Ignet

Gene Information

Gene symbol: STAT3

Gene name: signal transducer and activator of transcription 3 (acute-phase response factor)

HGNC ID: 11364

Synonyms: APRF

Related Genes

#	Gene Symbol	Number of hits
1	AKT1	1 hits
2	BCL2	1 hits
3	CD4	1 hits
4	CD8A	1 hits
5	CISH	1 hits
6	CXCL10	1 hits
7	CXCR3	1 hits
8	FASLG	1 hits
9	GATA3	1 hits
10	HAVCR2	1 hits
11	HLA-DRA	1 hits
12	ICAM1	1 hits
13	IFN1	1 hits
14	IFNG	1 hits
15	IL10	1 hits
16	IL13	1 hits
17	IL17A	1 hits
18	IL17C	1 hits
19	IL17RA	1 hits
20	IL1A	1 hits
21	IL23R	1 hits
22	IL26	1 hits
23	IL4	1 hits
24	IL5	1 hits
25	IL6	1 hits
26	IL8RB	1 hits
27	IRF1	1 hits
28	ITGB2	1 hits
29	JAK1	1 hits
30	JAK2	1 hits
31	MAPK3	1 hits
32	MCL1	1 hits
33	MIRN125A	1 hits
34	NDP	1 hits
35	PPARD	1 hits
36	PPARG	1 hits
37	RGS16	1 hits
38	RIPK1	1 hits
39	SELL	1 hits
40	SIRT1	1 hits
41	SMAD2	1 hits
42	SMAD7	1 hits
43	SOCS1	1 hits
44	SOCS2	1 hits
45	SOCS3	1 hits
46	STAT1	1 hits
47	STAT2	1 hits
48	STAT4	1 hits
49	STAT5A	1 hits
50	STAT5B	1 hits
51	STAT6	1 hits
52	TBX21	1 hits
53	TGFB1	1 hits
54	TH1L	1 hits
55	TLR4	1 hits
56	TNF	1 hits
57	TYK2	1 hits

Related Sentences

#	PMID	Sentence
1	29039977	The impact of these conditions on parameters of behavioral activity and mRNA levels of selected immune markers in the colonic mucosa of Wistar rats, namely TNFα (Tnf), IL1a (Il1a), IL17RA (Il17ra), STAT3 (Stat3) and Rgs16 (Rsg16), were detected.
2	28316372	The expression of genes, including IL10, JAK1, STAT3, SOCS3, IP10, ICAM1, IFNA, IFNG, STAT1, and IRF1, was investigated by RT-qPCR.
3	28316372	The expression of genes, including IL10, JAK1, STAT3, SOCS3, IP10, ICAM1, IFNA, IFNG, STAT1, and IRF1, was investigated by RT-qPCR.
4	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.
5	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.
6	27531854	These cells were the major source of IL21 in tumors and represented about 10% of the CD4⁺ T-cell population at levels comparable with the T_FH cells present in lymph nodes.
7	27531854	However, these T_FH-like cells displayed a unique CXCR5^-PD-1^lo/-BTLA^-CD69^hi tissue-resident phenotype with substantial IFNγ production, which differed from the phenotype of T_FH cells.
8	27531854	Toll-like receptor 4 (TLR4)-elicited innate monocyte inflammation was important for IL21⁺ T_FH-like cell induction in tumors, and activation of STAT1 and STAT3 was critical for T_FH-like cell polarization in this process.
9	27498708	BACKGROUND IL-23/IL-23R signaling plays a pivotal role during the course of inflammatory bowel diseases (IBD).
10	27498708	This study was performed to clarify the association between IL-23/IL-23R signaling and Foxp3+ regulatory T cells in colitis.
11	27498708	IL-23R, IL-23, IL-I7, and IFN-γ expression level, as well as regulatory T cell, Th17-, and Th1-related transcription factors Foxp3, RORgt, and T-bet were assayed by real-time PCR.
12	27498708	RESULTS We detected elevated IL-23R, IL-23, and IFN-γ expression in colon mucosa during acute and chronic colitis and found increased IL-17 in acute colitis mice.
13	27498708	Transcription factors Foxp3 and T-bet were elevated in colon mucosa during acute and chronic colitis.
14	27498708	Phosphorylation of Stat3 was greatly enhanced, indicating the activation of IL-23R function in colitis mice.
15	27179873	Genes that were differentially expressed over the transition period included those involved in neutrophil adhesion (SELL, ITGB2, and ITGBX), mediation of the immune response (TLR4, HLA-DRA, and CXCR2), maturation, cell cycle progression, apoptosis (MCL1, BCL2, FASLG, and RIPK1), and control of gene expression (PPARG, PPARD, and STAT3).
16	27179873	We noted reduced gene expression of proinflammatory cytokines (IFNG, TNF, IL12, and CCL2) on the day of calving, whereas anti-inflammatory cytokine gene expression (IL10) was upregulated.
17	27179873	Increased gene expression of antimicrobial peptides (BNBD4, DEFB10, and DEFB1) occurred on the day of calving.
18	26352148	To determine whether prediagnostic allergy-related serum proteins are associated with glioma, we conducted a nested case-control study of seven cytokines (IL4, IL13, IL5, IL6, IL10, IFNG, TGFB2), two soluble cytokine receptors (sIL4RA, sIL13RA2) and three allergy-related transcription factors (FOXP3, STAT3, STAT6) using serum specimens from the Janus Serum Bank Cohort in Oslo, Norway.
19	26352148	We first estimated individual effects of the 12 serum proteins and then interactions between IL4 and IL13 and their receptors using conditional logistic regression.
20	26300430	Using data integration of genome-wide TF binding profiles, we defined regions with combinatorial binding of lineage-specific master TFs (T-BET, GATA3, and ROR-γt) and STATs (STAT1 and STAT4, STAT6, and STAT3) in murine T helper (Th) 1, Th2, and Th17 cells, respectively.
21	26300430	Genes associated with super-enhancers, including relevant Th-cell genes (such as Ifng in Th1, Il13 in Th2, and Il17a in Th17 cells), showed strong transcriptional activity.
22	26170288	Opposing roles of STAT1 and STAT3 in IL-21 function in CD4+ T cells.
23	26170288	Opposing roles of STAT1 and STAT3 in IL-21 function in CD4+ T cells.
24	26170288	Opposing roles of STAT1 and STAT3 in IL-21 function in CD4+ T cells.
25	26170288	Opposing roles of STAT1 and STAT3 in IL-21 function in CD4+ T cells.
26	26170288	Opposing roles of STAT1 and STAT3 in IL-21 function in CD4+ T cells.
27	26170288	Opposing roles of STAT1 and STAT3 in IL-21 function in CD4+ T cells.
28	26170288	Opposing roles of STAT1 and STAT3 in IL-21 function in CD4+ T cells.
29	26170288	Opposing roles of STAT1 and STAT3 in IL-21 function in CD4+ T cells.
30	26170288	Opposing roles of STAT1 and STAT3 in IL-21 function in CD4+ T cells.
31	26170288	Although IL-21 can activate several STAT family transcription factors, previous studies focused mainly on the role of STAT3 in IL-21 signaling.
32	26170288	Although IL-21 can activate several STAT family transcription factors, previous studies focused mainly on the role of STAT3 in IL-21 signaling.
33	26170288	Although IL-21 can activate several STAT family transcription factors, previous studies focused mainly on the role of STAT3 in IL-21 signaling.
34	26170288	Although IL-21 can activate several STAT family transcription factors, previous studies focused mainly on the role of STAT3 in IL-21 signaling.
35	26170288	Although IL-21 can activate several STAT family transcription factors, previous studies focused mainly on the role of STAT3 in IL-21 signaling.
36	26170288	Although IL-21 can activate several STAT family transcription factors, previous studies focused mainly on the role of STAT3 in IL-21 signaling.
37	26170288	Although IL-21 can activate several STAT family transcription factors, previous studies focused mainly on the role of STAT3 in IL-21 signaling.
38	26170288	Although IL-21 can activate several STAT family transcription factors, previous studies focused mainly on the role of STAT3 in IL-21 signaling.
39	26170288	Although IL-21 can activate several STAT family transcription factors, previous studies focused mainly on the role of STAT3 in IL-21 signaling.
40	26170288	Here, we investigated the role of STAT1 and show that STAT1 and STAT3 have at least partially opposing roles in IL-21 signaling in CD4(+) T cells.
41	26170288	Here, we investigated the role of STAT1 and show that STAT1 and STAT3 have at least partially opposing roles in IL-21 signaling in CD4(+) T cells.
42	26170288	Here, we investigated the role of STAT1 and show that STAT1 and STAT3 have at least partially opposing roles in IL-21 signaling in CD4(+) T cells.
43	26170288	Here, we investigated the role of STAT1 and show that STAT1 and STAT3 have at least partially opposing roles in IL-21 signaling in CD4(+) T cells.
44	26170288	Here, we investigated the role of STAT1 and show that STAT1 and STAT3 have at least partially opposing roles in IL-21 signaling in CD4(+) T cells.
45	26170288	Here, we investigated the role of STAT1 and show that STAT1 and STAT3 have at least partially opposing roles in IL-21 signaling in CD4(+) T cells.
46	26170288	Here, we investigated the role of STAT1 and show that STAT1 and STAT3 have at least partially opposing roles in IL-21 signaling in CD4(+) T cells.
47	26170288	Here, we investigated the role of STAT1 and show that STAT1 and STAT3 have at least partially opposing roles in IL-21 signaling in CD4(+) T cells.
48	26170288	Here, we investigated the role of STAT1 and show that STAT1 and STAT3 have at least partially opposing roles in IL-21 signaling in CD4(+) T cells.
49	26170288	IL-21 induced STAT1 phosphorylation, and this was augmented in Stat3-deficient CD4(+) T cells.
50	26170288	IL-21 induced STAT1 phosphorylation, and this was augmented in Stat3-deficient CD4(+) T cells.
51	26170288	IL-21 induced STAT1 phosphorylation, and this was augmented in Stat3-deficient CD4(+) T cells.
52	26170288	IL-21 induced STAT1 phosphorylation, and this was augmented in Stat3-deficient CD4(+) T cells.
53	26170288	IL-21 induced STAT1 phosphorylation, and this was augmented in Stat3-deficient CD4(+) T cells.
54	26170288	IL-21 induced STAT1 phosphorylation, and this was augmented in Stat3-deficient CD4(+) T cells.
55	26170288	IL-21 induced STAT1 phosphorylation, and this was augmented in Stat3-deficient CD4(+) T cells.
56	26170288	IL-21 induced STAT1 phosphorylation, and this was augmented in Stat3-deficient CD4(+) T cells.
57	26170288	IL-21 induced STAT1 phosphorylation, and this was augmented in Stat3-deficient CD4(+) T cells.
58	26170288	RNA-Seq analysis of CD4(+) T cells from Stat1- and Stat3-deficient mice revealed that both STAT1 and STAT3 are critical for IL-21-mediated gene regulation.
59	26170288	RNA-Seq analysis of CD4(+) T cells from Stat1- and Stat3-deficient mice revealed that both STAT1 and STAT3 are critical for IL-21-mediated gene regulation.
60	26170288	RNA-Seq analysis of CD4(+) T cells from Stat1- and Stat3-deficient mice revealed that both STAT1 and STAT3 are critical for IL-21-mediated gene regulation.
61	26170288	RNA-Seq analysis of CD4(+) T cells from Stat1- and Stat3-deficient mice revealed that both STAT1 and STAT3 are critical for IL-21-mediated gene regulation.
62	26170288	RNA-Seq analysis of CD4(+) T cells from Stat1- and Stat3-deficient mice revealed that both STAT1 and STAT3 are critical for IL-21-mediated gene regulation.
63	26170288	RNA-Seq analysis of CD4(+) T cells from Stat1- and Stat3-deficient mice revealed that both STAT1 and STAT3 are critical for IL-21-mediated gene regulation.
64	26170288	RNA-Seq analysis of CD4(+) T cells from Stat1- and Stat3-deficient mice revealed that both STAT1 and STAT3 are critical for IL-21-mediated gene regulation.
65	26170288	RNA-Seq analysis of CD4(+) T cells from Stat1- and Stat3-deficient mice revealed that both STAT1 and STAT3 are critical for IL-21-mediated gene regulation.
66	26170288	RNA-Seq analysis of CD4(+) T cells from Stat1- and Stat3-deficient mice revealed that both STAT1 and STAT3 are critical for IL-21-mediated gene regulation.
67	26170288	Expression of some genes, including Tbx21 and Ifng, was differentially regulated by STAT1 and STAT3.
68	26170288	Expression of some genes, including Tbx21 and Ifng, was differentially regulated by STAT1 and STAT3.
69	26170288	Expression of some genes, including Tbx21 and Ifng, was differentially regulated by STAT1 and STAT3.
70	26170288	Expression of some genes, including Tbx21 and Ifng, was differentially regulated by STAT1 and STAT3.
71	26170288	Expression of some genes, including Tbx21 and Ifng, was differentially regulated by STAT1 and STAT3.
72	26170288	Expression of some genes, including Tbx21 and Ifng, was differentially regulated by STAT1 and STAT3.
73	26170288	Expression of some genes, including Tbx21 and Ifng, was differentially regulated by STAT1 and STAT3.
74	26170288	Expression of some genes, including Tbx21 and Ifng, was differentially regulated by STAT1 and STAT3.
75	26170288	Expression of some genes, including Tbx21 and Ifng, was differentially regulated by STAT1 and STAT3.
76	26170288	Moreover, opposing actions of STAT1 and STAT3 on IFN-γ expression in CD4(+) T cells were demonstrated in vivo during chronic lymphocytic choriomeningitis infection.
77	26170288	Moreover, opposing actions of STAT1 and STAT3 on IFN-γ expression in CD4(+) T cells were demonstrated in vivo during chronic lymphocytic choriomeningitis infection.
78	26170288	Moreover, opposing actions of STAT1 and STAT3 on IFN-γ expression in CD4(+) T cells were demonstrated in vivo during chronic lymphocytic choriomeningitis infection.
79	26170288	Moreover, opposing actions of STAT1 and STAT3 on IFN-γ expression in CD4(+) T cells were demonstrated in vivo during chronic lymphocytic choriomeningitis infection.
80	26170288	Moreover, opposing actions of STAT1 and STAT3 on IFN-γ expression in CD4(+) T cells were demonstrated in vivo during chronic lymphocytic choriomeningitis infection.
81	26170288	Moreover, opposing actions of STAT1 and STAT3 on IFN-γ expression in CD4(+) T cells were demonstrated in vivo during chronic lymphocytic choriomeningitis infection.
82	26170288	Moreover, opposing actions of STAT1 and STAT3 on IFN-γ expression in CD4(+) T cells were demonstrated in vivo during chronic lymphocytic choriomeningitis infection.
83	26170288	Moreover, opposing actions of STAT1 and STAT3 on IFN-γ expression in CD4(+) T cells were demonstrated in vivo during chronic lymphocytic choriomeningitis infection.
84	26170288	Moreover, opposing actions of STAT1 and STAT3 on IFN-γ expression in CD4(+) T cells were demonstrated in vivo during chronic lymphocytic choriomeningitis infection.
85	26170288	Finally, IL-21-mediated induction of STAT1 phosphorylation, as well as IFNG and TBX21 expression, were higher in CD4(+) T cells from patients with autosomal dominant hyper-IgE syndrome, which is caused by STAT3 deficiency, as well as in cells from STAT1 gain-of-function patients.
86	26170288	Finally, IL-21-mediated induction of STAT1 phosphorylation, as well as IFNG and TBX21 expression, were higher in CD4(+) T cells from patients with autosomal dominant hyper-IgE syndrome, which is caused by STAT3 deficiency, as well as in cells from STAT1 gain-of-function patients.
87	26170288	Finally, IL-21-mediated induction of STAT1 phosphorylation, as well as IFNG and TBX21 expression, were higher in CD4(+) T cells from patients with autosomal dominant hyper-IgE syndrome, which is caused by STAT3 deficiency, as well as in cells from STAT1 gain-of-function patients.
88	26170288	Finally, IL-21-mediated induction of STAT1 phosphorylation, as well as IFNG and TBX21 expression, were higher in CD4(+) T cells from patients with autosomal dominant hyper-IgE syndrome, which is caused by STAT3 deficiency, as well as in cells from STAT1 gain-of-function patients.
89	26170288	Finally, IL-21-mediated induction of STAT1 phosphorylation, as well as IFNG and TBX21 expression, were higher in CD4(+) T cells from patients with autosomal dominant hyper-IgE syndrome, which is caused by STAT3 deficiency, as well as in cells from STAT1 gain-of-function patients.
90	26170288	Finally, IL-21-mediated induction of STAT1 phosphorylation, as well as IFNG and TBX21 expression, were higher in CD4(+) T cells from patients with autosomal dominant hyper-IgE syndrome, which is caused by STAT3 deficiency, as well as in cells from STAT1 gain-of-function patients.
91	26170288	Finally, IL-21-mediated induction of STAT1 phosphorylation, as well as IFNG and TBX21 expression, were higher in CD4(+) T cells from patients with autosomal dominant hyper-IgE syndrome, which is caused by STAT3 deficiency, as well as in cells from STAT1 gain-of-function patients.
92	26170288	Finally, IL-21-mediated induction of STAT1 phosphorylation, as well as IFNG and TBX21 expression, were higher in CD4(+) T cells from patients with autosomal dominant hyper-IgE syndrome, which is caused by STAT3 deficiency, as well as in cells from STAT1 gain-of-function patients.
93	26170288	Finally, IL-21-mediated induction of STAT1 phosphorylation, as well as IFNG and TBX21 expression, were higher in CD4(+) T cells from patients with autosomal dominant hyper-IgE syndrome, which is caused by STAT3 deficiency, as well as in cells from STAT1 gain-of-function patients.
94	26170288	These data indicate an interplay between STAT1 and STAT3 in fine-tuning IL-21 actions.
95	26170288	These data indicate an interplay between STAT1 and STAT3 in fine-tuning IL-21 actions.
96	26170288	These data indicate an interplay between STAT1 and STAT3 in fine-tuning IL-21 actions.
97	26170288	These data indicate an interplay between STAT1 and STAT3 in fine-tuning IL-21 actions.
98	26170288	These data indicate an interplay between STAT1 and STAT3 in fine-tuning IL-21 actions.
99	26170288	These data indicate an interplay between STAT1 and STAT3 in fine-tuning IL-21 actions.
100	26170288	These data indicate an interplay between STAT1 and STAT3 in fine-tuning IL-21 actions.
101	26170288	These data indicate an interplay between STAT1 and STAT3 in fine-tuning IL-21 actions.
102	26170288	These data indicate an interplay between STAT1 and STAT3 in fine-tuning IL-21 actions.
103	25963922	Here we show that miR-125a is downregulated in peripheral CD4(+) T cells of human autoimmune diseases including systemic lupus erythematosus and Crohn's disease, and relevant autoimmune mouse models. miR-125a stabilizes both the commitment and immunoregulatory capacity of Treg cells.
104	25963922	The genome-wide target analysis reveals that miR-125a suppresses several effector T-cell factors including Stat3, Ifng and Il13.
105	25921106	Association Study of Single-Nucleotide Polymorphisms of STAT2/STAT3/IFN-γ Genes in Cervical Cancer in Southern Chinese Han Women.
106	25685909	STAT-3 and STAT-1 signaling have opposite effects in oncogenesis with STAT-3 acting as an oncogene and STAT-1 exerting anti-oncogenic activities through interferon-γ and interferon-α.
107	25685909	STAT-3 and STAT-1 signaling have opposite effects in oncogenesis with STAT-3 acting as an oncogene and STAT-1 exerting anti-oncogenic activities through interferon-γ and interferon-α.
108	25685909	The cytokine IL-6 promotes oncogenesis by stimulation of NFκB and STAT-3 signaling.
109	25685909	The cytokine IL-6 promotes oncogenesis by stimulation of NFκB and STAT-3 signaling.
110	25673564	IL10, TGF beta1, and IFN gamma modulate intracellular signaling pathways and cytokine production to control Toxoplasma gondii infection in BeWo trophoblast cells.
111	25673564	IL10, TGF beta1, and IFN gamma modulate intracellular signaling pathways and cytokine production to control Toxoplasma gondii infection in BeWo trophoblast cells.
112	25673564	Considering that interleukin 10 (IL10), transforming growth factor beta1 (TGFB1), and interferon gamma (IFNG) are involved in the susceptibility of BeWo trophoblast cells to Toxoplasma gondii infection, the aim of the present study was to investigate the effector mechanisms triggered by these cytokines in the control of T. gondii in BeWo cells.
113	25673564	Considering that interleukin 10 (IL10), transforming growth factor beta1 (TGFB1), and interferon gamma (IFNG) are involved in the susceptibility of BeWo trophoblast cells to Toxoplasma gondii infection, the aim of the present study was to investigate the effector mechanisms triggered by these cytokines in the control of T. gondii in BeWo cells.
114	25673564	For this purpose, infected/uninfected BeWo cells were treated with IL10, TGFB1 (50 ng/ml), and IFNG (20 or 100 ng/ml) in order to verify the phosphorylation of signal transducers and activators of transcription 1 (STAT1), STAT3, and Smad2, parasite intracellular proliferation, as well as the Th1/Th2/IL17A cytokine production.
115	25673564	For this purpose, infected/uninfected BeWo cells were treated with IL10, TGFB1 (50 ng/ml), and IFNG (20 or 100 ng/ml) in order to verify the phosphorylation of signal transducers and activators of transcription 1 (STAT1), STAT3, and Smad2, parasite intracellular proliferation, as well as the Th1/Th2/IL17A cytokine production.
116	25673564	The treatment of BeWo cells with IL10 and TGFB1 favored T. gondii proliferation, and these findings were associated with STAT3 and Smad2 phosphorylation, respectively (P < 0.05).
117	25673564	The treatment of BeWo cells with IL10 and TGFB1 favored T. gondii proliferation, and these findings were associated with STAT3 and Smad2 phosphorylation, respectively (P < 0.05).
118	25673564	Also, these cytokine treatments were able to down-modulate TNF alpha (TNFA) and IL6 production (P < 0.05).
119	25673564	Also, these cytokine treatments were able to down-modulate TNF alpha (TNFA) and IL6 production (P < 0.05).
120	25673564	Low concentration of IFNG was unable to control T. gondii infection but was able to trigger STAT1 phosphorylation and up-regulate IL6 and IL17A production; whereas a high concentration of IFNG was unable to activate STAT1 but down-modulated IL6 and TNFA and increased T. gondii proliferation (P < 0.05).
121	25673564	Low concentration of IFNG was unable to control T. gondii infection but was able to trigger STAT1 phosphorylation and up-regulate IL6 and IL17A production; whereas a high concentration of IFNG was unable to activate STAT1 but down-modulated IL6 and TNFA and increased T. gondii proliferation (P < 0.05).
122	25673564	IL10, TGFB1, and IFNG regulate a differential T. gondii proliferation in BeWo cells because they distinctly trigger intracellular signaling pathways and cytokine production, especially IL6 and TNFA.
123	25673564	IL10, TGFB1, and IFNG regulate a differential T. gondii proliferation in BeWo cells because they distinctly trigger intracellular signaling pathways and cytokine production, especially IL6 and TNFA.
124	25673564	Our data open new windows to understand the mechanisms triggered by IL10, TGFB1, and IFNG at the maternal-fetal interface in the presence of T. gondii, contributing to recognizing the importance of these effector mechanisms involved in the vertical transmission of this parasite.
125	25673564	Our data open new windows to understand the mechanisms triggered by IL10, TGFB1, and IFNG at the maternal-fetal interface in the presence of T. gondii, contributing to recognizing the importance of these effector mechanisms involved in the vertical transmission of this parasite.
126	24850427	SIRT1, a class III NAD+-dependent deacetylase, regulates negatively the expression of various proteins involved in the control of immune-inflammatory pathways, such as Stat3, Smad7, and NF-κB.
127	24850427	SIRT1 expression was downregulated in control LPMC by tumor necrosis factor (TNF)-α and interleukin (IL)-21, and upregulated in IBD LPMC by neutralizing TNF-α and IL-21antibodies.
128	24850427	Treatment of IBD LPMC with Cay10591, a specific SIRT1 activator, reduced NF-κB activation and inhibited inflammatory cytokine synthesis, whereas Ex527, an inhibitor of SIRT1, increased interferon (IFN)-γ in control LPMC.
129	24038588	The results showed that the JAK/STAT pathway activation by proinflammatory cytokine interleukin-6 and interferon-γ in CCA cells was suppressed by pretreatment with quercetin and EGCG, evidently by a decrease of the elevated phosphorylated-STAT1 and STAT3 proteins in a dose-dependent manner.
130	24038588	The cytokine-mediated up-regulation of inducible nitric oxide synthase (iNOS) and intercellular adhesion molecule-1 (ICAM-1) via JAK/STAT cascade was abolished by both quercetin and EGCG pretreatment.
131	24038588	Pretreatment with specific JAK inhibitors, AG490 and piceatannol, abolished cytokine-induced iNOS and ICAM-1 expression.
132	23668260	The infected mice displayed a significant up-regulation in the expression of chemokines (Cxcl1, Cxcl2 and Ccl2), numerous pro-inflammatory cytokines (Ifng, Il1b, Il6, and Il17f), as well as Il22 and a number of anti-microbial peptides (Defa1, Defa28, Defb1, Slpi and Reg3g) at the site(s) of infection.
133	23668260	However, CD4 T cells of the untreated and C. difficile-infected mice expressed similar levels of CD69 and CD25.
134	23668260	Neither tissue had up-regulated levels of Tbx21, Gata3 or Rorc.
135	23668260	They also displayed significantly higher phosphorylation of AKT and signal transducer and activator of transcription 3 (STAT3), an indication of pro-survival signalling.
136	23668260	These data underscore the local, innate, pro-inflammatory nature of the response to C. difficile and highlight eIF2α phosphorylation and the interleukin-22-pSTAT3-RegIIIγ axis as two of the pathways that could be used to contain and counteract the damage inflicted on the intestinal epithelium.
137	23144609	Tim-3-expressing CD4+ and CD8+ T cells in human tuberculosis (TB) exhibit polarized effector memory phenotypes and stronger anti-TB effector functions.
138	23144609	T-cell immune responses modulated by T-cell immunoglobulin and mucin domain-containing molecule 3 (Tim-3) during Mycobacterium tuberculosis (Mtb) infection in humans remain poorly understood.
139	23144609	Here, we found that active TB patients exhibited increases in numbers of Tim-3-expressing CD4(+) and CD8(+) T cells, which preferentially displayed polarized effector memory phenotypes.
140	23144609	Consistent with effector phenotypes, Tim-3(+)CD4(+) and Tim-3(+)CD8(+) T-cell subsets showed greater effector functions for producing Th1/Th22 cytokines and CTL effector molecules than Tim-3(-) counterparts, and Tim-3-expressing T cells more apparently limited intracellular Mtb replication in macrophages.
141	23144609	The increased effector functions for Tim-3-expressing T cells consisted with cellular activation signaling as Tim-3(+)CD4(+) and Tim-3(+)CD8(+) T-cell subsets expressed much higher levels of phosphorylated signaling molecules p38, stat3, stat5, and Erk1/2 than Tim-3- controls.
142	23144609	Furthermore, stimulation of Tim-3 signaling pathways by antibody cross-linking of membrane Tim-3 augmented effector function of IFN-γ production by CD4(+) and CD8(+) T cells, suggesting that Tim-3 signaling helped to drive stronger effector functions in active TB patients.
143	22659089	The CCBs nimodipine (NDP) and verapamil (VPM) both significantly suppressed toxic secretions from human astrocytes and astrocytoma U-373 MG cells that were induced by interferon (IFN)-γ.
144	22659089	In human astrocytes, both NDP and VPM reduced IFN-γ-induced phosphorylation of signal transducer and activator of transcription (STAT) 3.
145	22121102	JAK/STAT/SOCS-signaling pathway and colon and rectal cancer.
146	22121102	JAK/STAT/SOCS-signaling pathway and colon and rectal cancer.
147	22121102	JAK/STAT/SOCS-signaling pathway and colon and rectal cancer.
148	22121102	We evaluated the association between genetic variation in JAK1 (10 SNPs), JAK2 (9 SNPs), TYK2 (5 SNPs), suppressors of cytokine signaling (SOCS)1 (2 SNPs), SOCS2 (2 SNPs), STAT1 (16 SNPs), STAT2 (2 SNPs), STAT3 (6 SNPs), STAT4 (21 SNPs), STAT5A (2 SNPs), STAT5B (3 SNPs), STAT6 (4 SNPs) with risk of colorectal cancer.
149	22121102	We evaluated the association between genetic variation in JAK1 (10 SNPs), JAK2 (9 SNPs), TYK2 (5 SNPs), suppressors of cytokine signaling (SOCS)1 (2 SNPs), SOCS2 (2 SNPs), STAT1 (16 SNPs), STAT2 (2 SNPs), STAT3 (6 SNPs), STAT4 (21 SNPs), STAT5A (2 SNPs), STAT5B (3 SNPs), STAT6 (4 SNPs) with risk of colorectal cancer.
150	22121102	We evaluated the association between genetic variation in JAK1 (10 SNPs), JAK2 (9 SNPs), TYK2 (5 SNPs), suppressors of cytokine signaling (SOCS)1 (2 SNPs), SOCS2 (2 SNPs), STAT1 (16 SNPs), STAT2 (2 SNPs), STAT3 (6 SNPs), STAT4 (21 SNPs), STAT5A (2 SNPs), STAT5B (3 SNPs), STAT6 (4 SNPs) with risk of colorectal cancer.
151	22121102	JAK2, SOCS2, STAT1, STAT3, STAT5A, STAT5B, and STAT6 were associated with colon cancer; STAT3, STAT4, STAT6, and TYK2 were associated with rectal cancer.
152	22121102	JAK2, SOCS2, STAT1, STAT3, STAT5A, STAT5B, and STAT6 were associated with colon cancer; STAT3, STAT4, STAT6, and TYK2 were associated with rectal cancer.
153	22121102	JAK2, SOCS2, STAT1, STAT3, STAT5A, STAT5B, and STAT6 were associated with colon cancer; STAT3, STAT4, STAT6, and TYK2 were associated with rectal cancer.
154	22121102	Given the biological role of the JAK/STAT-signaling pathway and cytokines, we evaluated interaction with IFNG, TNF, and IL6; numerous statistically significant associations after adjustment for multiple comparisons were observed.
155	22121102	Given the biological role of the JAK/STAT-signaling pathway and cytokines, we evaluated interaction with IFNG, TNF, and IL6; numerous statistically significant associations after adjustment for multiple comparisons were observed.
156	22121102	Given the biological role of the JAK/STAT-signaling pathway and cytokines, we evaluated interaction with IFNG, TNF, and IL6; numerous statistically significant associations after adjustment for multiple comparisons were observed.
157	22121102	The following statistically significant interactions were observed: TYK2 with aspirin/NSAID use; STAT1, STAT4, and TYK2 with estrogen status; and JAK2, STAT2, STAT4, STAT5A, STAT5B, and STAT6 with smoking status and colon cancer risk; JAK2, STAT6, and TYK2 with aspirin/NSAID use; JAK1 with estrogen status; STAT2 with cigarette smoking and rectal cancer.
158	22121102	The following statistically significant interactions were observed: TYK2 with aspirin/NSAID use; STAT1, STAT4, and TYK2 with estrogen status; and JAK2, STAT2, STAT4, STAT5A, STAT5B, and STAT6 with smoking status and colon cancer risk; JAK2, STAT6, and TYK2 with aspirin/NSAID use; JAK1 with estrogen status; STAT2 with cigarette smoking and rectal cancer.
159	22121102	The following statistically significant interactions were observed: TYK2 with aspirin/NSAID use; STAT1, STAT4, and TYK2 with estrogen status; and JAK2, STAT2, STAT4, STAT5A, STAT5B, and STAT6 with smoking status and colon cancer risk; JAK2, STAT6, and TYK2 with aspirin/NSAID use; JAK1 with estrogen status; STAT2 with cigarette smoking and rectal cancer.
160	22121102	JAK2, SOCS1, STAT3, STAT5, and TYK2 were associated with colon cancer survival (hazard rate ratio (HRR) of 3.3 95% CI 2.01,5.42 for high mutational load).
161	22121102	JAK2, SOCS1, STAT3, STAT5, and TYK2 were associated with colon cancer survival (hazard rate ratio (HRR) of 3.3 95% CI 2.01,5.42 for high mutational load).
162	22121102	JAK2, SOCS1, STAT3, STAT5, and TYK2 were associated with colon cancer survival (hazard rate ratio (HRR) of 3.3 95% CI 2.01,5.42 for high mutational load).
163	22121102	JAK2, SOCS1, STAT1, STAT4, and TYK2 were associated with rectal cancer survival (HRR 2.80 95% CI 1.63,4.80).
164	22121102	JAK2, SOCS1, STAT1, STAT4, and TYK2 were associated with rectal cancer survival (HRR 2.80 95% CI 1.63,4.80).
165	22121102	JAK2, SOCS1, STAT1, STAT4, and TYK2 were associated with rectal cancer survival (HRR 2.80 95% CI 1.63,4.80).
166	20947410	Interleukin-26: an IL-10-related cytokine produced by Th17 cells.
167	20947410	IL-26 is classified as a member of the IL-10 cytokine family because it has limited sequence homology to IL-10 and the IL-10-related cytokines.
168	20947410	The human IL-26 gene, IL26, is located on chromosome 12q15 between the genes for two other important class-2 cytokines, IFNG (IFN-γ) and IL22 (IL-22).
169	20947410	IL-26 is often co-expressed with IL-22 by activated T cells, especially Th17 cells.
170	20947410	It signals through a heterodimeric receptor complex composed of the IL-20R1 and IL-10R2 chains.
171	20947410	Signaling through IL-26 receptor complexes results in the activation of STAT1 and STAT3 with subsequent induction of IL-26-responsive genes.