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Interaction IDMol ATypeSpeciesVerbNatureMol BTypeSpecies
4039CEBPBProteinHomo sapiens-eIncreases activityindirectIL1BDNAHomo sapiens-e
NF-IL6 (C/EBPbeta ) vigorously activates il1b gene expression via a Spi-1 (PU.1) protein-protein tether. / We now show that these two factors strongly cooperate on the il1b core promoter (-59/+12) in the absence of direct NF-IL6 binding to DNA.
Structure
Regulator
27628IL1BProteinHomo sapiens-eIncreases phosphorylationindirectMAPTProteinHomo sapiens-e
When such activated microglia were placed in coculture with primary neocortical neurons, a significant increase in the phosphorylation of neuronal tau was accompanied by a decline in synaptophysin levels. Similar effects were evoked by treatment of neurons with recombinant IL-1beta.
Disease
27629IL1BProteinHomo sapiens-eDecreases expressionindirectSYPProteinHomo sapiens-e
When such activated microglia were placed in coculture with primary neocortical neurons, a significant increase in the phosphorylation of neuronal tau was accompanied by a decline in synaptophysin levels. Similar effects were evoked by treatment of neurons with recombinant IL-1beta.
Disease
56392TNFProteinHomo sapiens-eIncreases expressionindirectIL1BProteinHomo sapiens-e
Our data shows that transfection of DCs with recombinant adenovirus AdV-TNF-alpha resulted in greater maturation of the DCs than occurred with control DCs cultured in exogenous TNF-alpha, as determined by up-regulated expression of pro-inflammatory cytokines (e.g. interleukins 1beta and 18), chemokines [e.g. interferon-gamma-inducible protein-10 and macrophage inflammatory protein-1beta (MIP-1beta)], the CC chemokine receptor CCR7, and immunologically important cell surface molecules (CD40, CD86 and intercellular adhesion molecule-1).
Disease
66181IL1BProteinHomo sapiens-eIncreases expressionindirectIl1r1RNAMus musculus
Using RT-PCR, we first showed that the expression of IL-1RI and IL-1RII, but not IL-1RacP, mRNAs are up-regulated by IL-1 beta in a time-dependent manner.
77527IL1BProteinHomo sapiens-eDecreases expressionindirectMt3RNARattus norvegicus
Among interleukin-1beta (IL-1beta), fibroblast growth factor-2, epidermal growth factor (EGF), amyloid beta1-42, and 50% O2, only EGF and IL-1beta altered the level of GIF in confluent astrocytes: EGF increased both GIF mRNA and protein, and IL-1beta decreased GIF mRNA, but did not alter GIF protein.
Disease
103171IL1BProteinHomo sapiens-eDecreases expressionindirectPPARGProteinHomo sapiens
RT-PCR and Western blot analysis revealed that PPARgamma expression was decreased by IL-1beta.
Disease
119200IL1BProteinHomo sapiens-eIncreases activityindirectMap2k4ProteinRattus norvegicus
Furthermore, our experiments confirm that IL-1beta activates MAP kinase kinase-4 (MKK4)/SEK1, MKK3, and MKK6 in renal mesangial cells.
128308IL1BProteinHomo sapiens-eIncreases expressionindirectCCL2ProteinHomo sapiens
The findings presented herein demonstrate that both human astroglioma cell lines and primary human astrocytes express the CXC chemokines IP-10 and IL-8 and the CC chemokines MCP-1 and RANTES in response to TNF-alpha and IL-1beta.
191595IL1BProteinHomo sapiens-eIncreases degradationindirectNfkbiaProteinRattus norvegicus
Transient nuclear factor kappaB (NF-kappaB) activation stimulated by interleukin-1beta may be partly dependent on proteasome activity, but not phosphorylation and ubiquitination of the IkappaBalpha molecule, in C6 glioma cells. Regulation of NF-kappaB linked to chemokine production. / Nascent IkappaBalpha began to degrade 5 min after treatment with IL-1beta and disappeared completely after 15 min.
202568IL1BProteinHomo sapiens-eBinddirectIl1r1ProteinRattus norvegicus
In the present study, the role of IL-1 receptor binding sites in the regulation of NGF release was evaluated by determining the pharmacological properties of astroglially localized IL-1 receptors, and, by comparing the effects of both the agonists (IL-1 alpha and IL-1 beta) and the antagonist (IL-1ra)-members of the IL-1 family on NGF secretion from rat neonatal cortical astrocytes in primary culture. / IL-1 receptor agonists IL-1 alpha (K(i) of 341.1 pM) and IL-1 beta (K(i) 59.9 pM), as well as the antagonist IL-1ra (K(i) 257.6 pM), displaced specific [(125)I] IL-1 beta binding from cultured astrocytes in a monophasic manner. / We concluded that IL-1 beta-induced NGF secretion from cultured rat cortical astrocytes is mediated by functional type I IL-1 receptors, whereas IL-1 alpha and IL-1ra, in spite of their affinity for IL-1RI, have no effect on NGF secretion from these cells.
232091IL1BProteinHomo sapiens-eIncreases expressionindirectTNFAIP2RNAHomo sapiens
We utilized cDNA representational difference analysis to identify the genes in which expression is induced by the proinflammatory cytokines tumor necrosis factor-alpha and interleukin-1beta in primary human bronchial epithelial cells and hence are relevant to airway inflammation. Hybridization of the subtraction product to arrayed cDNAs indicated that known tumor necrosis factor-alpha- and interleukin-1beta-inducible genes such as B94, Zfp36, and regulated on activation normal T cell expressed and secreted were represented, confirming the success of the subtraction experiment.
421528NF-kappa-BProteinRattus norvegicusIncreases expressiondirectIl1bProteinRattus norvegicus
Chronic ethanol intake induces brain damage, although the mechanisms involved in this effect are not well understood. / We used cerebral cortex from control and chronic ethanol-fed rats, which received ethanol-liquid diet for 5 months and cultured of astrocytes exposed to 75 mM ethanol for 7 days. Our results demonstrate that chronic ethanol treatment up-regulates iNOS, COX-2 and IL-1beta in rat cerebral cortex and in cultured astrocytes. Under both experimental conditions, up-regulation of these inflammatory mediators and IL-1RI concomitantly occurs with the stimulation of IRAK and MAP kinases, including ERK1/2, p-38 and JNK, which trigger the downstream activation of oxidant-sensitive transcription factors NF-KB and AP-1.
Regulator
422289IL1BProteinHomo sapiens-eIncreases activityindirectActivator protein 1ProteinHomo sapiens
The present study was undertaken to investigate the mechanism of expression of inducible nitric oxide synthase (iNOS) in human primary astrocytes. / All three cytokines alone induced the activation of AP-1 while IL-1beta and TNF-alpha but not IFN-gamma induced the activation of NF-kappaB. / Consistently, JNK-I, a specific inhibitor of JNK, inhibited IL-1beta-mediated activation of AP-1 and expression of iNOS.
422297IL1BProteinHomo sapiens-eIncreases activityindirectCEBPBProteinHomo sapiens
The present study was undertaken to investigate the mechanism of expression of inducible nitric oxide synthase (iNOS) in human primary astrocytes. / However, among the three cytokines, only IL-1beta was capable of inducing the activation of CCAAT/enhancer-binding proteinbeta (C/EBPbeta), suggesting an essential role of C/EBPbeta in the expression of iNOS in astrocytes.

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