Gene interactions and pathways from curated databases and text-mining

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REL — TNF

Pathways - manually collected, often from reviews:

Text-mined interactions from Literome

Martin et al., J Biol Chem 2000 : Thus, TNFalpha induced phosphorylation of Ser-471 seems to be absolutely necessary for TNFalpha activation of c-Rel
Kang et al., J Pharmacol Exp Ther 2002 : Silymarin also inhibited tumor necrosis factor-alpha induced NF-kappaB/Rel activation , whereas okadaic acid induced NF-kappaB/Rel activation was not affected
Kang et al., FEBS Lett 2003 : Moreover, silymarin suppressed the TNF-alpha induced DNA binding of NF-kappaB/Rel in HUVECs
Morello et al., J Immunol 2006 : IL-1beta and TNF-alpha rapidly activated p50 and p65, but not C-Rel , RelB, or p52, and both IL-1beta- and TNF-alpha stimulated A2AR expression was inhibited by the IkappaB kinase 2 inhibitor AS602868 in a concentration dependent manner
Wang et al., J Biol Chem 2007 (Thrombosis) : By electrophoretic mobility shift assay analyses, TNF-alpha and lipopolysaccharide induce strong p65/p50 and p65/c-Rel heterodimer binding to both NF-kappaB and TF-kappaB probes
Jahnke et al., FEBS Lett 1994 (Melanoma) : Synergistic activation of intercellular adhesion molecule 1 ( ICAM-1 ) by TNF-alpha and IFN-gamma is mediated by p65/p50 and p65/c-Rel and interferon-responsive factor Stat1 alpha ( p91 ) that can be activated by both IFN-gamma and IFN-alpha
Beg et al., Oncogene 1994 : Activation of multiple NF-kappa B/Rel DNA binding complexes by tumor necrosis factor
Jahnke et al., Immunobiology 1995 (Melanoma) : Using electrophoretic mobility shift assays and specific antibodies we observed that the NF-kappa B like sequence at -187 bound both p65/p50 and p65/c-Rel in the presence of TNF-alpha , while the interferon responsive region at -75 bound Stat1 alpha ( p91 )
Kochetkova et al., J Clin Invest 1997 (Leukemia, Myelomonocytic, Chronic) : The constitutive and TNFalpha induced NF-kappaB/Rel complexes were identical and were composed mainly of p50 and c-Rel proteins ... These results indicate that the aberrant, constitutive GM-CSF gene activation in JMML is maintained by TNFalpha mediated activation of NF-kappaB/Rel proteins
Tobin et al., Proc Natl Acad Sci U S A 1998 : Therefore, UVB induced activation of Rel proteins via TNF receptor 1, independent of ligand activation, is a key component in the UV response in keratinocytes