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Short peptides that bind tightly to anti-apoptotic protein Bfl-1 but not other Bcl-2 family members provide a tool for diagnosing cancer cell survival mechanisms and a lead for developing new therapeutics.

Skin inflammation in Sharpin-deficient mice is primarily due to TNFR1-dependent apoptosis, but necroptosis appears to play a bigger role in inflammation of internal organs.

In postnatal retina, neuronal apoptosis promotes a spectrum of microglial transcriptional states with varied dependence on CSF1R; TAM receptor Mer and complement receptor 3 mediate phagocytosis of dying neurons while altered CSF1R dependence requires Axl.

During ES cell differentiation, Yap1 directly regulates apoptosis-related genes like Bcl-2 and Mcl-1 to attenuate apoptosis and promote cell survival to allow for successful cell fate changes.

Cleavage of pannexin-1 channel by caspases facilitates the loss of intracellular ATP level and attenuates glycolytic metabolism of apoptotic cells.

SIMR-1 acts downstream of the piRNA pathway to promote siRNA amplification by the Mutator complex and localizes to perinuclear foci distinct from Mutator foci, P granules and Z granules.

ATR/Chk1 contribute to G2 arrest in developing tracheoblasts, and arrest in G2 facilitates cellular and hypertrophic organ growth.

In vitro analyses reveal how vertical DNA transmission from the mother to the pre-implantation embryo via endometrial extracellular vesicles can impact embryo bioenergetics.

A phosphorylation of receptor interacting RIPK3 switches its pro-necroptosis function to apoptosis that promotes luteal regression which induced by Prostaglandin F2alpha.

A biomechanical approach inducing confined cell migration reveals that mechanical stress has a profound effect on cancer cell survival.