Nature Structural & Molecular Biology, Published online: 28 September 2026; doi:10.1038/s41594-026-01871-yLu and Du et al. show that HERC4 E3 ligase ubiquitinates S166-phosphorylated RIPK1 to initiate prodeath complex assembly and TNF-induced cell death, acting as the pivotal prodeath switch and that loss of HERC4 protects mice from TNF-driven inflammation and liver injury.

Nature Structural & Molecular Biology, Published online: 28 September 2026; doi:10.1038/s41594-026-01871-yLu and Du et al. show that HERC4 E3 ligase ubiquitinates S166-phosphorylated RIPK1 to initiate prodeath complex assembly and TNF-induced cell death, acting as the pivotal prodeath switch and that loss of HERC4 protects mice from TNF-driven inflammation and liver injury.

And of course, Texas is appealing.

YouTube video by MeidasTouch

Vitamins are essential micronutrients traditionally viewed as passive cofactors that sustain cellular homeostasis. Emerging evidence challenges this notion, identifying vitamins as active regulators of cell fate that tune the threshold for regulated cell death. Through coordinated control of redox balance, metabolic pathways, and signaling networks, vitamins shape cellular susceptibility to diverse death programs. Their effects are highly context-dependent, enabling both prosurvival and prodeath outcomes depending on dose, cell type, and metabolic state. Recent studies further uncover noncanonical mechanisms linking vitamins to lipid remodeling, membrane trafficking, and organelle integrity. Collectively, these advances establish vitamins as dynamic modulators of cellular vulnerability and highlight their potential as therapeutic targets for selectively manipulating cell death in disease.

This cross-sectional study assesses the association of state-level abortion bans with spontaneous abortion management and receipt of mifepristone plus misoprostol among commercially insured individual...