Disease relevance of Cebpb

• LAP (NF-IL-6), a tissue-specific transcriptional activator, is an inhibitor of hepatoma cell proliferation [1].
• Induction of interleukin (IL)-6 by hypoxia is mediated by nuclear factor (NF)-kappa B and NF-IL6 in cardiac myocytes [2].
• NF-IL6, a less potent transactivator, attenuates NF-kappa B mediated transcription late in the evolution of the acute-phase response [3].

High impact information on Cebpb

• Expression of the liver-enriched transcriptional activator protein DBP follows a stringent circadian rhythm [4].
• The liver-enriched transcriptional activator protein DBP accumulates in hepatocytes of adult rats according to a strictly controlled circadian rhythm [4].
• Here we show that consolidation but not reconsolidation of inhibitory avoidance memory requires the expression of the transcription factor CCAAT enhancer binding protein beta (C/EBPbeta) in the hippocampus [5].
• Protein kinase A and C site-specific phosphorylations of LAP (NF-IL6) modulate its binding affinity to DNA recognition elements [6].
• Here we demonstrate that CCAAT enhancer binding protein beta (C/EBPbeta) is induced by 1,25(OH)(2)D(3) in kidney and in osteoblastic cells and is a potent enhancer of vitamin D receptor (VDR)-mediated 24(OH)ase transcription [7].

Biological context of Cebpb

• AF-2-dependent potentiation of CCAAT enhancer binding protein beta-mediated transcriptional activation by glucocorticoid receptor [8].
• Both c-Jun and CRE binding protein (CREB) bound to the CRE, while C/EBP-beta bound to NF-IL-6 [9].
• Deletion and mutational analysis identified critical nuclear factor (NF)-kB and NF-IL-6 binding sites required for NO regulation of MIP-2 [10].
• A computer homology search for a 1.5-kb promoter region showed that there are several consensus cis DNA elements such as C/EBP, NF-IL6, and AP-1 in this region [11].
• Downregulation of the CCAAT-enhancer binding protein beta in deltaFosB transgenic mice and by electroconvulsive seizures [12].

Anatomical context of Cebpb

• The induction of RANTES expression by JEV infection in glial cells needed the coordinate activation of NF-kappaB and NF-IL-6 [13].
• These results indicate that NF-IL6 inactivation could be the major determinant for the suppression of NO production by baicalein in microglia [14].

Associations of Cebpb with chemical compounds

• Cyclic GMP-dependent protein kinase regulates CCAAT enhancer-binding protein beta functions through inhibition of glycogen synthase kinase-3 [15].
• A nuclear factor for interleukin-6 expression (NF-IL6) and the glucocorticoid receptor synergistically activate transcription of the rat alpha 1-acid glycoprotein gene via direct protein-protein interaction [16].
• Herbimycin A suppressed NF-kappaB but not NF-IL6 [17].
• SF-B that binds to a negative element in glutathione transferase P gene is similar or identical to trans-activator LAP/IL6-DBP [18].

Regulatory relationships of Cebpb

• Altogether, these results demonstrated that infection of glial cells by JEV provided the early ERK-, NF-kappaB-, and NF-IL-6-mediated signals that directly activated RANTES expression, which might be involved in the initiation and amplification of inflammatory responses in the CNS [13].

Other interactions of Cebpb

• This effect is mediated by activation of the CT-1 gene promoter and requires the transcription factor C/EBPbeta/NF-IL6 [19].
• However, JEV replication was not dependent on the activation of ERK, NF-kappaB, and NF-IL-6 [13].
• Since stress activates NF-kappaB and NF-IL6, we examined that the effect of herbimycin A, which suppresses CINC mRNA expression, on NF-kappaB and NF-IL6 activation [17].
• One of these elements contains a consensus binding site for the liver-enriched transcription factor hepatocyte nuclear factor-1 alpha, while the other is a consensus binding site for the liver-specific factors D-binding protein and liver-enriched transcriptional activator protein [20].
• The 5'-flanking region of AT2-R contained several cis-regulatory elements, such as AP-1, AP-2, C/EBP, NF-1, NF-IL6, NF-kappa B, and glucocorticoid- and cAMP-responsive elements (CRE) [21].

Analytical, diagnostic and therapeutic context of Cebpb

• Electrophoretic mobility shift assays were performed using oligonucleotides containing the binding site for NF-kappa B or NF-IL6 as a probe [2].

References