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Overexpression of BAG2—a novel mutant p53 binding protein—in tumors inhibits MDM2-mediated mutant p53 degradation, which leads to the accumulation of mutant p53 protein and promotes tumorigenesis.

Mitochondrial flashes counteract the imbalance of ATP supply-and-demand and constitute an auto-regulator of ATP homeostasis in the heart.

Alternative splicing of multiple apoptotic genes is enhanced by CD28 costimulation to promote cell survival.

The nuclear protein Sam68 plays a role in the genotoxic stress-initiated "nuclear to cytoplasmic" activation of NF-κB and is involved in the development and survival of colon cancer.

Arginine methylation regulates mRNA translation of key protooncogenes via an RGG/RG motif-containing protein called Aven.

PPM1D-mutant leukemia cells exhibit a dysregulated redox landscape, a diminished response to oxidative stress, and rely on SOD1 for their survival.

The RNA-binding protein polypyrimidine tract-binding protein 1 (PTBP1) is essential for B cell development at the pro-B cell stage where it suppresses S-phase entry and promotes progression through mitosis.

CD4 lineage commitment requires HDAC3 to prevent premature upregulation of CD8 lineage genes during T cell development.

Building on previous work (Fu et al., 2016), we demonstrate the critical role of Sam68 in orchestrating genotoxic stress-initiated NF-κB signaling in the colon and the pathophysiological relevance of Sam68-dependent NF-κB activation in colonic cell survival/recovery from extrinsic DNA damage.

The new cancer treatment strategy reduces the volume of mouse cutaneous squamous cell carcinoma and reverses the expression of tumor marker proteins by stimulating the production of serum-based antibodies.