TRADD-TRAF2 and TRADD-FADD interactions define two distinct TNF receptor 1 signal transduction pathways

Article Abstract:

Tumor necrosis factor (TNF) can either induce apoptosis or activate the NF-kappaB transcription factor depending on which signal tranducer the TNF receptor 1 (TNFR1)-associated signal transducer TRADD, interacts with. If TRADD interacts with TRAF2, TNF follows the apoptosis pathway. If TRADD interacts with FADD, the NF-kappaB transcription pathway is activated. Thus the signals emanating from the TNFR1-TRADD signaling complex divides at the TRADD portion.

Gene expression, Cell interaction, Cell interactions

---

Involvement of MACH, a novel MORT1/FADD-interacting protease, in Fas/APO-1- and TNF receptor-induced cell death

Article Abstract:

A new protein, MACH, has exhibited binding activity with the MORT1/FADD system. The expression of MACH in conjunction with the activation of the Fas/APO-1 p55 tumor necrosis factor(TNF)receptor (p-55R) results in cell death. Analysis of several of the MACH isoforms has shown that the protein is the highest enzymatic component in the cell death signaling process in the Fas/APO-1 -p55R signaling system.

Usage, Proteins, Tumor necrosis factor

---

Similar abstracts:

• Abstracts: A requirement for NF-protocadherin and TAF1/Set in cell adhesion and neural tube formation. The mouse Ovol2 gene is required for cranial neural tube development
• Abstracts: Determinants of regulated proteolysis in signal transduction. Crystal structure of the DegS stress sensor: how a PDZ domain recognizes misfolded protein and activates a protease
• Abstracts: Genetic association of apolipoprotein E with age-related macular degeneration. A critical appraisal of the scientific basis of commercial genomic profiles used to assess health risks and personalize health interventions
• Abstracts: The RAG1 and RAG2 proteins establish the 12/23 rule in V(D)J recombination. Initiation of V(D)J recombination in a cell-free system
• Abstracts: Cytokine rescue of p53-dependent apoptosis and cell cycle arrest is mediated by distinct Jak kinase signaling pathways

This website is not affiliated with document authors or copyright owners. This page is provided for informational purposes only. Unintentional errors are possible.