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Tnf  -  tumor necrosis factor

Mus musculus

Synonyms: Cachectin, DIF, TNF alpha, TNF-a, TNF-alpha, ...
 
 
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Disease relevance of Tnf

 

Psychiatry related information on Tnf

 

High impact information on Tnf

 

Chemical compound and disease context of Tnf

 

Biological context of Tnf

 

Genetic context of TNF

 

 

 

Anatomical context of Tnf

 

Associations of Tnf with chemical compounds

  • Tumor-necrosis factor (TNF), a pleiotropic cytokine, triggers physiological and pathological responses in several organs [29].
  • Tpl2 knockout mice produce low levels of TNF-alpha when exposed to lipopolysaccharide (LPS) and they are resistant to LPS/D-Galactosamine-induced pathology [26].
  • These effects of TNF-alpha and IL-1 on target cells may contribute to their reported protective activity against radiation as well as their ability to induce resistance to cell killing induced by the combination of TNF-alpha and cycloheximide [27].
  • In a dose-dependent manner, PGE2 inhibits LPS-induced release of TNF-alpha and IL-6, but not of lactate or nitric oxide [30].
  • Tartrate-resistant acid phosphatase-positive osteoclasts were also formed when M-BMM phi were further cultured for 3 d with mouse tumor necrosis factor alpha (TNF-alpha) in the presence of M-CSF [31].
  • By the use of HIF-1-deficient cells and by obliterating NF-kappaB activation, it was determined that the hypoxic TACE response is mediated by HIF-1 signaling, whereas the regulation by TNFalpha also requires NF-kappaB activation [32].
  • Activation of the protein kinase C pathway by treatment with phorbol ester, which has been shown previously to result in CUGBP1 phosphorylation, also causes TNF mRNA stabilization [33].
  • PDTC accelerated death and aggravated liver apoptosis in the GalN/LPS model, although it reduced nitric oxide production, attenuated glutathione depletion, and inhibited the expression of TNF-alpha in liver [34].
  • CcO isolated after TNFalpha treatment showed tyrosine phosphorylation on CcO catalytic subunit I and was approximately 50 and 70% inhibited at high cytochrome c concentrations in the presence of allosteric activator ADP and inhibitor ATP, respectively [35].
  • Accordingly, c-Flip(L/S) protein levels were elevated in livers of TNFalpha-tolerant mice, which correlated to a switch from JNK and ERK to p38 signaling after galactosamine/TNF re-challenge [36].
  • In BDL mice, cardiac mRNA and protein expression of NFkappaBp65, p38MAPK, iNOS, NOx, anandamide, and plasma TNFa were increased, whereas glutathione, Cu/Zn-SOD, and Mn-SOD were decreased [37].
 

Physical interactions of Tnf

  • Following its induction, TNFalpha gene transcription is rapidly attenuated, in part due to the accumulation of NF-kappaB p50 homodimers that bind to three kappaB sites in the TNFalpha promoter [38].
  • Furthermore, RA inhibited activator protein-1 binding to 12-O-tetradecanoylphorbol 13-acetate-response element (TRE) in the cells treated with TNF-alpha, suggesting that RA acts as a potent negative regulator for activator protein-1 binding activity to TRE in the osteoblastic cells [39].
  • We also found that LPL caused the nuclear migration of one member of the NFkB family that appears to bind to a site in the murine TNF alpha gene promoter [40].
  • Expression and purification of recombinant tristetraprolin that can bind to tumor necrosis factor-alpha mRNA and serve as a substrate for mitogen-activated protein kinases [41].
  • It efficiently antagonizes the effect of TNF-alpha binding to the TNF receptor (I) [42].
  • Using chromatin immunoprecipitation assays, we demonstrated that treatment of adipocytes with TNFalpha led to increased binding of NFkappaB p50, and decreased binding of p65 and Sp1, to this region of the apoE promoter in living cells [43].
 

Enzymatic interactions of Tnf

  • Jo2 and, to a lesser extent, TNF-alpha phosphorylate Akt [44].
  • Collectively, these findings suggest that pp130 and pp95 are constitutively associated with CD120a (p55) and become inducibly phosphorylated in macrophages in response to TNFalpha [45].
  • Both the insulin receptor and IRS-1 are tyrosine-phosphorylated to the same extent in response to acute insulin stimulation following cellular TNF-alpha exposure [46].
  • Western blot analyses showed significantly increased levels of TNF-alpha (1.8-fold) and phosphorylated-SAPK/JNK1/2 (1.5-fold) in transgenic hearts [47].
  • Here we demonstrate that Ser311 accounts for zetaPKC phosphorylation of RelA and that this site is phosphorylated in vivo in response to TNF-alpha [48].
 

Co-localisations of Tnf

 

Regulatory relationships of Tnf

 

Other interactions of Tnf

 

Analytical, diagnostic and therapeutic context of Tnf

References

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