Cleavage of a membrane-bound transcription factor by the chemotherapeutic reagent doxorubicin can block the proliferation of tumor cells.

By using immune cells called dendritic cells to deliver drugs, it is possible to target and kill specific members of another class of immune cell, known as T cells, and to prevent these cells from attacking the body's own tissues in cases of autoimmune disease.

A transmembrane protein uses distinct mechanisms to regulate the movement of specific toll-like receptors-key immune system components involved in detecting pathogens-to their final locations inside cells.

The receptor EBI2 is essential for correctly positioning CD4+ dendritic cells in the spleen so that they can present blood-borne antigens to T cells and thereby provoke an antibody response.

Lysine-specific demethylase 1 (Lsd1) has an essential role during both the early and later stages of blood cell development.

The proteins Bax and Bak, which increase the permeability of the mitochondrial membrane during apoptosis, are also crucial for generating a mitochondrial membrane pore that is specifically involved in necrosis.

While intact mir-17-92 acts as a potent oncogene in a mouse model of Burkitt’s lymphoma, one of the six mir-17-92 components antagonizes its oncogenic cooperation with c-Myc by promoting c-Myc-induced apoptosis.

Mechanisms that enable wild mice to survive infection with strains of the Toxoplasma gondii parasite virulent enough to kill laboratory mice offer an explanation for how these parasites have been able to persist in the mouse population.

The cancer drug vemurafenib has potent off-target effects on JNK signaling that contribute to the development of squamous cell carcinomas in humans and in mice.

A CO₂ receptor and a mechanism for the CO₂-mediated opening of gap junction hemichannels have been identified.