Impaired apoptosis is both critical in cancer development and a major barrier to effective
treatment. In response to diverse intracellular damage signals, including those evoked by�…

Unicellular organisms respond to the presence of DNA lesions by activating cell cycle
checkpoint and repair mechanisms, while multicellular animals have acquired the further�…

The Bcl-2 family proteins are key regulators of apoptosis in human diseases and cancers.
Though known to block apoptosis, Bcl-2 promotes cell death through an undefined�…

Background—Endothelial dysfunction and injury are thought to play an important role in the
progression of coronary artery disease (CAD). High-density lipoprotein from healthy subjects�…

Trophic factor deprivation (TFD) activates c-Jun N-terminal kinases (JNKs), culminating in
coordinate AP1-dependent transactivation of the BH3-only BCL-2 proteins BIM EL and HRK�…

A paradox for the cancer biology field has been the revelation that oncogenes, once thought
to simply provide advantages to a cancer cell, actually put it at dire risk of cell suicide. Myc is�…

Post-translational modifications (PTMs) dramatically enhance the capabilities of proteins.
They introduce new functionalities and dynamically control protein activity by modulating�…

The tumor suppressor p53 exerts its versatile function to maintain the genomic integrity of a
cell, and the life of cancerous cells with DNA damage is often terminated by induction of�…

Apoptosis is a critical process for the maintenance of tissue homeostasis and prevention of
tumorigenesis. The members of the Bcl-2 family of proteins are the central regulators of the�…

It is assumed that the survival factors Bcl-2 and Bcl-xL are mainly functional on mitochondria
and therefore must contain mitochondrial targeting sequences. Here we show, however, that�…