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A single point mutation in a Ras activator leads to aberrant constitutive mTOR signaling in peripheral T cells that consequently accumulate as abnormal T helper cells and stimulate the production of autoantibodies by B cells.

No single molecular change is uniquely necessary to cause neuropathic changes in primary afferent excitability; multiple different changes are sufficient.

The repair of spontaneous DNA damage can introduce mutators that lead to further genetic changes, which could underlie evolutionary change, disease and aging.

A mouse model of atopic dermatitis provides mechanistic evidence for an association between allergic disease and skin cancer.

IL-6 signaling in T cells controls how sensitive they are to suppression by T regulatory cells, and the way mature to become memory T cells.

In addition to its cytoplasmic role for translation, the seryl-tRNA synthetase also antagonizes the c-Myc transcription factor in the nucleus to transcriptionally repress the growth factor VEGFA and ensure proper development of the vasculature in vertebrates.

Rapid acquisition of chromosome rearrangements, together with independently acting transmission distorter alleles on each chromosome, drive near complete sterility in fission yeast hybrids.

A new computational model of the Warburg Effect reveals that the rate-limiting step of glycolysis is variable, identifies new control mechanisms, and could help to predict the responses to targeting glycolysis to treat cancer.

Serum amyloid A proteins bind retinol with nanomolar affinity, and do so by forming oligomers that create a hydrophobic pocket that shields retinol from the aqueous environment.

A comprehensive catalogue of somatic mutations accumulating in MMR-deficient tumors highlights their relevance in the context of human genetic evolution, for the diagnosis of microsatellite instability and the provision of targeted treatment options.