TGF-beta1 and PGD2 have a common regulator IL-1beta
TGF-beta1 is regulated by IL-1beta |
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Positive_regulation(C: IL-1beta, T: Protein_catabolism(T: TGF-beta1))
Confidence: High
Interleukin-1beta (IL-1beta), a key-cytokine in osteoarthritis, impairs TGFbeta signaling through TbetaRII down-regulation by increasing its degradation. Described in 2 sentences
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Positive_regulation(C: IL-1beta, T: Localization(T: TGF-beta1))
Confidence: High
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Positive_regulation(C: IL-1beta, T: Gene_expression(T: TGF-beta1))
Confidence: High
CONCLUSIONS: Diltiazem suppressed collagen synthesis of human PMCs and inhibited IL-1beta-induced TGF-beta1 production on human PMCs. Described in 34 sentences
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Positive_regulation(C: IL-1beta, T: Binding(T: AP4, T: TGF-beta1))
Confidence: High
CONCLUSION: IL-1beta induces an increase of TGFbeta1 in articular chondrocytes through activation of AP-4 and AP-1 binding to the TGFbeta1 gene promoter. Described in 1 sentence
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Positive_regulation(C: IL-1beta, T: Binding(T: TGF-beta1, T: c-jun))
Confidence: High
CONCLUSION: IL-1beta induces an increase of TGFbeta1 in articular chondrocytes through activation of AP-4 and AP-1 binding to the TGFbeta1 gene promoter. Described in 1 sentence
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Regulation(C: IL-1beta, T: Binding(T: IL-2, T: TGF-beta1))
Confidence: High
Other cytokines (IL-1, IL-3, IL-4, IL-5, TNF, LT, IFN-gamma, and TGF-beta) had no effect on IL-2 binding, suggesting that IL-6 may mediate the enhanced expression of HIL-2-R. Described in 1 sentence
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Positive_regulation(C: IL-1beta, T: Transcription(T: TGF-beta1))
Confidence: High
NF-kappaB and activator protein 1 response elements and the role of histone modifications in IL-1beta-induced TGF-beta1 gene transcription. Described in 5 sentences
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Positive_regulation(C: Binding(T: IL-1beta), T: Localization(T: TGF-beta1))
Confidence: Average
These results demonstrate that the interaction of D-glucose and IL-1 beta lead to secretion of TGF-beta 1 by HPTC. Described in 1 sentence
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Positive_regulation(C: IL-1beta, T: TGF-beta1)
Confidence: Average
In PANC-1 cells, IL-1beta and TNF-alpha induced a rapid activation of nuclear factor (NF)-kappaB, and TGF-beta1 enhanced this activation slightly. Described in 32 sentences
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Negative_regulation(C: IL-1beta, T: Localization(T: TGF-beta1))
Confidence: Low
Inhibition of TGF-beta(1) activity secreted from PSCs by TGF-beta(1)-neutralizing antibody attenuated IL-1beta secretion from PSCs. Described in 2 sentences
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Regulation(C: IL-1beta, T: Gene_expression(T: TGF-beta1))
Confidence: Low
IL-1beta acts directly on T cells and affects Foxp3 and TGF-beta1 expression in them in a concentration dependent manner Described in 8 sentences
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Regulation(C: IL-1beta, T: Localization(T: TGF-beta1))
Confidence: Low
The question of whether tumor necrosis factor alpha (TNF-alpha) and/or interleukin 1 beta (IL-1 beta) regulate the release of TGF-beta1 was investigated by incubation of adipose tissue explants with a soluble human TNF-alpha receptor (etanercept) and a neutralizing antihuman IL-1 beta antibody. Described in 4 sentences
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Positive_regulation(C: Positive_regulation(T: IL-1beta), T: Localization(T: TGF-beta1))
Confidence: Low
Secretion of IL-6, IL-8, and TNF-alpha, but not TGF-beta1, was increased by IL-1beta stimulation. Described in 1 sentence
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Negative_regulation(C: IL-1beta, T: Gene_expression(T: TGF-beta1))
Confidence: Very low
These observations indicated that IL-1beta and IL-12 can directly act on T cells upon activation and modulate Foxp3+ and TGF-beta1 expression. Described in 9 sentences
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Negative_regulation(C: IL-1beta, T: TGF-beta1)
Confidence: Very low
IL-1beta and its downstream mediator TAK1 inhibit SMAD3-mediated TGFbeta target gene activation, whereas SMAD3 nuclear translocation and DNA binding in response to TGFbeta are not affected. Described in 11 sentences
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Regulation(C: IL-1beta, T: TGF-beta1)
Confidence: Very low
CONCLUSION: In summary, IL-1 has a biphasic effect on PTC TGF beta signalling, with early NF-kappaB-mediated inhibition and delayed sensitization via an autocrine IL-6 loop. Described in 10 sentences
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Negative_regulation(C: Gene_expression(T: IL-1beta), T: Gene_expression(T: TGF-beta1))
Confidence: Very low
Overexpression of TGF-beta1 or IL-1beta increased activated microglia and reduced Abeta load in the brains of AD mouse models [24,27]. Described in 1 sentence
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Positive_regulation(C: Binding(T: IL-1beta), T: TGF-beta1)
Confidence: Very low
Moreover, IL-1beta has been shown to increase TGF-beta1 in articular chondrocytes through the activation of AP-4 and AP-1 binding to the TGF-beta1 gene promoter [72]. Described in 1 sentence
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Regulation(C: IL-1beta, T: Binding(T: IL-1beta, T: TGF-beta1))
Confidence: Very low
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Positive_regulation(C: Positive_regulation(T: IL-1beta), T: Positive_regulation(C: IL-1beta, T: TGF-beta1))
Confidence: Very low
Since substantial cross-talk between pro-inflammatory cytokines IL-1beta, TNF-alpha, IL-6, and IL-17 is essential to induce joint destruction in RA,1 IL-1beta and TNF-alpha promote IL-6 and tumor growth factor-beta (TGF-beta) driven process of Th17 cell commitment and IL-17 production.73 Th17 cell polarization further induces IL-1beta, TNF-alpha, IL-6, IL-8, and IL-17 production (Figure 1).74-77 Numerous studies have also demonstrated the critical role of B-cells in RA pathogenesis. Described in 1 sentence
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Positive_regulation(C: Positive_regulation(T: IL-1beta), T: Positive_regulation(C: TNF-alpha, T: TGF-beta1))
Confidence: Very low
Since substantial cross-talk between pro-inflammatory cytokines IL-1beta, TNF-alpha, IL-6, and IL-17 is essential to induce joint destruction in RA,1 IL-1beta and TNF-alpha promote IL-6 and tumor growth factor-beta (TGF-beta) driven process of Th17 cell commitment and IL-17 production.73 Th17 cell polarization further induces IL-1beta, TNF-alpha, IL-6, IL-8, and IL-17 production (Figure 1).74-77 Numerous studies have also demonstrated the critical role of B-cells in RA pathogenesis. Described in 1 sentence
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PGD2 is regulated by IL-1beta |
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Positive_regulation(C: IL-1beta, T: Transcription(T: PGD2))
Confidence: High
The interleukin-1-beta (IL-1beta)-induced upregulation of lipocalin-type prostaglandin D synthase (L-PGDS) mRNA expression requires de novo protein synthesis. Described in 2 sentences
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Positive_regulation(C: IL-1beta, T: PGD2)
Confidence: Average
These results suggest that the activation of JNK and p38 MAPK as well as NF-kappaB is essential to the induction of L-PGDS by IL-1beta in chondrocytes. Described in 3 sentences
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Regulation(C: IL-1beta, T: Gene_expression(T: PGD2))
Confidence: Low
Effect of interleukin-1-beta (IL-1beta) on lipocalin-type prostaglandin D synthase (L-PGDS) expression in osteoarthritis chondrocytes. Described in 3 sentences
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