Publication for STAT1 and DDX58

Species	Symbol	Function*	Entrez Gene ID*	Other ID	Gene coexpression	CoexViewer
hsa	STAT1	signal transducer and activator of transcription 1	6772			[link]
hsa	DDX58	DExD/H-box helicase 58	23586

Pubmed ID	Priority	Text
32152220	0.98	RIG-I plays an important role in diminishing the interaction between SHP1 and STAT1, which is consistent with our results, and we also confirmed that RIG-I and STAT1 interact with each other with or without IFN-alpha via immunoprecipitation (figure 3D).
	0.97	STAT1 in RIG-I-overexpressing and Vec TRCs and found that activation of STAT1 was enhanced in RIG-I-overexpressing TRCs (figure 3G).
	0.97	STAT1 is mediated by the downregulation of retinoic acid inducible gene-I (RIG-I).
	0.94	RIG-I repression and then affect STAT1 activation to cause resistance to IFN-alpha-induced apoptosis.
	0.94	RIG-I expression may lead to diminished activation of STAT1, resulting in the attenuated effect of IFN-alpha on TRCs.
	0.93	RIG-I in melanoma TRCs led to diminished activation of STAT1 via enhancing the interaction between Src homology region 2 domain-containing phosphatase-1 and STAT1.
	0.92	STAT1 activation and mediate resistance to IFN-alpha through downregulated RIG-I expression and that RIG-I is a prognostic marker in patients with melanoma.
	0.89	STAT1 can be influenced by PARK7 and RIG-I. We next determined the expression of genes that can influence the interaction between SHP1 and STAT1 via RT-PCR and found that PARK7 expression was no different between TRCs and control tumor cells, while RIG-I expression was significantly lower in TRCs (figure 3B, C and online supplementary figure S3c).
	0.84	STAT1 via RIG-I and decrease the effect of IFN-alpha on tumor cells.
29348488	0.98	STAT1 and DDX58 mRNA in HNSCC was analysed using the TCGA database (Pearson's correlation coefficient: 0.58, Spearman's correlation coefficient: 0.77).
	0.97	RIG-I expression in both HN4 and HN30 cells (Figure 7A), supporting the hypothesis that STAT1 activation plays a major role in IFNalpha-induced RIG-I expression.
	0.96	STAT1 binding sites in DDX58 promoter region were predicted by the JASPAR database (Supplementary Figure 10).
	0.96	Stat1 (Tyr701) bound the promoter region of the DDX58 gene in IFNalpha-stimulated HN4 and HN30 cells in the ChIP assay (Figure 7B).
	0.93	RIG-I expression through STAT1 activation.
	0.80	RIG-I transcription in HNSCC cells through p-STAT1 (Tyr701).
	0.50	RIG-I by activating signal transducers and activators of transcription 1 (STAT1) in HNSCC cells.
29403485	0.98	RIG-I, phosho-IRF7, STAT1, IFIT1, RABV N, and GAPDH.
	0.97	RIG-I, MDA5, MAVS, IRF7, IFN-beta, STAT1, and IFIT1, were significantly upregulated by B2c compared with DRV in both CHX-treated and mock-treated astrocytes, indicating that viral RNA rather than proteins activates IFN pathway depending on MAVS (Figures 3C-I).
	0.96	RIG-I, p-IRF7, STAT1, and IFIT1 in B2c-infected astrocytes were higher than those in DRV-infected cells (Figure 3A).
	0.90	RIG-I, melanoma differentiation-associated protein 5, MAVS, IRF7, interferon-beta, STAT1, and IFIT1 transcription levels were measured by qRT-PCR.
	0.88	RIG-I, p-IRF7, STAT1 and IFIT1 (ISG56), was measured by Western blot.
22483866	0.98	STAT1-mediated pathway (Figs. 3 and S3) that resembles the sustained response to interferon stimulation (Table 3); it induces an MDA5- and RIG-I-dependent innate antiviral response in the absence of RNA virus infection (Table 4); it binds to a large family of MER85 repetitive elements that are dispersed throughout the genome, potentially providing a mechanism for regulating expression of nearby genes (Fig. 4); as expected from conservation of the CSB-PGBD3 fusion protein, the interferon-like and innate antiviral responses are both dramatically repressed by coexpression of intact CSB (Tables 2 and S1C); and finally, expression of CSB in CS1AN cells that naturally express the fusion protein induces many of the same antiviral proteins as expression of the fusion protein in CSB-null UVSS1KO cells (Tables 4A,B and S5), suggesting that CSB and CSB-PGBD3 fusion protein both contribute to the normal cellular antiviral state and interferon response.
	0.95	RIG-I and MDA5 are normally activated by intracellular double-stranded or uncapped RNA indicative of viral infection, and are known to signal through the mitochondrial adaptor protein IPS-1 (IFN-beta promoter stimulator 1, also called Signaling can stimulate the IFN-alpha and/or IFN-beta promoters, generating secreted interferons that activate STAT1 through an autocrine circuit involving interferon cell-surface receptors and the canonical JAK-STAT pathway.
	0.95	STAT1 by RIG-I overexpression in the U937 acute myeloid leukemia (AML) cell line results in STAT1 phosphorylation on both Tyr 701 and Ser 727 whereas expression of the CSB-PGBD3 fusion protein in UVSS1KO fibroblasts induces STAT1 phosphorylated on Ser 727 alone (Figs. 3 and S3) as well as many of the same genes induced by the unphosphorylatable Y701F STAT1 mutant in normal BJ fibroblasts (Tables 2, 3 and S3).
	0.82	RIG-I can also activate STAT1 through a newly discovered noncanonical pathway that is independent of cell-surface interferon receptors and possibly of the receptor-associated kinases JAK1, JAK2, and TYK2 as well.
28593618	0.98	RIG-I triggers STAT1-dependent signaling pathway by the stimulation of endogenous RNAs in the exosomes released by stromal cells.
	0.97	RIG-I was detected in HCC, wherein RIG-I promotes STAT1 activation by competing the SH2-TA binding domain with SHP1.
	0.96	RIG-I also enhances the expression of other numerous IFN stimulatory genes (ISGs) by promoting STAT1 activation in a MAVS-independent manner.
	0.91	RIG-I acts as a tumor suppressor through either augmenting STAT1 activation by competitively binding STAT1 against its negative regulator SHP1 or inhibiting AKT-mTOR signaling pathway by directly interacting with Src respectively.
24260178	0.98	STAT1-57 also included DEAD (Asp-Glu-Ala-Asp) box polypeptide 58 (DDX58), which is located near a chromosome 9 psoriasis susceptibility locus.
	0.96	STAT1-57 genes were in fact elevated following RNAi knockdown of each of these three targets (i.e., p63, ZNF750 and KLF4; e.g., DDX58, IRF9, OAS2, OAS3 and STAT1; P<0.05 for each RNAi treatment by moderated t-test).
	0.85	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).
26535695	0.97	RIG-I and type I IFN response, we analyzed RIG-I, MDA5, STAT1, IFN-a and IFN-b mRNA levels from post-mortem brain tissues collected from HAND patients, HIV serum-positive patients without dementia, and HIV serum negative individuals.
	0.97	STAT1 (P-STAT1), STAT1, RIG-I, MyD88 and P24 were detected by western blot.
	0.96	RIG-I expression and STAT1 expression and phosphorylation.
	0.96	RIG-I knockdown inhibits activation of STAT1 and enhances HIV-1 replication in HIV-1-infected MDMs
	0.96	RIG-I expression and STAT1 activation.
	0.95	RIG-I pathways genes was employed and STAT1 expression and phosphorylation levels were examined to explore the molecular mechanisms of HAND.
	0.95	STAT1 (P-STAT1), STAT1, RIG-I, MyD88 and P24 were detected by western blot.
	0.93	RIG-I silencing can inhibit activation of STAT1 and enhance HIV-1 replication in HIV-1-infected MDMs.
	0.93	RIG-I with ratio of phosphorylated STAT1 to total STAT1 was determined by Spearman's correlation.
	0.92	RIG-I expression and STAT1 activation
	0.85	RIG-I protein expression and increased STAT1 phosphorylation as expected.
	0.84	STAT1 phosphorylation was found in MDMs transfected with siRNA for RIG-I (Figure 6A, E).
	0.71	RIG-I and the ratio of phosphorylated STAT1 to total STAT1 (Figure 3E).
	0.65	RIG-I highly correlated with those of STAT1 (P < 0.0001) (Figure 2A), indicating that the regulation of RIG-I may act as an immune response to HIV-1 infection of the CNS.
	0.57	RIG-I silencing inhibits activation of STAT1 and enhances HIV-1 replication in HIV-1-infected MDMs.
27662626	0.97	STAT1 (-1331/-1323), ISRE (-901/-887), c-Rel (-306/-297), and IRF-E (-17/-5) were identified in the RIG-I promoter region (Fig 4A).
	0.97	STAT1, ISRE, c-Rel and IRF-E on the RIG-I promoter are shown.
	0.97	STAT1 is required for the enhanced expression of RIG-I in response to RLR signaling.
	0.97	RIG-I is limited; specifically, the involvement of IRF-1 in RLR signaling-mediated RIG-I expression is likely to depend on STAT1 (Fig 2B), whereas IRF-3 affects the expression of RIG-I in a STAT1-independent manner.
	0.94	STAT1-binding site (-1323), ISRE (-887), or c-Rel-binding site (-291) from the 2-kb RIG-I promoter exerted an insignificant effect on the luciferase activities of the transfected cells (Fig 4B).
	0.91	STAT1-null U3A cells, type I IFN receptor (IFNAR)-null U5A cells, and their parental 2fTGH cells to examine the effects of STAT1 and type I IFN on the expression of RIG-I in response to RLR signaling.
	0.89	STAT1, leading to the robust expression of RIG-I in neighboring cells.
	0.87	RIG-I even in the absence of STAT1 or IFNAR and that the kinetics of RIG-I expression was similar under all conditions for up to 4 hours (Fig 1, U3A and U5A cells).
	0.83	RIG-I, type I IFN-activated STAT1 initiates RIG-I induction.
	0.80	STAT1 has been demonstrated to serve as a crucial transcriptional factor for the induction of RIG-I. Indeed, both type I and type II IFNs induce the expression of RIG-I in HeLa cells (S1B Fig).
31992798	0.97	RIG-I/MDA5 pathway leading to activation of NF-kappaB through induction of IRF7 and phosphorylation of IRF3 - both events detected in CD95 stimulated cells - eventually resulting in induction of IFN-I. We detected a dramatic mobilization of two of the four tested ERVs (MER21C and MLT1C49) in response to CD95 stimulation which was strongly dependent on the presence of STAT1 (Fig. 5B).
	0.91	STAT1 and STAT2 resulting in upregulation of the double stranded (ds)RNA sensor proteins RIG-I and MDA5, and a release of a subset of endogenous retroviruses.
	0.87	STAT1, PLSCR1, RIG-I, MDA5, and IRF7 of Cas9 control (wt, clone C1) and STAT1 k.o.
	0.84	RIG-I, MDA5, TLR3, MAVS, IRF3, and IRF7 of two Cas9 control clones (C1 and C2) and two STAT1 k.o.
	0.74	STAT1, PLSCR1, RIG-I, MDA5 and IRF7 induction could be detected and their expression levels dramatically increased after two days (Fig. 5A).
29402958	0.97	STAT1 and STAT2 dimerise, translocate to the nucleus and trigger transcription of Ddx58 (RIG-I), Eif2ak2 (PKR) and Oas1a, as well as Stat1/2.
	0.96	STAT1 activation triggers expression of its target genes, including Stat1, Stat2, Ddx58 (RIG-I), Socs1, Eif2ak2 (PKR) and Oas1a, which peak at 6-10 h (Fig. 4b, d), and is followed by the accumulation of corresponding proteins (Fig. 4a, c).
	0.94	STAT1 activation after poly(I:C), but the presence of residual RIG-I allows for poly(I:C) recognition, phosphorylation of IKKalpha/beta and TBK1, and subsequent activation of IRF3 (Fig. 4a).
	0.81	STAT1/2-regulated genes, Stat1, Stat2, Ddx58 (RIG-I), Socs1, Eif2ak2 (PKR) and Oas1a, in response to LPS, IFNbeta or poly(I:C).
29416786	0.97	STAT1, STAT2, EIF2AK2, TGM2, DDX58, PARP9, SASH1, RBL2 and USP18 and their expression levels were up-regulated by 1.581 to 2.337 folds by 4-OH-TAM.
	0.94	DDX58, PARP9, STAT2, STAT1, PGR and CCND1 were all significantly higher in ER+-tumor tissues than in their corresponding tumor-adjacent tissues.
	0.66	STAT1, STAT2, EIF2AK2, TGM2, DDX58, PARP9, SASH1, RBL2 and USP18 as well as down-regulated genes including CCDN1, S100A9, S100A8, ANXA1 and PGR were confirmed by quantitative real-time PCR (qRT-PCR).
	0.64	DDX58, PARP9, STAT1 and STAT2 were not significantly different between ER--tumor tissues and their corresponding tumor-adjacent tissues.
22629479	0.97	STAT1, including its phosphorylated form, and RIG-I protein.
	0.86	STAT1 (p-STAT1), STAT1 (STAT1), ISG15 (ISG15), RIG-I (RIG-I) and beta-actin (actin) proteins.
	0.77	STAT1 (p-STAT1), STAT1 (STAT1), ISG15 (ISG15), viral NP protein (NP), RIG-I (RIG-I), IRF3 (IRF3) and beta-actin (actin).
24594370	0.97	STAT1 and STAT2, leads to the induction of many genes, some of which give rise to antiviral proteins such as OAS and MX1, others to RIG-I which is instrumental in detecting the virus, and to IRF7, which in infected cells enhances IFNbeta induction and is the transcription factor of IFNalpha.
28991176	0.96	RIG-I-like receptors (RLRs) signalling transduction by HCV NS4B; cleaving STING by dengue virus (DENV) NS2B3; interacting with TANK-binding Kinase (TBK1) by HCV NS2 and NS3; inhibiting TBK1 phosphorylation by West Nile virus (WNV) NS4B and DENV4 NS2A and NS4B; inhibiting interferon regulatory factor-3 (IRF3) phosphorylation by DENV4 NS2A and NS4B and HCV NS3/4A; inhibiting interferon regulatory factor-7 (IRF7) activation by interacting with IRF7; interacting with IFNAR1 by Langat virus (LGTV) NS5; reducing Tyk2 phosphorylation by Japanese encephalitis virus (JEV), DENV and JEV NS5; interacting with STAT1 by DENV NS2A, NS4A and NS4B and JEV NS5; cleaving STAT1 by DENV NS5; inhibiting STAT1 phosphorylation by HCV NS5A, yellow fever virus (YFV) and WNV NS4B; inhibiting STAT2 phosphorylation by Kunjin virus (KUNV) NS2A, NS2B, NS3, NS4A and NS4B; and suppressing double-stranded RNA-activated protein kinase (PKR) and 2'-5' OAS function by HCV NS5A.
29581268	0.95	DDX58, a canonical U-ISGF3 target gene, was also decreased after 48 h compared with 24 h of IFNbeta treatment in BJ cells (SI Appendix, Fig. S1F), but the induction of STAT1, IRF9, and STAT2 were not decreased at 48 h (Fig. 1E), similarly to the induction of IL6.
	0.92	DDX58, was less in IFNbeta-treated STAT1-null cells than in wild-type cells (Fig. 1E and SI Appendix, Fig. S1F).
	0.88	STAT1-null fibroblasts and by about 3-fold in wild-type fibroblasts (Fig. 1J), similarly to the effects on DDX58 expression (SI Appendix, Fig. S3B).
28819164	0.95	RIG-I and STAT1.
	0.95	RIG-I and STAT1.
28248290	0.95	STAT1 phosphorylation (pSTAT), key steps in RIG-I/IFN signaling, in a dose-dependent manner relative to control (LacZ; Fig. 3d right).
29872431	0.94	STAT1, signal transducer and activator of transcription 1; RIG-I, retinoic acid-inducible gene I; MAVS, mitochondrial antiviral signaling; TRAF2, tumor necrosis factor receptor-associated factor 2; IRF3, 5, 7, and 9, interferon regulatory factors 3, 5, 7, and 9; beta-TrCP, beta-transducin repeat-containing protein; MyD88, myeloid differentiation primary response protein; NF-kappaB, nuclear factor kappaB; IKBalpha, inhibitory kappaB alpha; MHC-I, major histocompatibility complex class I; HLA-A, -B, -C, and -E, HLA class I histocompatibility antigens A, B, C, and E; ICAM-1, intercellular adhesion molecule 1; B7.2, cytotoxic T-lymphocyte-associated antigen 4 counter-receptor; CD83 and 4, CD_antigens 83 and 4.
28152048	0.93	RIG-I agonist induced up-regulation of the RLRs (RIG-I, MDA5, and LGP2), STAT proteins (STAT1 and STAT2), and multiple proteins directly involved in restriction of viral replication (IFIT1, IFIT3, and viperin) (Fig 6C).
	0.90	RIG-I agonist treatment potently restricted ZIKV replication, while type I IFN was significantly less effective due to ZIKV antagonism of STAT1 and STAT2 phosphorylation.
17325370	0.93	RIG-I-mediated pathway, it is reasonable to assume that the IFN response observed in MPRV-infected cells was due to activation of (and failure to inhibit) RIG-I. MPRV clearly did eventually block IFN signalling since the addition of exogenous IFN did not bring the levels of STAT1 up in MPRV-infected cells to those observed in IFN-treated uninfected cells.
23633948	0.92	STAT1 pTyr-701, STAT1, ISG56, RIG-I, IkappaBalpha pSer-32, IkBalpha and beta-actin; all immunoblots are from the same samples.
	0.88	STAT1, IFIT1, RIG-I, and beta-Actin.
26187414	0.88	Ddx58-/-), or STAT1-deficient A549 cells were infected with YFV-WT or YFV-E218A (MOI 1) and IFIT1 mRNA was measured 8 hr after infection by RT-PCR.
	0.80	Ddx58-/-), or STAT1-deficient A549 cells were infected with YFV-WT or YFV-E218A (MOI 0.01) and virus production was quantified as in (C) 72 hr after infection.
28680969	0.86	RIG-I, TBK1, IRF-3, and STAT1 and STAT2 in NSs-containing, round, cytoplasmic inclusion bodies (IB) or viroplasms.
30018336	0.86	STAT1 expression and promotes ISGs induction including RIG-I, which further facilitates the activation of the NF-kappaB, IRF3 (Fig. 4b) and the production of type I IFN and inflammatory cytokines (Supplementary Fig. 2g) at the 8 h after VSV infection.
25417103	0.85	RIG-I and STAT1 are necessary for stroma-mediated resistance, separation of breast cancer cells from stromal fibroblasts using a transwell filter large enough for exosome passage resulted in retained IRDS induction but loss of RT resistance (Figure 4A).
	0.84	RIG-I is a driver of the IRDS, 2) breast cancer NOTCH3 and stromal JAG1 are important regulators of NOTCH target gene expression, 3) NOTCH3 and STAT1 are localized to sites of tumor-stroma interaction, 4) STAT1 facilitates the transcriptional response to NOTCH3, 5) IRDS/STAT1 and NOTCH3 identify patients with both high NOTCH target genes and chemo/RT resistant tumors, and 6) high IRDS/NOTCH3 is preferentially observed in basal and claudin-low subtype primary tumors, which are known to be enriched in cancer stem cell-like features.
	0.82	RIG-I to activate STAT1-dependent anti-viral signaling.
	0.73	STAT1) in response to exosomes (Exo, n=5) or co-culture CM (n=6) plotted against RIG-I levels after knockdown in 1833 IRDS-R. F) IRDS gene expression from two representative data points used to generate plot in Figure 3E are shown relative to siControl.
22590680	0.85	STAT1, RIG-I, Mx1, and PKR functions.
31798565	0.84	RIG-I, STAT1, and IRF3, which promotes innate immune activation and thwart the replication of diverse viruses.
27034163	0.81	Stat1, Ddx58, and Cdkn1a gene expression values in WT and MAVS-/- MEFs after IR treatment.
24391501	0.68	RIG-I-dependent pathway, but IFN-lambda-induced phosphorylation of the signal transducer and activator of transcription protein 1 (STAT1) was dramatically inhibited in the infected cells.
29109527	0.65	RIG-I, TLR-3, OAS1 and OAS2, are expressed following STAT1/STAT2 activation, leading to the inhibition of transcription and translation of viral proteins, along with induction and synthesis of MHC class I expression.
25869307	0.59	RIG-I stimulated by HCV PAMP in a cell culture model of pDCs, through the reduced levels of IRF7 and of phosphorylated STAT1 protein.
27308362	0.53	RIG-I CARD's association with IPS-1, but allows CARDs and PxxP motif of RIG-I accessible for the interaction with STAT1 or Src, by which RIG-I constrains the tumorigenicity of host cells.