen did not significantly prolong the survival of IFN-gamma-deficient (B6.129S7-Ifng(tm1Ts)) mice compared with mice treated with IFN-alpha alone. |
| 146 | 15187113 | However, this treatment regimen did not significantly prolong the survival of IFN-gamma-deficient (B6.129S7-Ifng(tm1Ts)) mice compared with mice treated with IFN-alpha alone. |
| 147 | 15187113 | These results suggest that the response to IFN-alpha immunotherapy can be significantly enhanced by IL-12 pretreatment, and this effect is dependent upon endogenous IFN-gamma production and its actions on melanoma cells. |
| 148 | 15187113 | These results suggest that the response to IFN-alpha immunotherapy can be significantly enhanced by IL-12 pretreatment, and this effect is dependent upon endogenous IFN-gamma production and its actions on melanoma cells. |
| 149 | 15187113 | These results suggest that the response to IFN-alpha immunotherapy can be significantly enhanced by IL-12 pretreatment, and this effect is dependent upon endogenous IFN-gamma production and its actions on melanoma cells. |
| 150 | 15187113 | These results suggest that the response to IFN-alpha immunotherapy can be significantly enhanced by IL-12 pretreatment, and this effect is dependent upon endogenous IFN-gamma production and its actions on melanoma cells. |
| 151 | 15187113 | These results suggest that the response to IFN-alpha immunotherapy can be significantly enhanced by IL-12 pretreatment, and this effect is dependent upon endogenous IFN-gamma production and its actions on melanoma cells. |
| 152 | 15187113 | These results suggest that the response to IFN-alpha immunotherapy can be significantly enhanced by IL-12 pretreatment, and this effect is dependent upon endogenous IFN-gamma production and its actions on melanoma cells. |
| 153 | 15004750 | To identify a key genetic factor in the pathogenesis of sarcoidosis, we investigated single nucleotide polymorphisms within 10 candidate genes involved in type 1 immune process ( IFNA17, IFNB, IFNG, IFNGR1, IFNGR2, IL12B, IL12RB1, IL12RB2, ETA-1, and NRAMP1) in an association-based study of 102 Japanese patients with sarcoidosis, 114 with tuberculosis, and 110 control subjects. |
| 154 | 15004750 | We further typed another IFNA polymorphism ( IFNA10 60T-->A) and confirmed two major haplotypes of the IFNA gene, viz., allele 1: IFNA10 [60T]- IFNA17 [551T] and allele 2: IFNA10 [60A]- IFNA17 [551G], in the Japanese population. |