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Interaction IDMol ATypeSpeciesVerbNatureMol BTypeSpecies
2239TNFProteinHomo sapiens-eIncreases expressionindirectCebpbProteinMus musculus
In fully differentiated adipocytes, TNF-alpha rapidly induced C/EBPbeta and C/EBPdelta, whereas it downregulated the expression of C/EBPalpha and PPARgamma.
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
88744CEBPBProteinHomo sapiens-eIncreases activitydirectBCL2DNAHomo sapiens-e
Expression of C/EBPalpha increased bcl-2 expression, and two regions of the bcl-2 P2 promoter that mediated this effect were identified. C/EBPbeta was also able to increase bcl-2 promoter activity through these sites. / Decreased expression of C/EBP factors due to targeting of their transcripts by siRNA molecules resulted in downregulation of Bcl-2 protein.
Structure
Disease
115979CEBPBProteinHomo sapiensIncreases expressiondirectCCL2RNAHomo sapiens
RANTES secretion was induced more slowly and was induced mainly by TNF-alpha. / The increase in transcriptional activation of chemokine genes correlated with the NF-kappaB and NF-IL6 activation.
Disease
145576Calcium/calmodulin-dependent protein kinaseFamilyHomo sapiens-eIncreases activitydirectCEBPBProteinHomo sapiens-e
In pituitary cells C/EBP beta was phosphorylated in response to increased intracellular calcium concentrations as a consequence of the activation of a calcium-calmodulin-dependent protein kinase. Phosphorylation of serine at position 276 within the leucine zipper of C/EBP beta appeared to confer calcium-regulated transcriptional stimulation of a promoter that contained binding sites for C/EBP beta.
Structure
145578Calcium/calmodulin-dependent protein kinaseFamilyHomo sapiens-ePhosphorylatedirectCEBPBProteinHomo sapiens-e
In pituitary cells C/EBP beta was phosphorylated in response to increased intracellular calcium concentrations as a consequence of the activation of a calcium-calmodulin-dependent protein kinase. Phosphorylation of serine at position 276 within the leucine zipper of C/EBP beta appeared to confer calcium-regulated transcriptional stimulation of a promoter that contained binding sites for C/EBP beta.
Structure
156878MAPK3ProteinHomo sapiens-eIncreases activitydirectCEBPBProteinHomo sapiens-e
ERK1 and ERK2 activate CCAAAT/enhancer-binding protein-beta-dependent gene transcription in response to interferon-gamma. / We show that ERKs are activated by IFN-gamma to stimulate C/EBP-beta-dependent expression. / Mutant MKK1, its inhibitors, and mutant ERK suppressed IFN-gamma-stimulated gene induction through the gamma-IFN-activated transcriptional element.
Regulator
163428CEBPBProteinHomo sapiens-eIncreases activitydirectPtgs2DNAMus musculus
We investigated the cis-acting elements of the COX-2 5'-flanking sequence, the transcription factors and signaling pathways responsible for transcriptional activation of the COX-2 gene in endotoxin-treated murine RAW 264.7 macrophages. / Overexpression of c-Jun, C/EBPbeta, and C/EBPdelta enhances induction of the COX-2 reporter, while overexpression of cyclic AMP-response element-binding protein or "dominant negative" C/EBPbeta represses COX-2 induction.
Structure
212184MAPK1ProteinHomo sapiensIncreases activitydirectCEBPBProteinHomo sapiens
The present study was undertaken to investigate the effect of the HIV-1 tat gene on the expression of inducible nitric-oxide synthase (iNOS) in human U373MG astroglial cells and primary astroglia. / In addition, we show that extracellular signal-regulated kinase (ERK) but not that p38 mitogen-activated protein kinase (MAPK) is involved in RSV-tat induced production of NO. Interestingly, PD98059, an inhibitor of the ERK pathway, and deltaERK2, a dominant-negative mutant of ERK2, inhibited RSV-tat-induced production of NO through the inhibition of C/EBPbeta but not that of NF-kappaB.
411970CEBPBProteinHomo sapiens-eIncreases activityindirectCCL2DNAHomo sapiens-e
Ectopic expression of any of these transcription factors is sufficient to confer lipopolysaccharide (LPS)-inducible expression of interleukin-6 (IL-6) and monocyte chemoattractant protein-1 (MCP-1) to a B lymphoblast cell line, which normally lacks C/EBP factors and does not display LPS induction of proinflammatory cytokines. / Surprisingly, the bZIP region of C/EBPbeta, which lacks any previously described activation domains, can also confer LPS-inducible expression of IL-6 and MCP-1 in stable transfectants. Transient transfections reveal that the bZIP regions of C/EBPbeta, C/EBPdelta, and, to a lesser extent, C/EBPalpha can activate the IL-6 promoter and augment its induction by LPS. Furthermore, the transdominant inhibitor, LIP, can activate expression from the IL-6 promoter. The ability of the C/EBPbeta bZIP region to activate the IL-6 promoter in transient transfections is completely dependent upon an intact NF-kappaB-binding site, supporting a model where the bZIP protein primarily functions to augment the activity of NF-kappaB.
Structure
Regulator
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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