Gene interactions and pathways from curated databases and text-mining

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SLC2A4 — TNF

Pathways - manually collected, often from reviews:

  • OpenBEL Selventa BEL large corpus: SLC2A4 → TNF (decreases)
    Evidence: Furthermore, TNF-? induces lipolysis and down-regulates IRS-1 and the insulin sensitive glucose transporter (GLUT)-4

Text-mined interactions from Literome

Rachdaoui et al., Am J Physiol Endocrinol Metab 2003 : Taken together, these results suggest that TNF-alpha induced desensitization of endothelin-1 stimulated GLUT4 translocation and glucose uptake in 3T3-L1 adipocytes is due, at least in part, to a decreased expression of Galphaq/11, leading to a suppression in tyrosine phosphorylation of PYK2
Ferrier et al., Diabetologia 2004 (Obesity) : In contrast, exercise training did not significantly change TNF-alpha protein expression, but GLUT4 protein expression increased by 105 +/- 37 % ( p < 0.05 )
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
Nishiumi et al., Toxicological sciences : an official journal of the Society of Toxicology 2010 (Insulin Resistance) : Anti-TNF-alpha neutralization antibody and silencing of TNF-alpha receptor 1 (TNFR1) diminished the TCDD induced downregulation of IRbeta, IRS1, and GLUT4 ... Taken together, TCDD stimulates expression and secretion of TNF-alpha in adipocytes through activation of AhR, ERK1/2, and JNK, and the secreted TNF-alpha causes the downregulation of IRbeta, IRS1, and GLUT4 through TNFR1, resulting in insulin resistance
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
Stephens et al., J Biol Chem 1997 (Insulin Resistance) : These results are consistent with earlier studies indicating that TNF-alpha reduces the transcriptional activity of the GLUT4 gene in murine adipocytes, and reduced mRNA transcription of a number of relevant genes may be the general mechanism by which TNF-alpha causes insulin resistance in adipocytes