Na Zhang

TL;DR: The protein kinase receptor-interacting protein 3 (RIP3) was identified as a molecular switch between TNF-induced apoptosis and necrosis in NIH 3T3 cells and found that RIP3 was required for necrosisin other cells.

TL;DR: It is suggested that a full complement of actin is required for transduction of a cell death signal to mitochondria in TNF-treated L929 cells, indicating that actin-deficiency-mediated TNF resistance is most likely due to impaired mitochondrial responses to TNF stimulation.

TL;DR: LIP is a common denominator of ferritin both in the enhancement of cell death by basal steady-state H-ferritin and in protection againstcell death by induced H- Ferritin, thereby acting as a key determinant of TNF-induced cell death.

TL;DR: It is found that nuclear import, but not export, determines the subcellular localization of p38α-PRAK and p38β-PraK complexes, and the location of PRAK plays a role in its function.

TL;DR: A quantitative MS based analysis was performed to compare TNF‐induced changes in the global phosphoproteome of wild‐type (RIP3+/+) and RIP3‐knockdown L929 cells at different time points after TNF treatment, revealing 174, 167, and 177 distinct phosphorylation sites were revealed to be dependent on RIP3 at the 0.5, 2, and 4 h time points afterwards.