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CEBPA — TNF

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: CEBPA → TNF (decreases, TNF Activity)
  Evidence: expression of TNF-a suppresses the transcription factor C/EBP-a, which in turn activates the GLUT4 gene. TNF-a also suppresses the expression of PPARG. Gene ablation of TNF-a or the TNF-a receptor leads to improved insulin sensitivity in rodents.
• OpenBEL Selventa BEL large corpus: CEBPA → TNF (increases, TNF Activity)
  Evidence: Modified assertion

Text-mined interactions from Literome

Alaaeddine et al., Arthritis Rheum 1999 (Osteoarthritis) : IL-4 and IL-13 decreased the TNFa induced C/EBP accumulation in a dose dependent manner, while IL-10 up-regulated its basal level
Granger et al., Biochim Biophys Acta 2000 (Kidney Diseases) : Both cell-type- and stimulus-specific regulation of C/EBP mRNA expression and DNA binding activity were identified, with C/EBPalpha being induced by LPS, C/EBPbeta by LPS, IL-1, TNF-alpha and C/EBPdelta by LPS, IL-1, IFN-gamma, TNF-alpha and PDGF
Kurebayashi et al., Endocr J 2001 : In fully differentiated adipocytes, TNF-alpha rapidly induced C/EBPbeta and C/EBPdelta, whereas it downregulated the expression of C/EBPalpha and PPARgamma
Liu et al., J Biochem Mol Toxicol 2002 : Based on the knowledge that TNFalpha preferentially affects C/EBPalpha and that TGFbeta specifically controls C/EBPbeta and delta in their antiadipogenic action, we hypothesized that the major cause for the differential response of these two similar cell lines could be the insensitivity of C/EBPbeta and/or delta of F442A cells to the action of TCDD
Stephens et al., J Biol Chem 1992 : Transcriptional repression of the C/EBP-alpha and GLUT4 genes in 3T3-L1 adipocytes by tumor necrosis factor-alpha
Stephens et al., J Biol Chem 1991 : Transcriptional repression of the GLUT4 and C/EBP genes in 3T3-L1 adipocytes by tumor necrosis factor-alpha
Hau et al., Am J Pathol 2013 (Psoriasis) : Visfatin and/or TNF-a enhanced C/EBP transcriptional activity and C/EBPa phosphorylation, which were suppressed by p38 mitogen activated protein kinase ( MAPK ) inhibition
Ohsumi et al., Endocrinology 1994 : Treatment of 3T3-L1 cells with troglitazone ( 1-10 microM ) partially prevented this inhibitory effect of TNF on adipogenesis, and enhanced expression of C/EBP alpha and GLUT4, even in the presence of TNF
Lee et al., J Neuroimmunol 1998 : We determined that binding sites for both NF-kappaB ( -186 bp region ) and C/EBP ( -198 bp region ) are involved in TNF-alpha and IL-1beta mediated ICAM-1 upregulation