IndraLab

"TABLE 1. Cytokine/chemokines, their receptors, and functions."

"TABLE 1. Cytokine/chemokines, their receptors, and functions."

"The results support the following pathway, whereby TNF-alpha enhances expression of ICAM-1 in NHBE cells: TNF-alpha --> TNF-RI --> PC-PLC --> DAG --> PKC --> (NF-kappaB?) --> ICAM-1 mRNA --> ICAM-1 surface expression."

"After being processed by such metalloproteinases as TNF-a-converting enzyme (TACE) between residues alanine76 and valine77, the soluble form of TNF-a of 157 amino acid residues (17 kDa) is released and mediates its biological activities through Type 1 and 2 TNF receptors (TNF-R1 also known as TNFRSF1A, CD120a and TNF-R2 also known as"

"Fig. 4. Both cIAP1 and 2 are recruited to TNF-R1 upon TNFa treatment and are required for Rip1 polyubiquitination."

"Consistent with the in vivo findings, p75 blockade resulted in significant reduction of TNF-induced VCAM-1 and E-selectin expression by 28 and 23%, respectively (P < 0.05), but had no significant effect on ICAM-1 (Fig. 4A). On the other hand, as with in vivo experiments, p55 blockade significantly decreased the expression of all adhesion molecules"

"To investigate whether either or both TNF receptors control the expression of these cell adhesion molecules, HUVEC were stimulated from 0 to 10 h with human TNF-a binding to both receptor types, and with receptor type-specific agonists. The specific activation of TNF-R55 was achieved using three independent reagents: first the agonistic mAb htr-1, second the RaTNF-K55 agonistic antibodies, and third a recombinant mutant of human TNF-a, 32W/S86T-TNF-a (Trp32 Thr86 TNF), which binds exclusively to TNF-K55. TNF-R75 activation was achieved with RaTNF-R75 agonistic antibodies."

"he binding of TNF to the cell surface receptor TNF-R1 causes the recruitment of the adapter protein TRADD to the cytoplasmic domain of the receptor. TRADD then serves to recruit additional signaling molecules, including FADD, TRAF2, and RIP1 (Chen and Goeddel 2002)."

"he binding of TNF to the cell surface receptor TNF-R1 causes the recruitment of the adapter protein TRADD to the cytoplasmic domain of the receptor. TRADD then serves to recruit additional signaling molecules, including FADD, TRAF2, and RIP1 (Chen and Goeddel 2002)."

"To determine the cytotoxic effects and the type of cell death facilitated by TNF in A549 cells, we treated cells with TNF and analyzed cell death based on morphological and biochemical assays. The death rate of A549 cells increased with increasing concentration of TNF (Fig. 1b), and cell death was characterized by cytoplasmic condensation and pyknotic nuclei without apoptotic body formation (Fig. 1c). Dose-dependent release of LDH into the culture medium was also noted (Fig. 1d); this is frequently encountered after necrotic cell death due to rupture of the cell membrane....Thus, TNF triggers necrotic rather than apoptotic cell death in A549 cells."

"Because RIP1 and TRAF2 are downstream effectors of the TNF receptor, it is possible that MNNG induces TNF through RIP1 and TRAF2 to trigger cell death. To investigate this possibility, we examined the sensitivity of TNFR1-/- MEF cells to MNNG treatment and found that it is comparable with that of WT MEF cells (Fig. 6c). As expected, TNFR1-/- MEF cells are resistant to TNF-induced cell death (Fig. 6c). These results exclude the possibility that RIP1 and TRAF2 function in the TNF signaling pathway in MNNG-treated cells."

"To determine the cytotoxic effects and the type of cell death facilitated by TNF in A549 cells, we treated cells with TNF and analyzed cell death based on morphological and biochemical assays. The death rate of A549 cells increased with increasing concentration of TNF (Fig. 1b), and cell death was characterized by cytoplasmic condensation and pyknotic nuclei without apoptotic body formation (Fig. 1c). Dose-dependent release of LDH into the culture medium was also noted (Fig. 1d); this is frequently encountered after necrotic cell death due to rupture of the cell membrane....Thus, TNF triggers necrotic rather than apoptotic cell death in A549 cells."

"After being processed by such metalloproteinases as TNF-a-converting enzyme (TACE) between residues alanine76 and valine77, the soluble form of TNF-a of 157 amino acid residues (17 kDa) is released and mediates its biological activities through Type 1 and 2 TNF receptors (TNF-R1 also known as TNFRSF1A, CD120a and TNF-R2 also known as"

"The results support the following pathway, whereby TNF-alpha enhances expression of ICAM-1 in NHBE cells: TNF-alpha --> TNF-RI --> PC-PLC --> DAG --> PKC --> (NF-kappaB?) --> ICAM-1 mRNA --> ICAM-1 surface expression."

"To confirm that TNFalpha protein synthesized in the brain of the transgenic animal is biologically active, we quantified expression of TRADD protein. Homogenates of brain sampled from TNFalpha-Tg and non-Tg rats were incubated with a primary antibody that recognizes rat TRADD only after it has been activated through binding of TNFalpha to p55/TNFR1, thereby implying biological activity of the cytokine. Regional expression of TRADD protein was uniformly higher in TNFalpha-Tg rat brain than in non-Tg controls by statistically significant margins."