Publication for STAT1 and ISG15

Species	Symbol	Function*	Entrez Gene ID*	Other ID	Gene coexpression	CoexViewer
hsa	STAT1	signal transducer and activator of transcription 1	6772			[link]
hsa	ISG15	ISG15 ubiquitin like modifier	9636

Pubmed ID	Priority	Text
29040650	0.98	STAT1 (e), ISG15 (f), and USP18 (g) gene expression.
	0.98	STAT1, ISG15, and USP18 mRNA Gene Expression, and IL-6 Protein
	0.98	STAT1 (fold change [fc]=2.7 and 3.1, respectively), ISG15 (fc=2.1 and 3.3), and USP18 (fc=2.1 and 3.4) (Figure 1e-g).
	0.98	STAT1 is involved also in the downstream mechanisms by which ISG15, USP18, and IL-6, respectively, reduce neurogenesis and increase apoptosis.
	0.98	ISG15, and All Proteins Increase UBA7, UBE2L6, and HERC5 Gene Expression via Activation of STAT1 Protein
	0.98	ISG15 was able to induce UBA7, UBE2L6, and HERC5, and whether such effect was mediated by further downstream STAT1 activation.
	0.98	STAT1-mediated upregulation of UBA7, UBE2L6, and HERC5 is a downstream mechanism involved in the ISG15-dependent pathway by which IFN-alpha reduces neurogenesis.
	0.97	ISG15, USP18, STAT1, IRF7, UBA7, UBE2L6, and HERC5) (supplementary Table 5), and found a very high correlation between the fold-changes detected by Affymetrix and those detected by qPCR (r=0.99; supplementary Figure 2b).
	0.96	ISG15, USP18, and IL-6 (Figure 4e-g), thus indicating that STAT1 activation is required for the IFN-alpha-induced upregulation of these 3 molecules.
	0.96	STAT1 Inhibitor Prevents the Effect of ISG15 on Neurogenesis and of IL-6 on Apoptosis
	0.96	ISG15, but not USP18 and IL-6, induces UBA7, UBE2L6, and HERC5 genes via further downstream activation of STAT1 (see supplementary Figure 4 for a summary of the findings).
	0.95	STAT1, ISG15, USP18, and IL-6.
	0.95	STAT1, ISG15, USP18, and IL-6 as potentially relevant mechanisms, we next investigated if and how these mechanisms were inter-connected.
	0.95	signal transducer and activator of transcription-1 (STAT1) inhibitor reverts the effects of interferon (IFN)-alpha on neurogenesis and apoptosis by preventing the upregulation of interferon-stimulated gene 15 (ISG15), ubiquitin-specific peptidase 18 (USP18), and interleukin (IL)-6.
	0.95	signal transducer and activator of transcription-1 (STAT1) inhibitor prevents the effect of interferon-stimulated gene 15 (ISG15) on neurogenesis and of interleukin (IL)-6 on apoptosis.
	0.94	STAT1 Inhibitor Reverts the Effects of IFN-alpha on Neurogenesis and Apoptosis by Preventing the Upregulation of ISG15, USP18, and IL-6
	0.94	ISG15-dependent STAT1 activation, we decided to investigate which downstream mechanisms STAT1 can modulate once induced by ISG15.
	0.94	ISG15 and USP18, via STAT1-dependent mechanisms, and that either of these molecules alone can induce the same reduction in neurogenesis induced by IFN-alpha.
	0.94	STAT1-mediated upregulation of UBA7, UBE2L6, and HERC5 as a potential mechanism in the ISG15-dependent reduction in neurogenesis by IFN-alpha.
	0.86	ISG15, USP18, and IL-6, via STAT1-dependent mechanisms and that those molecules are ultimately responsible for the effects seen upon in vitro treatment with IFN-alpha.
	0.86	STAT1, ISG15, USP18, and IL-6 in these cells and investigate whether these proteins are mechanistically involved in the effects of IFN-alpha.
	0.84	ISG15 and IL-6 on, respectively, neurogenesis and apoptosis are also mediated by further STAT1 activation, while the effects of USP18 on neurogenesis are mediated by a different mechanism (see supplementary Figure 4 for a summary of the findings).
	0.81	ISG15), ubiquitin-specific peptidase 18 (USP18), and interleukin-6 (IL-6) via activation of STAT1.
	0.79	ISG15, USP18, and IL-6 was able to reduce neurogenesis and enhance apoptosis via further downstream activation of STAT1.
	0.56	ISG15 and USP18 via STAT1, and that, in turn, each of these 2 proteins alone can mimic the effects of IFN-alpha on neurogenesis.
26022350	0.98	ISG15, STAT1, TAP1 and HLA-C, which were positively regulated upon KSR1 overexpression in the presence of genotoxic agents, with longer relapse free survival in patients who underwent chemotherapy (Fig. 5b).
	0.98	ISG15 and STAT1.
	0.97	ISG15, STAT1, TAP1, MX1 and HLA-C gene expressions from TCGA dataset.
	0.96	STAT1, ISG15 and TAP1 that are positively associated with KSR1 expression in patient samples.
	0.94	STAT1, ISG15 and TAP1 are also found to be positively associated with KSR1 expression in patient samples.
	0.94	ISG15, STAT1, TAP1, MX1 and HLA-C in the case of genotoxic agents.
	0.92	ISG15, STAT1, TAP1, MX1 and HLA-C and their relevance in chemotherapy response, we carried out a series of analyses using extensive data from breast cancer patients.
	0.87	STAT1, ISG15, TAP1 and HLA-C with relapse free survival (RFS) in breast cancer patients who underwent systematic chemotherapy
	0.85	ISG15, STAT1, TAP1, MX1 and HLA-C, were up-regulated upon KSR1 overexpression in the presence of genotoxic agents.
	0.84	ISG15, STAT1, TAP1, MX1 and HLA-C (Tables 1, 2).
	0.84	ISG15, STAT1, TAP1 and HLA-C, are correlated with better outcome in patients who underwent chemotherapy.
	0.80	ISG15, STAT1, TAP1, MX1 and HLA-C on relapse free survival (RFS) in breast cancer patients who received chemotherapy was analysed.
	0.79	ISG15, STAT1, TAP1, MX1 and HLA-C was also seen in the tumour samples from the TCGA database.
	0.70	ISG15 and STAT1 upon chemotherapeutic drugs and supports their role as responsive markers.
24726362	0.98	STAT1 and ISG15 activation.
	0.98	STAT1-ISG15 signaling cascade
	0.96	STAT1-ISG15 signaling axis
	0.96	STAT1 and ISG15.
	0.96	STAT1 or ISG15 activation.
	0.95	STAT1-ISG15 signaling axis.
	0.95	STAT1 and ISG15, and TNBC cell lines are sensitive to STAT1 depletion.
	0.94	STAT1 depletion also expressed the highest level of ISG15 among the TNBC cell lines assayed (Figure S5A).
	0.94	STAT1 and ISG15 can inhibit proliferation of TNBC cell lines and also demonstrate that other deregulated pathways in addition to ARF/p53 are likely capable of inducing ISG expression.
	0.93	ISG15/STAT1 (TNBC-2).
	0.92	STAT1 and ISG15 (Figures 7A and 7B).
	0.81	ISG15 expression in dp53R-shARF MEFs is dependent upon STAT1 (Figure 5D), so we hypothesized ISG15 might represent one of the pro-tumorigenic targets activated downstream of STAT1.
23237992	0.98	ISG15, PKR and STAT1, induced by the JAK/STAT pathway play a role in the anti-viral responses of IFN-alpha.
	0.98	ISG15, PKR and STAT1 mRNA expression by RT-qPCR.
	0.98	ISG15 (Figure 4C), PKR (Figure 4B), and STAT1 (Figure 4D) from 15.2 fold to 7.7 fold, from 44.7 to 26.7 fold, from 8.3 to 5.8 fold, from 4.9 fold to 3.9 fold, respectively.
	0.98	ISG15, PKR and STAT1 and found that these IFN-induced ISGs were also inhibited by SOCS1 overexpression in both Huh7.5.1 and OR6 cells.
	0.98	ISG15 (B), PKR (C) or STAT1 (D) were determined by quantitative real time PCR normalized beta-actin.
	0.97	ISG15 (Figure 5B), PKR (Figure 5C) and STAT1 (Figure 5D) by from 9.1 fold to 6.2 fold, from 43.6 to 31.4 fold, from 9.9 to 5.6 fold, from 8.2 fold to 5.1 fold, respectively.
	0.97	ISG15, PKR and STAT1 mRNA and protein levels in OR6 cells
	0.97	ISG15, PKR and STAT1 mRNA and protein levels in JFH1 infected Huh7.5.1 cells
	0.72	ISG15, PKR and STAT1 mRNA and protein levels
	0.50	ISG15 (B), PKR (C) or STAT1 (D) were determined by quantitative real time PCR normalized to beta-actin.
21147189	0.98	STAT1, MxA and ISG15) by IL28B was reduced by IL10R2 antibody.
	0.98	STAT1, MxA and ISG15) by IL28B was also reduced by silencing of IL28R1, indicating that the downstream JAK-STAT pathway was inhibited.
	0.98	STAT1, the induction of STAT1 and MxA by IL28B was reduced; however, ISG15 protein levels remained similar to that of control siRNA (Fig. 6A and D).
	0.98	STAT1, MxA, and ISG15 by IL28B was reduced (Fig. 6B, C, E and F).
	0.97	ISG15, MxA, OAS1, PKR, and STAT1 stimulated by IL28A, IL28B or IL29 are similar.
	0.97	STAT1, MxA and ISG15) by IL28B was reduced and HCV core protein levels inhibited by IL28B were rescued by JAK inhibitor I. These data indicate that Jak1 and Tyk2 are required for IL28B's antiviral effect.
	0.97	STAT1, MxA and ISG15 was measured to reflect the activation of the JAK-STAT pathway.
	0.92	ISG15, MxA, OAS1, PKR, and STAT1 in a time dependent manner, while mock treatment failed to induce the expression of ISGs (Fig. 3A).
29580840	0.98	STAT1 and STAT3 and ISG induction were starkly reduced, with removal of Vif (IIIBDeltaVif), partially restoring pSTATs, ISG15 and MxB induction.
	0.98	STAT1 and STAT3 protein levels and ISG15 induction in a Vif-dependent manner and only infectivity of IIIBDeltaVif is sensitive to IFN-alpha.
	0.98	STAT1 and STAT3 Protein Levels, Impaired IFN-alpha-Mediated Phosphorylation and Reduced ISG15 Induction
	0.96	STAT1 and STAT3 protein expression and IFN-alpha-induced ISG15, we wondered if HIV infection also reduced expression of phosphorylated STAT1 and STAT3 in primary human immune cells.
	0.96	STAT1 and STAT3 expression, it was no surprise to observe that IFN-alpha induction of ISG15 was significantly reduced.
	0.91	STAT1 and STAT3 protein levels, IFN-alpha-induced STAT activation and lower levels of ISG15 induction.
	0.73	STAT1 and STAT3 phosphorylation and ISG induction, while removal of Vif in IIIBDeltaVif-infected PBMCs partially restores induction of pSTAT1, pSTAT3, ISG15 and MxB, but not MxA.
19551150	0.98	ISG15 expression (Fig. 2), also exhibited normal kinetics of STAT1 phosphorylation, as expected (Fig. S1).
	0.97	STAT1, STAT2 and IRF9) to a DNA probe containing the ISRE of the ISG15 promoter indicated that IFN-alpha-induced binding to the probe was equivalent within extracts of EBV-negative (A.2) and EBV-positive (A.15) Akata cells for at least 4 h following addition of IFN-alpha.
	0.86	STAT1 correlates with sustained ISG15 expression following IFN treatment.
	0.85	ISG15ylated proteins, however, is not required for the inhibition of STAT1 phosphorylation, which appears to be mediated instead through direct inhibition by UBP43 of the interaction of JAK1 with the type I IFN receptor.
27716962	0.98	STAT1 posttranslational modification (ISGylation) by de-conjugation of a small ubiquitin-like protein, ISG15 that is increased in response to IFNalpha treatment.
	0.97	ISG15 (or isotype-specific antibody) followed by immunoblotting with anti-STAT-1.
	0.96	STAT1 by an ISG15-specific protease, USP18.
	0.93	STAT1 (protein conjugation of a small ubiquitin-like modifier, ISG15, Western blot), which preserves STAT1 activation.
24260178	0.98	STAT1-57 gene expression program in KCs, the neutrophil chemoattractant property of ISG15 suggests another mechanism by which STAT1-57 activation may become self-sustaining and chronic (Figure 8).
	0.52	STAT1-57 genes, there was strong overrepresentation of genes involved in response to virus (e.g., DDX58, DDX60, EIF2AK2, HERC5, IFI35, IFI44, IFI44L, IFIT1, IFITM1, IRF9, ISG15, MX1, MX2, OAS2, OAS3, PLSCR1, STAT1 and TRIM22; P = 8.4x10-16).
25620967	0.98	STAT1, IRF9, ISG15, BST2, and several members of the GBP, OAS, and IFI families were upregulated with a very high statistical significance (B > 7).
	0.92	ISG15 or lncISG15 expression was observed with a milder inhibition of STAT1 or inhibition of IRF1 using RNA interference (data not shown).
27427993	0.98	ISG15, the enzymes responsible for its conjugation, and cellular target proteins such as DDX58, IRF3, PKR, and STAT1 are strongly induced by treatment of type I IFNs or viral infection.
	0.85	Isg15, and Stat1, was significantly increased in ISGylation-deficient Ube1l-/- MEFs (Fig 1C); the same was observed for Ifnb1.
29769653	0.98	signal transducer and activator of transcription 1 (STAT1) and STAT2 and forms the interferon-stimulated gene factor 3 (ISGF3) complex, which recognizes the interferon-sensitive response element (ISRE) promoters of ISG15 and its conjugation enzymes to induce their expression.
	0.93	STAT1-STAT2 (refs), to induce the expression of a subset of interferon-stimulated genes (ISGs), including ISG15 (ref.).
31434934	0.98	STAT1 and translocation in the nucleus of STAT phosphorylated dimers and finally activation of ISRE promotors and increase of transcription of corresponding genes (ex: ISG15, MxA, IFNbeta1 and Tyk2).
	0.96	ISG15, MxA, IFNbeta, Tyk2, Jak1 and Stat1 in IFNalpha-stimulated cells (Fig. S4A-F).
22590680	0.98	ISG15 substrates have been identified and many of them play important roles for type I IFN responses including JAK1, STAT1, RIG-I, Mx1, and PKR functions.
24787290	0.98	ISG15 to STAT1 and JAK1 and components of other signaling pathways (ERK1, phospholipase C, and heat shock proteins) suggest that regulation of ISG15 family molecules may have profound effects in the tumor microenvironment.
29176033	0.98	ISG15, PSMB9, TAP1, STAT1, three guanylate-binding proteins (GBP1, GBP4, and GBP5), and three 2'5'-oligoadenylate synthetases (OAS1, OAS2, and OAS3).
30283459	0.98	STAT1 targets; IFIT1, IFIT2, IFIT3, OAS1, OAS2, MX1, MX2, ISG15 as STAT1-STAT2 targets; SOCS3, CCND1, MMP3, FAS PIM1, VEGF, S1PR1 as STAT3 targets).
22629479	0.97	ISG15 protein expression at similar levels, along with similarly elevated levels of STAT1, including its phosphorylated form, and RIG-I protein.
	0.97	STAT1 (p-STAT1), STAT1 (STAT1), ISG15 (ISG15), RIG-I (RIG-I) and beta-actin (actin) proteins.
	0.97	ISG15 protein expression and STAT1 phosphorylation as expected (Figure 4B).
	0.96	STAT1 (p-STAT1), STAT1 (STAT1), ISG15 (ISG15), viral NP protein (NP), RIG-I (RIG-I), IRF3 (IRF3) and beta-actin (actin).
	0.69	STAT1 (p-STAT1), STAT1 protein (STAT1), ISG15 (ISG15), virus NP protein (NP) and human beta-actin (actin).
28129744	0.97	ISG15, ISG20, MX1 MX2, OASL, PTPN6, PSMB8, (Additional file 4: Figure S1)]; b) Type II IFN (IFN-gamma) signaling pathway [IRF9, PRKCD, EIF2AK2 (PKR), STAT1 (Fig. 4)]; c) IFN signaling related to inflammation [MICB, IRF9, ISG20, STAT1, TAP1, MX2, IFI44, PTPN6 (Fig. 3b)]; d) Cytokine related pathways (28 in total) (Fig. 3c) (IL-13 signaling (STAT1, PTPN6, STAT6, PRKCD] and IL-2 activation (NFKB2, HMGA1, PTPN6 and SYK, among others).
	0.96	STAT1/IRF9/ISG15 complex, variable colors = NF-kB (connected to several hubs).
	0.94	STAT1, with 18 interactions was found to be involved in the most number of pairings, followed by PRKCD, IRF9 and ISG15.
	0.88	STAT1, FCGR2B, PRKCD, PSMB9, PSMB8, PTPN6, MX1, MX2, IFIT1, TOMM34, IFIT3, SERPING1, NCF4, TAP1 and ISG15) in the VL-blood profile (representing TFs, receptors, kinases, proteases, phosphatases, enzymes and other general proteins) that are significantly "over-connected" with objects both within the VL-blood profile as well as the larger metabase (Table 2).
22634037	0.97	STAT1 expression, a component of the IFN signaling cascade, and induced expression of the cellular ISGs, Mx1 and ISG15 (Fig. 1).
30951861	0.96	STAT1, IRF1, B2M, ISG15, and MHC Class I molecules (Fig. 5B vs 5A and Supplementary Fig. 2).
	0.89	STAT1, I and EIF1, J) and proteins that are IFITM1/3 dependent (ISG15; G, HLA-B, L).
	0.89	ISG15 (Fig. 5), whilst the maintenance of STAT1 protein in response to IFNgamma involves by a different signalling mechanism that is IFITM1/3-independent (Fig. 9B).
	0.77	STAT1, B2M, and ISG15.
	0.76	STAT1 and B2M, some of the IFNgamma stimulated factors are IFITM1 dependent including MHC Class I molecules and ISG15 (Fig. 5G and L).
31861450	0.96	p-STAT1 (F) and the mRNA expression of ISG15, Viperin and IFITM1 (G) were detected according to the method described above.
24065129	0.95	STAT1 S708 phosphorylation by IKKe is essential for expression of the anti-viral genes IFIT2 and ADAR1, but not the related genes IFIT1, IFIT3, and ISG15 (G1P2).
	0.76	ISGF3-induced mRNAs and proteins, including IFI27 (ISG12), IFITM1 (LEU13), ISG15 (G1P2) and BST2, are upregulated in various types of cancers compared to normal tissues and in metastatic or recurrent cancers compared to the original lesions.
31781061	0.94	STAT1 signaling pathway requires Phosphorylated STAT1 (Tyr 701) enters the nucleus to activate interferon-stimulating factors ISGs (including MX1, MX2, PKR, OAS, ISG15, and ZAP).
	0.88	ISG15, and OASL, respectively, after targeting gene silencing STAT1.
20159032	0.94	ISG-15 gene, IRF9 binds the ISRE sequence and interacts with STAT1, which binds the neighbouring half GAS site (highlighted in bold in Table 3), thus stabilizing the complex.
25307056	0.93	ISG15-RFP or ISG15(DeltaGG)-RFP genes were used to transduce hTert-immortalized fibroblasts from C1, a STAT1-/- subject, P1, P2 and P3.
21994583	0.92	ISG15 target proteins have important roles in the IFN response, for example Jak1, STAT1, RIG-I, MxA, PKR and RNaseL. Consistent with its role in the IFN system, mice deficient in ISG15 have increased susceptibility to infection with several viruses.
30186768	0.92	STAT1, IFI44, IFIT3, OAS1, IFIT1, ISG15, MX1, and USP18, was also shown to predict poor outcomes in glioblastomas post RT.
25170834	0.91	ISG15 (3-fold), XAF1 (3-fold), OAS3 (3-fold), CCL8 (3-fold), OAS2 (3-fold), DDX58 (2.5-fold), STAT1 (2-fold), MX2 (2-fold), IRF7 (2-fold) and CCL2 (2-fold) were the most highly up-regulated genes, whereas THBS1 (3-fold), HLA-DQA (3-fold), TLR7 (2.6-fold), CD74 (2.5-fold), CXCL2 (2-fold), CCR2 (2-fold) and CXCL9 (2-fold) were the most highly down-regulated genes in Donor 2 (Table 1).
	0.91	STAT1, ISG15, ISG20, APOBEC3A, and TRAIL in MDMs.
	0.69	STAT1, IRF7, MX1, MX2, ISG15, ISG20, IFIT1, IFIT2, IFIT3, IFI27, IFI44L, APOBEC3A, DDX58 (RIG-I), TNFSF10 (TRAIL), and RSAD2 (viperin) were confirmed by real-time quantitative PCR and were consistent with the microarray data.
31288481	0.88	ISG15, IRF1, and STAT1 were measured by qPCR analysis.
19879619	0.87	Stat-1 was phosphorylated after IFNalpha treatment in cells infected with the ICP27- virus, ISG15 expression was not induced (Fig. 4, lane 6).
	0.84	Stat-1 phosphorylation and nuclear accumulation is ICP27-dependent, there is ICP27-independent inhibition of IFNalpha-induced ISG15 expression.
	0.80	Stat-1 and ISG15 expression were induced in mock-infected cells after treatment with IFNalpha (Fig. 4 lane 2).
	0.62	Stat-1 phosphorylation and no evidence of ISG15 expression (Fig. 4, lane 4).
22242177	0.86	ISG15 interaction and the STAT1-ISG15 interactions are discovered, which lends support to the role of USP18 as a modulator of STAT1 signaling.
	0.74	STAT1 -> ISG15 is a known protein-DNA interaction, and USP18 - ISG15 is a known protein-protein interaction).
	0.69	STAT1 signaling cascade, and indeed MX1, IFI44, ISG15, OAS1, and STAT1, which are predicted to be up-regulated with increased Interferon signaling, are shown to have significantly increased hazard ratios in the single gene analysis (Figure 1 and Table 1).
30177931	0.86	Isg15, Gbp1, Ifi30, Ifit2, Ifit3, Isg20, Atg7, Adrm1, and Stat1 (Figure 7).
	0.82	Isg15, Gbp1, Ifi30, Ifit2, Ifit3, Isg20, Atg7, Adrm1 and Stat1.
30837340	0.86	Stat1 activation and expression of Isg15.
22100648	0.80	STAT1 activation and cellular protein conjugation to ISG15.
16934001	0.79	ISG15 (the promoter of which was used for EMSA), MX1, and IRF1 (the promoter of which was used for EMSA) were induced following stimulation with IFNA and IFNG, as appropriate, in control cells, but not in cells from a patient lacking STAT1 (P5, homozygous for the 1928insA STAT1 allele, which encodes no detectable protein).
	0.60	ISG15, and MX1, and cDNAs from EBV-transformed B cells derived from a healthy control (C), three patients under study (P1, P2, P3), and a patient with recessive complete STAT1 deficiency (P5) homozygous for the 1928insA STAT1 mutation or from parental fibrosarcoma cell line (2C4) and STAT1-deficient U3C fibrosarcoma cell clones, untransfected (U3C) or stably cotransfected with a zeocin-resistance vector and a vector containing a mock, WT, E320Q, Q463H, or L706S STAT1 allele stimulated or not stimulated with 105 IU/ml of IFNG or IFNA for 1 h and 2 h for EBV-transformed B cells and fibroblasts, respectively, for IRF1, and for 6 h for both cellular types for ISG15 and MX1.
22573496	0.77	ISG15 are STAT1-dependent, we used STAT1 null EBV-B cells as a negative control and indeed, induction of these genes was not observed in these cells.
27867263	0.77	ISG15 could increase phosphorylation of JAK2, STAT1, and IRF-3, promoting type I IFN signaling pathway, our results also revealed an activated type I IFN signaling characterized by amplified expressions of some ISGs.
27626177	0.76	ISG15 targets many cellular proteins, including Janus kinase 1 (JAK1), STAT1 and ISGs via ISGlation, a process that can regulate HBV pathogenesis.
29502462	0.72	ISG15, NEMO, IRF8, and TYK2), and cellular responses to IFN-gamma (IFNGR1, IFNGR2, STAT1, IRF8 and CYBB).
18604270	0.68	ISG15 also targets proteins that play a role in the innate antiviral response, including: PKR, MXA, STAT1, JAK1 and RIG-I. ISGylation of these antiviral molecules may regulate their activity during viral infection.
28671669	0.52	ISG15 promoter that has multiple STAT1 binding sites (Figure 5D).