IndraLab

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Notch decreases the amount of CYLD. 9 / 9
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"Previous studies have reported that the Notch and Hes -1 pathway repressed the expression of CYLD XREF_BIBR, XREF_BIBR, a deubiquitination protease, and that CYLD can regulate the activation of TAK1 XREF_BIBR, XREF_BIBR, which is a member of the mitogen activated protein kinase kinase family."
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"A previous study found that Notch stimulates NF-κB activation by initiating the transcription of Hes1, which then suppresses the expression of CYLD, a negative regulator of IKK activity in T-ALL cells [23]; however, this finding does not rule out the possibility that other mechanisms co-exist."
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"Next, we confirmed that miRNA-9-5p and Thbs-2-induced activation of the Notch pathway can inhibit the expression of CYLD and increase the phosphorylation of TAK1 in neurons, thus promoting activation of ERK and AKT and the expression of synapse proteins."
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"On the other hand, activation of Notch signaling in macrophages led to increased inflammatory cytokine production and NF-kappaB activation and decreased CYLD expression in vitro."
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"In T cell acute lymphoblastic leukemia (T-ALL), CYLD expression is repressed by the Notch and Hes1 pathway to promote persistent IKK activation and cell survival [XREF_BIBR]."
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"Previous reports have demonstrated that Notch signal represses the expression of CYLD that negatively regulates NF-kappaB activation in macrophages XREF_BIBR."
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"The results showed that blockade of Notch signal up-regulated expression of CYLD in BMDMs treated with CM from I/R injured hepatocytes (XREF_FIG)."
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"Furthermore, suppression of Notch signaling by DAPT upregulated Cylindromatosis (CYLD) expression but downregulated TRAF6 expression, IκB kinase (IKK) α/β phosphorylation, and subsequently, phosphorylation and degradation of IκB-α, indicating that DAPT inhibited NF-κB activation triggered by TLR-4."
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"To test whether the Notch pathway and specifically Hes1 was directly repressing CYLD transcription, we used the Genomatix software to identify putative Hes1 binding sites, and found three distinct N-box consensus sites in the promoter and 5 ' UTR of the CYLD transcriptional start site (XREF_FIG, denoted as PRO1 and PRO2)."
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