Ignet

Gene Information

Gene symbol: JUP

Gene name: junction plakoglobin

HGNC ID: 6207

Synonyms: DP3, PDGB, PKGB, DPIII

Related Genes

#	Gene Symbol	Number of hits
1	AHR	1 hits
2	AKT1	1 hits
3	APC	1 hits
4	CCL7	1 hits
5	CCND1	1 hits
6	CD4	1 hits
7	CD83	1 hits
8	CD8A	1 hits
9	CDKN1B	1 hits
10	CIITA	1 hits
11	CTNNA1	1 hits
12	CTNNB1	1 hits
13	CXCL12	1 hits
14	FZD2	1 hits
15	GSK3B	1 hits
16	IL10	1 hits
17	IL2RA	1 hits
18	IL6	1 hits
19	INDO	1 hits
20	KIT	1 hits
21	LGMN	1 hits
22	LRP5	1 hits
23	LY75	1 hits
24	MAGEA1	1 hits
25	MAGEA3	1 hits
26	MLANA	1 hits
27	MMP9	1 hits
28	MUC1	1 hits
29	MYC	1 hits
30	NOD2	1 hits
31	PIK3CA	1 hits
32	PSMD9	1 hits
33	PTGS2	1 hits
34	RORC	1 hits
35	SILV	1 hits
36	SOCS3	1 hits
37	STAT3	1 hits
38	TCF4	1 hits
39	TCF7	1 hits
40	TCF7L2	1 hits
41	TGFB1	1 hits
42	TNFRSF11B	1 hits
43	TPBG	1 hits
44	TYR	1 hits
45	WNT3A	1 hits

Related Sentences

#	PMID	Sentence
1	8640065	Such antigens include MAGE-1, MAGE-3, MART-1/Melan-A, gp100, tyrosinase, the tyrosinase-related antigen gp75, the antigen gp15 and the mutated CDK4 and beta-catenin gene-products.
2	8640065	This should include examination of melanoma antigen and MHC class I allele expression in the individual patient's tumour, assessment of the status of the peptide transporter molecules TAP1/TAP2 and evaluation of T-cell mediated immune responses reactive against peptides and autologous melanoma.
3	11050151	Regulation of beta -catenin transformation by the p300 transcriptional coactivator.
4	11050151	The beta-catenin protein plays a critical role in embryonic development and mature tissue homeostasis through its effects on E-cadherin-mediated cell adhesion and Wnt-dependent signal transduction.
5	11050151	In colon and other cancers, mutations of beta-catenin or the adenomatous polyposis coli (APC) tumor suppressor appear to stabilize beta-catenin and enhance its interaction with T cell factor (TCF) or lymphoid enhancer factor (Lef) transcription factors.
6	11050151	At present, a complete picture of the means by which beta-catenin's interactions with TCF/Lef proteins contribute to neoplastic transformation is lacking.
7	11050151	We report that the transcriptional coactivator p300 interacts with beta-catenin in vitro and in vivo and is critical for beta-catenin-mediated neoplastic transformation. p300 synergistically activates beta-catenin/TCF transcription, and their biochemical association requires the CH1 domain of p300 and a region of beta-catenin that includes its NH(2)-terminal transactivation domain and the first two armadillo repeats.
8	11050151	Lowering of cellular p300 levels by using a ribozyme directed against p300 reduced TCF transcriptional activity and inhibited the neoplastic growth properties of a beta-catenin-transformed rat epithelial cell line and a human colon carcinoma line with a beta-catenin mutation.
9	11050151	These findings demonstrate a critical role for p300 in beta-catenin/TCF transcription and in cancers arising from defects in beta-catenin regulation.
10	11050151	Regulation of beta -catenin transformation by the p300 transcriptional coactivator.
11	11050151	The beta-catenin protein plays a critical role in embryonic development and mature tissue homeostasis through its effects on E-cadherin-mediated cell adhesion and Wnt-dependent signal transduction.
12	11050151	In colon and other cancers, mutations of beta-catenin or the adenomatous polyposis coli (APC) tumor suppressor appear to stabilize beta-catenin and enhance its interaction with T cell factor (TCF) or lymphoid enhancer factor (Lef) transcription factors.
13	11050151	At present, a complete picture of the means by which beta-catenin's interactions with TCF/Lef proteins contribute to neoplastic transformation is lacking.
14	11050151	We report that the transcriptional coactivator p300 interacts with beta-catenin in vitro and in vivo and is critical for beta-catenin-mediated neoplastic transformation. p300 synergistically activates beta-catenin/TCF transcription, and their biochemical association requires the CH1 domain of p300 and a region of beta-catenin that includes its NH(2)-terminal transactivation domain and the first two armadillo repeats.
15	11050151	Lowering of cellular p300 levels by using a ribozyme directed against p300 reduced TCF transcriptional activity and inhibited the neoplastic growth properties of a beta-catenin-transformed rat epithelial cell line and a human colon carcinoma line with a beta-catenin mutation.
16	11050151	These findings demonstrate a critical role for p300 in beta-catenin/TCF transcription and in cancers arising from defects in beta-catenin regulation.
17	11050151	Regulation of beta -catenin transformation by the p300 transcriptional coactivator.
18	11050151	The beta-catenin protein plays a critical role in embryonic development and mature tissue homeostasis through its effects on E-cadherin-mediated cell adhesion and Wnt-dependent signal transduction.
19	11050151	In colon and other cancers, mutations of beta-catenin or the adenomatous polyposis coli (APC) tumor suppressor appear to stabilize beta-catenin and enhance its interaction with T cell factor (TCF) or lymphoid enhancer factor (Lef) transcription factors.
20	11050151	At present, a complete picture of the means by which beta-catenin's interactions with TCF/Lef proteins contribute to neoplastic transformation is lacking.
21	11050151	We report that the transcriptional coactivator p300 interacts with beta-catenin in vitro and in vivo and is critical for beta-catenin-mediated neoplastic transformation. p300 synergistically activates beta-catenin/TCF transcription, and their biochemical association requires the CH1 domain of p300 and a region of beta-catenin that includes its NH(2)-terminal transactivation domain and the first two armadillo repeats.
22	11050151	Lowering of cellular p300 levels by using a ribozyme directed against p300 reduced TCF transcriptional activity and inhibited the neoplastic growth properties of a beta-catenin-transformed rat epithelial cell line and a human colon carcinoma line with a beta-catenin mutation.
23	11050151	These findings demonstrate a critical role for p300 in beta-catenin/TCF transcription and in cancers arising from defects in beta-catenin regulation.
24	11050151	Regulation of beta -catenin transformation by the p300 transcriptional coactivator.
25	11050151	The beta-catenin protein plays a critical role in embryonic development and mature tissue homeostasis through its effects on E-cadherin-mediated cell adhesion and Wnt-dependent signal transduction.
26	11050151	In colon and other cancers, mutations of beta-catenin or the adenomatous polyposis coli (APC) tumor suppressor appear to stabilize beta-catenin and enhance its interaction with T cell factor (TCF) or lymphoid enhancer factor (Lef) transcription factors.
27	11050151	At present, a complete picture of the means by which beta-catenin's interactions with TCF/Lef proteins contribute to neoplastic transformation is lacking.
28	11050151	We report that the transcriptional coactivator p300 interacts with beta-catenin in vitro and in vivo and is critical for beta-catenin-mediated neoplastic transformation. p300 synergistically activates beta-catenin/TCF transcription, and their biochemical association requires the CH1 domain of p300 and a region of beta-catenin that includes its NH(2)-terminal transactivation domain and the first two armadillo repeats.
29	11050151	Lowering of cellular p300 levels by using a ribozyme directed against p300 reduced TCF transcriptional activity and inhibited the neoplastic growth properties of a beta-catenin-transformed rat epithelial cell line and a human colon carcinoma line with a beta-catenin mutation.
30	11050151	These findings demonstrate a critical role for p300 in beta-catenin/TCF transcription and in cancers arising from defects in beta-catenin regulation.
31	11050151	Regulation of beta -catenin transformation by the p300 transcriptional coactivator.
32	11050151	The beta-catenin protein plays a critical role in embryonic development and mature tissue homeostasis through its effects on E-cadherin-mediated cell adhesion and Wnt-dependent signal transduction.
33	11050151	In colon and other cancers, mutations of beta-catenin or the adenomatous polyposis coli (APC) tumor suppressor appear to stabilize beta-catenin and enhance its interaction with T cell factor (TCF) or lymphoid enhancer factor (Lef) transcription factors.
34	11050151	At present, a complete picture of the means by which beta-catenin's interactions with TCF/Lef proteins contribute to neoplastic transformation is lacking.
35	11050151	We report that the transcriptional coactivator p300 interacts with beta-catenin in vitro and in vivo and is critical for beta-catenin-mediated neoplastic transformation. p300 synergistically activates beta-catenin/TCF transcription, and their biochemical association requires the CH1 domain of p300 and a region of beta-catenin that includes its NH(2)-terminal transactivation domain and the first two armadillo repeats.
36	11050151	Lowering of cellular p300 levels by using a ribozyme directed against p300 reduced TCF transcriptional activity and inhibited the neoplastic growth properties of a beta-catenin-transformed rat epithelial cell line and a human colon carcinoma line with a beta-catenin mutation.
37	11050151	These findings demonstrate a critical role for p300 in beta-catenin/TCF transcription and in cancers arising from defects in beta-catenin regulation.
38	11050151	Regulation of beta -catenin transformation by the p300 transcriptional coactivator.
39	11050151	The beta-catenin protein plays a critical role in embryonic development and mature tissue homeostasis through its effects on E-cadherin-mediated cell adhesion and Wnt-dependent signal transduction.
40	11050151	In colon and other cancers, mutations of beta-catenin or the adenomatous polyposis coli (APC) tumor suppressor appear to stabilize beta-catenin and enhance its interaction with T cell factor (TCF) or lymphoid enhancer factor (Lef) transcription factors.
41	11050151	At present, a complete picture of the means by which beta-catenin's interactions with TCF/Lef proteins contribute to neoplastic transformation is lacking.
42	11050151	We report that the transcriptional coactivator p300 interacts with beta-catenin in vitro and in vivo and is critical for beta-catenin-mediated neoplastic transformation. p300 synergistically activates beta-catenin/TCF transcription, and their biochemical association requires the CH1 domain of p300 and a region of beta-catenin that includes its NH(2)-terminal transactivation domain and the first two armadillo repeats.
43	11050151	Lowering of cellular p300 levels by using a ribozyme directed against p300 reduced TCF transcriptional activity and inhibited the neoplastic growth properties of a beta-catenin-transformed rat epithelial cell line and a human colon carcinoma line with a beta-catenin mutation.
44	11050151	These findings demonstrate a critical role for p300 in beta-catenin/TCF transcription and in cancers arising from defects in beta-catenin regulation.
45	11050151	Regulation of beta -catenin transformation by the p300 transcriptional coactivator.
46	11050151	The beta-catenin protein plays a critical role in embryonic development and mature tissue homeostasis through its effects on E-cadherin-mediated cell adhesion and Wnt-dependent signal transduction.
47	11050151	In colon and other cancers, mutations of beta-catenin or the adenomatous polyposis coli (APC) tumor suppressor appear to stabilize beta-catenin and enhance its interaction with T cell factor (TCF) or lymphoid enhancer factor (Lef) transcription factors.
48	11050151	At present, a complete picture of the means by which beta-catenin's interactions with TCF/Lef proteins contribute to neoplastic transformation is lacking.
49	11050151	We report that the transcriptional coactivator p300 interacts with beta-catenin in vitro and in vivo and is critical for beta-catenin-mediated neoplastic transformation. p300 synergistically activates beta-catenin/TCF transcription, and their biochemical association requires the CH1 domain of p300 and a region of beta-catenin that includes its NH(2)-terminal transactivation domain and the first two armadillo repeats.
50	11050151	Lowering of cellular p300 levels by using a ribozyme directed against p300 reduced TCF transcriptional activity and inhibited the neoplastic growth properties of a beta-catenin-transformed rat epithelial cell line and a human colon carcinoma line with a beta-catenin mutation.
51	11050151	These findings demonstrate a critical role for p300 in beta-catenin/TCF transcription and in cancers arising from defects in beta-catenin regulation.
52	15956591	To further improve immunogenicity of the native proteins, we generated expression vectors producing fusion of the proteins Gag and Env to the secreted chemokine MCP3, targeting the viral proteins to the secretory pathway and to a beta-catenin (CATE) peptide, targeting the viral proteins to the intracellular degradation pathway.
53	15956591	Interestingly, macaques immunized with a combination of vectors expressing three forms of antigens (native protein and MCP3 and CATE fusion proteins) showed the strongest decrease in viral load (P = 0.0059).
54	17128152	Indeed, MUC1 can interact with B-catenin competitively for E-cadherin, thus destabilizing intercellular junctions and favouring metastatic dissemination.
55	18806872	Contradicting the previous finding, we found that the levels of E-cadherin, beta-catenin, Glycogen Synthase Kinase 3ss (GSK3beta), axin and alpha-catenin were not affected by the expression of LMP1 sequences from normal B cells or nasopharyngeal carcinoma.
56	18806872	Moreover, we also show that LMP1 expression had no detectable effect on the E-cadherin and beta-catenin interaction and did not induce transcriptional activation of beta-catenin.
57	18806872	Contradicting the previous finding, we found that the levels of E-cadherin, beta-catenin, Glycogen Synthase Kinase 3ss (GSK3beta), axin and alpha-catenin were not affected by the expression of LMP1 sequences from normal B cells or nasopharyngeal carcinoma.
58	18806872	Moreover, we also show that LMP1 expression had no detectable effect on the E-cadherin and beta-catenin interaction and did not induce transcriptional activation of beta-catenin.
59	20574838	And GSK-3beta and beta-catenin, which are involved in Wnt canonical pathway, showed a 45% and 39% reduction in mRNA levels, respectively.
60	20574838	PLC, CaMKII, DVL, and JNK, which are involved in Wnt non-canonical pathway, showed no reduction.
61	20688898	Wnt/beta-catenin signaling in T-cell immunity and cancer immunotherapy.
62	20705860	Activation of beta-catenin in dendritic cells regulates immunity versus tolerance in the intestine.
63	20705860	We report here that the Wnt-beta-catenin signaling in intestinal dendritic cells regulates the balance between inflammatory versus regulatory responses in the gut. beta-catenin in intestinal dendritic cells was required for the expression of anti-inflammatory mediators such as retinoic acid-metabolizing enzymes, interleukin-10, and transforming growth factor-beta, and the stimulation of regulatory T cell induction while suppressing inflammatory effector T cells.
64	20705860	Furthermore, ablation of beta-catenin expression in DCs enhanced inflammatory responses and disease in a mouse model of inflammatory bowel disease.
65	20705860	Thus, beta-catenin signaling programs DCs to a tolerogenic state, limiting the inflammatory response.
66	20705860	Activation of beta-catenin in dendritic cells regulates immunity versus tolerance in the intestine.
67	20705860	We report here that the Wnt-beta-catenin signaling in intestinal dendritic cells regulates the balance between inflammatory versus regulatory responses in the gut. beta-catenin in intestinal dendritic cells was required for the expression of anti-inflammatory mediators such as retinoic acid-metabolizing enzymes, interleukin-10, and transforming growth factor-beta, and the stimulation of regulatory T cell induction while suppressing inflammatory effector T cells.
68	20705860	Furthermore, ablation of beta-catenin expression in DCs enhanced inflammatory responses and disease in a mouse model of inflammatory bowel disease.
69	20705860	Thus, beta-catenin signaling programs DCs to a tolerogenic state, limiting the inflammatory response.
70	20705860	Activation of beta-catenin in dendritic cells regulates immunity versus tolerance in the intestine.
71	20705860	We report here that the Wnt-beta-catenin signaling in intestinal dendritic cells regulates the balance between inflammatory versus regulatory responses in the gut. beta-catenin in intestinal dendritic cells was required for the expression of anti-inflammatory mediators such as retinoic acid-metabolizing enzymes, interleukin-10, and transforming growth factor-beta, and the stimulation of regulatory T cell induction while suppressing inflammatory effector T cells.
72	20705860	Furthermore, ablation of beta-catenin expression in DCs enhanced inflammatory responses and disease in a mouse model of inflammatory bowel disease.
73	20705860	Thus, beta-catenin signaling programs DCs to a tolerogenic state, limiting the inflammatory response.
74	20705860	Activation of beta-catenin in dendritic cells regulates immunity versus tolerance in the intestine.
75	20705860	We report here that the Wnt-beta-catenin signaling in intestinal dendritic cells regulates the balance between inflammatory versus regulatory responses in the gut. beta-catenin in intestinal dendritic cells was required for the expression of anti-inflammatory mediators such as retinoic acid-metabolizing enzymes, interleukin-10, and transforming growth factor-beta, and the stimulation of regulatory T cell induction while suppressing inflammatory effector T cells.
76	20705860	Furthermore, ablation of beta-catenin expression in DCs enhanced inflammatory responses and disease in a mouse model of inflammatory bowel disease.
77	20705860	Thus, beta-catenin signaling programs DCs to a tolerogenic state, limiting the inflammatory response.
78	22843095	Potential targets of future therapy may include osteoprotegerin, RANK ligand, cathepsins and also the Wnt-β-catenin pathway.
79	22930493	Genetic studies have provided the opportunity to determine which proteins link vitamin D to PD pathology, e.g., Nurr1 gene, toll-like receptor, gene related to lipid disorders, vascular endothelial factor, tyrosine hydroxylase, and angiogenin.
80	22930493	Vitamin D also exerts its effects on cancer through nongenomic factors, e.g., bacillus Calmette-Guerin vaccination, interleukin-10, Wntβ-catenin signaling pathways, mitogen-activated protein kinase pathways, and the reduced form of the nicotinamide adenine dinucleotide phosphate.
81	23071285	p27(Kip1) negatively regulates the magnitude and persistence of CD4 T cell memory.
82	23071285	Our studies ascribe a novel role for the cell cycle regulator p27(Kip1) as a prominent negative regulator of the establishment and long-term maintenance of Th1 CD4 T cell memory.
83	23071285	We demonstrate that p27(Kip1) might restrict the differentiation and survival of memory precursors by increasing the T-bet/Bcl-6 ratio in effector CD4 T cells.
84	23071285	By promoting apoptosis and contraction of effector CD4 T cells by mechanisms that are at least in part T cell intrinsic, p27(Kip1) markedly limits the abundance of memory CD4 T cells.
85	23071285	Furthermore, we causally link p27(Kip1)-dependent apoptosis to the decay of CD4 T cell memory, possibly by repressing the expression of γ-chain receptors and the downstream effector of the Wnt/β-catenin signaling pathway, Tcf-1.
86	23071285	We extend these findings by showing that the antagonistic effects of p27(Kip1) on CD4 T cell memory require its cyclin-dependent kinase-binding domain.
87	23071285	Collectively, these findings provide key insights into the mechanisms underlying the governance of peripheral CD4 T cell homeostasis and identify p27(Kip1) as a target to enhance vaccine-induced CD4 T cell memory.
88	23633115	We further investigated several MUC1-related molecules of the β-catenin pathway, and found that the expression of MUC1 decreased the translocation of β-catenin into the nucleus, reduced the activity of T cell factor (TCF) and blocked the expression of cyclin D1 and c-Myc.
89	23958949	Here, we report that patients with melanoma receiving DD immediately before a dendritic cell (DC) vaccine failed to develop a tumor-antigen-specific CD4 and CD8 T-cell immune response even after repeated vaccinations.
90	23958949	First, DD modulated DCs toward tolerance by downregulating costimulatory receptors such as CD83 and CD25 while upregulating tolerance-associated proteins/pathways including Stat-3, β-catenin, and class II transactivator-dependent antigen presentation.
91	24023259	B16 melanoma-bearing mice, when vaccinated with DC-targeting anti-DEC-205 mAb fused with tumor antigens, exhibited dampened CD8⁺ immunity, similar to DC-β-catenin(active) mice.
92	24728077	PD-1/B7-H1 is an important inhibitory axis in the tumor microenvironment.
93	24728077	We observed that using anti-PD-1 antibody and a multipeptide vaccine (consisting of immunogenic peptides derived from breast cancer antigens, neu, legumain, and β-catenin) as a combination therapy regimen for the treatment of breast cancer-bearing mice prolonged the vaccine-induced progression-free survival period.
94	24728077	This prolonged survival was associated with increase in number of Tc1 and Tc2 CD8 T cells with memory precursor phenotype, CD27+IL-7RhiT-betlo, and decrease in number of PD-1+ dendritic cells (DC) in regressing tumors and enhanced antigen reactivity of tumor-infiltrating CD8 T cells.
95	24728077	It was also observed that blockade of PD-1 on tumor DCs enhanced IL-7R expression on CD8 T cells.
96	24728077	Taken together, our results suggest that PD-1 blockade enhances breast cancer vaccine efficacy by altering both CD8 T cell and DC components of the tumor microenvironment.
97	24967879	Among others, we found several genes related to the canonical Wnt/beta-catenin signaling pathway.
98	25066861	Thus 5T4 expression is mechanistically associated with the directional movement of cells through epithelial mesenchymal transition, facilitation of CXCL12/CXCR4 chemotaxis, blocking of canonical Wnt/beta-catenin while favouring non-canonical pathway signalling.
99	25730849	β-Catenin in dendritic cells exerts opposite functions in cross-priming and maintenance of CD8+ T cells through regulation of IL-10.
100	25730849	Recent studies have demonstrated that β-catenin in DCs serves as a key mediator in promoting both CD4(+) and CD8(+) T-cell tolerance, although how β-catenin exerts its functions remains incompletely understood.
101	25730849	Here we report that activation of β-catenin in DCs inhibits cross-priming of CD8(+) T cells by up-regulating mTOR-dependent IL-10, suggesting blocking β-catenin/mTOR/IL-10 signaling as a viable approach to augment CD8(+) T-cell immunity.
102	25730849	Further studies revealed that DC-β-catenin(-/-) mice were deficient in generating CD8(+) T-cell immunity despite normal clonal expansion, likely due to impaired IL-10 production by β-catenin(-/-) DCs.
103	25730849	Deletion of β-catenin in DCs or blocking IL-10 after clonal expansion similarly led to reduced CD8(+) T cells, suggesting that β-catenin in DCs plays a positive role in CD8(+) T-cell maintenance postclonal expansion through IL-10.
104	25730849	Thus, our study has not only identified mTOR/IL-10 as a previously unidentified mechanism for β-catenin-dependent inhibition of cross-priming, but also uncovered an unexpected positive role that β-catenin plays in maintenance of CD8(+) T cells.
105	25730849	Despite β-catenin's opposite functions in regulating CD8(+) T-cell responses, selectively blocking β-catenin with a pharmacological inhibitor during priming phase augmented DC vaccine-induced CD8(+) T-cell immunity and improved antitumor efficacy, suggesting manipulating β-catenin signaling as a feasible therapeutic strategy to improve DC vaccine efficacy.
106	25730849	β-Catenin in dendritic cells exerts opposite functions in cross-priming and maintenance of CD8+ T cells through regulation of IL-10.
107	25730849	Recent studies have demonstrated that β-catenin in DCs serves as a key mediator in promoting both CD4(+) and CD8(+) T-cell tolerance, although how β-catenin exerts its functions remains incompletely understood.
108	25730849	Here we report that activation of β-catenin in DCs inhibits cross-priming of CD8(+) T cells by up-regulating mTOR-dependent IL-10, suggesting blocking β-catenin/mTOR/IL-10 signaling as a viable approach to augment CD8(+) T-cell immunity.
109	25730849	Further studies revealed that DC-β-catenin(-/-) mice were deficient in generating CD8(+) T-cell immunity despite normal clonal expansion, likely due to impaired IL-10 production by β-catenin(-/-) DCs.
110	25730849	Deletion of β-catenin in DCs or blocking IL-10 after clonal expansion similarly led to reduced CD8(+) T cells, suggesting that β-catenin in DCs plays a positive role in CD8(+) T-cell maintenance postclonal expansion through IL-10.
111	25730849	Thus, our study has not only identified mTOR/IL-10 as a previously unidentified mechanism for β-catenin-dependent inhibition of cross-priming, but also uncovered an unexpected positive role that β-catenin plays in maintenance of CD8(+) T cells.
112	25730849	Despite β-catenin's opposite functions in regulating CD8(+) T-cell responses, selectively blocking β-catenin with a pharmacological inhibitor during priming phase augmented DC vaccine-induced CD8(+) T-cell immunity and improved antitumor efficacy, suggesting manipulating β-catenin signaling as a feasible therapeutic strategy to improve DC vaccine efficacy.
113	25730849	β-Catenin in dendritic cells exerts opposite functions in cross-priming and maintenance of CD8+ T cells through regulation of IL-10.
114	25730849	Recent studies have demonstrated that β-catenin in DCs serves as a key mediator in promoting both CD4(+) and CD8(+) T-cell tolerance, although how β-catenin exerts its functions remains incompletely understood.
115	25730849	Here we report that activation of β-catenin in DCs inhibits cross-priming of CD8(+) T cells by up-regulating mTOR-dependent IL-10, suggesting blocking β-catenin/mTOR/IL-10 signaling as a viable approach to augment CD8(+) T-cell immunity.
116	25730849	Further studies revealed that DC-β-catenin(-/-) mice were deficient in generating CD8(+) T-cell immunity despite normal clonal expansion, likely due to impaired IL-10 production by β-catenin(-/-) DCs.
117	25730849	Deletion of β-catenin in DCs or blocking IL-10 after clonal expansion similarly led to reduced CD8(+) T cells, suggesting that β-catenin in DCs plays a positive role in CD8(+) T-cell maintenance postclonal expansion through IL-10.
118	25730849	Thus, our study has not only identified mTOR/IL-10 as a previously unidentified mechanism for β-catenin-dependent inhibition of cross-priming, but also uncovered an unexpected positive role that β-catenin plays in maintenance of CD8(+) T cells.
119	25730849	Despite β-catenin's opposite functions in regulating CD8(+) T-cell responses, selectively blocking β-catenin with a pharmacological inhibitor during priming phase augmented DC vaccine-induced CD8(+) T-cell immunity and improved antitumor efficacy, suggesting manipulating β-catenin signaling as a feasible therapeutic strategy to improve DC vaccine efficacy.
120	25730849	β-Catenin in dendritic cells exerts opposite functions in cross-priming and maintenance of CD8+ T cells through regulation of IL-10.
121	25730849	Recent studies have demonstrated that β-catenin in DCs serves as a key mediator in promoting both CD4(+) and CD8(+) T-cell tolerance, although how β-catenin exerts its functions remains incompletely understood.
122	25730849	Here we report that activation of β-catenin in DCs inhibits cross-priming of CD8(+) T cells by up-regulating mTOR-dependent IL-10, suggesting blocking β-catenin/mTOR/IL-10 signaling as a viable approach to augment CD8(+) T-cell immunity.
123	25730849	Further studies revealed that DC-β-catenin(-/-) mice were deficient in generating CD8(+) T-cell immunity despite normal clonal expansion, likely due to impaired IL-10 production by β-catenin(-/-) DCs.
124	25730849	Deletion of β-catenin in DCs or blocking IL-10 after clonal expansion similarly led to reduced CD8(+) T cells, suggesting that β-catenin in DCs plays a positive role in CD8(+) T-cell maintenance postclonal expansion through IL-10.
125	25730849	Thus, our study has not only identified mTOR/IL-10 as a previously unidentified mechanism for β-catenin-dependent inhibition of cross-priming, but also uncovered an unexpected positive role that β-catenin plays in maintenance of CD8(+) T cells.
126	25730849	Despite β-catenin's opposite functions in regulating CD8(+) T-cell responses, selectively blocking β-catenin with a pharmacological inhibitor during priming phase augmented DC vaccine-induced CD8(+) T-cell immunity and improved antitumor efficacy, suggesting manipulating β-catenin signaling as a feasible therapeutic strategy to improve DC vaccine efficacy.
127	25730849	β-Catenin in dendritic cells exerts opposite functions in cross-priming and maintenance of CD8+ T cells through regulation of IL-10.
128	25730849	Recent studies have demonstrated that β-catenin in DCs serves as a key mediator in promoting both CD4(+) and CD8(+) T-cell tolerance, although how β-catenin exerts its functions remains incompletely understood.
129	25730849	Here we report that activation of β-catenin in DCs inhibits cross-priming of CD8(+) T cells by up-regulating mTOR-dependent IL-10, suggesting blocking β-catenin/mTOR/IL-10 signaling as a viable approach to augment CD8(+) T-cell immunity.
130	25730849	Further studies revealed that DC-β-catenin(-/-) mice were deficient in generating CD8(+) T-cell immunity despite normal clonal expansion, likely due to impaired IL-10 production by β-catenin(-/-) DCs.
131	25730849	Deletion of β-catenin in DCs or blocking IL-10 after clonal expansion similarly led to reduced CD8(+) T cells, suggesting that β-catenin in DCs plays a positive role in CD8(+) T-cell maintenance postclonal expansion through IL-10.
132	25730849	Thus, our study has not only identified mTOR/IL-10 as a previously unidentified mechanism for β-catenin-dependent inhibition of cross-priming, but also uncovered an unexpected positive role that β-catenin plays in maintenance of CD8(+) T cells.
133	25730849	Despite β-catenin's opposite functions in regulating CD8(+) T-cell responses, selectively blocking β-catenin with a pharmacological inhibitor during priming phase augmented DC vaccine-induced CD8(+) T-cell immunity and improved antitumor efficacy, suggesting manipulating β-catenin signaling as a feasible therapeutic strategy to improve DC vaccine efficacy.
134	25730849	β-Catenin in dendritic cells exerts opposite functions in cross-priming and maintenance of CD8+ T cells through regulation of IL-10.
135	25730849	Recent studies have demonstrated that β-catenin in DCs serves as a key mediator in promoting both CD4(+) and CD8(+) T-cell tolerance, although how β-catenin exerts its functions remains incompletely understood.
136	25730849	Here we report that activation of β-catenin in DCs inhibits cross-priming of CD8(+) T cells by up-regulating mTOR-dependent IL-10, suggesting blocking β-catenin/mTOR/IL-10 signaling as a viable approach to augment CD8(+) T-cell immunity.
137	25730849	Further studies revealed that DC-β-catenin(-/-) mice were deficient in generating CD8(+) T-cell immunity despite normal clonal expansion, likely due to impaired IL-10 production by β-catenin(-/-) DCs.
138	25730849	Deletion of β-catenin in DCs or blocking IL-10 after clonal expansion similarly led to reduced CD8(+) T cells, suggesting that β-catenin in DCs plays a positive role in CD8(+) T-cell maintenance postclonal expansion through IL-10.
139	25730849	Thus, our study has not only identified mTOR/IL-10 as a previously unidentified mechanism for β-catenin-dependent inhibition of cross-priming, but also uncovered an unexpected positive role that β-catenin plays in maintenance of CD8(+) T cells.
140	25730849	Despite β-catenin's opposite functions in regulating CD8(+) T-cell responses, selectively blocking β-catenin with a pharmacological inhibitor during priming phase augmented DC vaccine-induced CD8(+) T-cell immunity and improved antitumor efficacy, suggesting manipulating β-catenin signaling as a feasible therapeutic strategy to improve DC vaccine efficacy.
141	25730849	β-Catenin in dendritic cells exerts opposite functions in cross-priming and maintenance of CD8+ T cells through regulation of IL-10.
142	25730849	Recent studies have demonstrated that β-catenin in DCs serves as a key mediator in promoting both CD4(+) and CD8(+) T-cell tolerance, although how β-catenin exerts its functions remains incompletely understood.
143	25730849	Here we report that activation of β-catenin in DCs inhibits cross-priming of CD8(+) T cells by up-regulating mTOR-dependent IL-10, suggesting blocking β-catenin/mTOR/IL-10 signaling as a viable approach to augment CD8(+) T-cell immunity.
144	25730849	Further studies revealed that DC-β-catenin(-/-) mice were deficient in generating CD8(+) T-cell immunity despite normal clonal expansion, likely due to impaired IL-10 production by β-catenin(-/-) DCs.
145	25730849	Deletion of β-catenin in DCs or blocking IL-10 after clonal expansion similarly led to reduced CD8(+) T cells, suggesting that β-catenin in DCs plays a positive role in CD8(+) T-cell maintenance postclonal expansion through IL-10.
146	25730849	Thus, our study has not only identified mTOR/IL-10 as a previously unidentified mechanism for β-catenin-dependent inhibition of cross-priming, but also uncovered an unexpected positive role that β-catenin plays in maintenance of CD8(+) T cells.
147	25730849	Despite β-catenin's opposite functions in regulating CD8(+) T-cell responses, selectively blocking β-catenin with a pharmacological inhibitor during priming phase augmented DC vaccine-induced CD8(+) T-cell immunity and improved antitumor efficacy, suggesting manipulating β-catenin signaling as a feasible therapeutic strategy to improve DC vaccine efficacy.
148	26343197	This review provides an appraisal of some of the key signaling pathways that may contribute to immune suppression in ovarian cancer, with a particular focus on the potential involvement of the c-KIT/PI3K/AKT, wnt/β-catenin, IL-6/STAT3 and AhR signaling pathways in regulation of indoleamine 2,3-dioxygenase expression in tumor-associated macrophages.
149	26391398	Ac2PIM-responsive miR-150 and miR-143 target receptor-interacting protein kinase 2 and transforming growth factor beta-activated kinase 1 to suppress NOD2-induced immunomodulators.
150	26391398	While Ac2PIM treatment of macrophages compromised their ability to induce NOD2-dependent immunomodulators like cyclooxygenase (COX)-2, suppressor of cytokine signaling (SOCS)-3, and matrix metalloproteinase (MMP)-9, no change in the NOD2-responsive NO, TNF-α, VEGF-A, and IL-12 levels was observed.
151	26391398	Further, genome-wide microRNA expression profiling identified Ac2PIM-responsive miR-150 and miR-143 to target NOD2 signaling adaptors, RIP2 and TAK1, respectively.
152	26391398	Interestingly, Ac2PIM was found to activate the SRC-FAK-PYK2-CREB cascade via TLR2 to recruit CBP/P300 at the promoters of miR-150 and miR-143 and epigenetically induce their expression.
153	26391398	Loss-of-function studies utilizing specific miRNA inhibitors establish that Ac2PIM, via the miRNAs, abrogate NOD2-induced PI3K-PKCδ-MAPK pathway to suppress β-catenin-mediated expression of COX-2, SOCS-3, and MMP-9.
154	26474975	The Al content of femora and serum, bone histological structure, bone mineral density (BMD) of the distal and proximal femoral metaphysis and Wnt/β-catenin signaling pathway (the mRNA expressions of Wnt3a, Fzd2, LRP-5, β-catenin, Tcf4, cyclin D1 and c-Myc, the protein levels of Wnt3a and β-catenin, the activities of Fzd2 and LRP-5) in rat femora were determined on day 30, 60, 90 or 120, respectively.
155	26474975	The results showed that the Al contents of femora and serum were increased, the BMD of the distal and proximal femoral metaphysis were decreased, the femora histological structure were disrupted, the mRNA expressions of Wnt3a, Fzd2, LRP-5, β-catenin, Tcf4, cyclin D1 and c-Myc, the protein levels of Wnt3a and β-catenin, the activities of Fzd2 and LRP-5 were all decreased in the treatment group compared with the control group with time prolonged.
156	26474975	The Al content of femora and serum, bone histological structure, bone mineral density (BMD) of the distal and proximal femoral metaphysis and Wnt/β-catenin signaling pathway (the mRNA expressions of Wnt3a, Fzd2, LRP-5, β-catenin, Tcf4, cyclin D1 and c-Myc, the protein levels of Wnt3a and β-catenin, the activities of Fzd2 and LRP-5) in rat femora were determined on day 30, 60, 90 or 120, respectively.
157	26474975	The results showed that the Al contents of femora and serum were increased, the BMD of the distal and proximal femoral metaphysis were decreased, the femora histological structure were disrupted, the mRNA expressions of Wnt3a, Fzd2, LRP-5, β-catenin, Tcf4, cyclin D1 and c-Myc, the protein levels of Wnt3a and β-catenin, the activities of Fzd2 and LRP-5 were all decreased in the treatment group compared with the control group with time prolonged.