Hypermethylation of the tumor necrosis factor receptor superfamily 6 (APT1, Fas, CD95/Apo-1) gene promoter at rel/nuclear factor κB sites in prostatic carcinoma

2001 ◽  
Vol 32 (1) ◽  
pp. 36-43 ◽  
Author(s):  
Simon Santourlidis ◽  
Ulrich Warskulat ◽  
Andrea R. Florl ◽  
Simone Maas ◽  
Thomas Pulte ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Prostatic Carcinoma ◽  
Tumor Necrosis Factor Receptor ◽  
Gene Promoter ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Necrosis Factor

scholarly journals The Human Toll Signaling Pathway: Divergence of Nuclear Factor κB and JNK/SAPK Activation Upstream of Tumor Necrosis Factor Receptor–associated Factor 6 (TRAF6)

1998 ◽  
Vol 187 (12) ◽  
pp. 2097-2101 ◽  
Author(s):  
Marta Muzio ◽  
Gioacchino Natoli ◽  
Simona Saccani ◽  
Massimo Levrero ◽  
Alberto Mantovani
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Interleukin 1 ◽  
Tumor Necrosis Factor Receptor ◽  
Nuclear Factor Κb ◽  
Dominant Negative ◽  
Nuclear Factor ◽  
Kinase C ◽  
Toll Signaling ◽  
Necrosis Factor

The human homologue of Drosophila Toll (hToll) is a recently cloned receptor of the interleukin 1 receptor (IL-1R) superfamily, and has been implicated in the activation of adaptive immunity. Signaling by hToll is shown to occur through sequential recruitment of the adapter molecule MyD88 and the IL-1R–associated kinase. Tumor necrosis factor receptor–activated factor 6 (TRAF6) and the nuclear factor κB (NF-κB)–inducing kinase (NIK) are both involved in subsequent steps of NF-κB activation. Conversely, a dominant negative version of TRAF6 failed to block hToll-induced activation of stress-activated protein kinase/c-Jun NH2-terminal kinases, thus suggesting an early divergence of the two pathways.

Sign in / Sign up

Export Citation Format

Share Document