COPII vesicles regulate the metabolism of cholesterol through the selective transport of secretory proteins.

Nutrient limitation elicits differential responses in cells lacking the tumor suppressor PTEN and in normal cells, resulting in hyperplastic overgrowth of PTEN mutant tissue independent of additional mutations.

A protein called Megf8 regulates the activity of key signaling molecules involved in the development of the peripheral nervous system.

In individuals with a missing hand, the area of the brain that would otherwise control that hand is recruited by either the remaining hand or the residual limb, depending on the usage preference of the individual.

Genetic studies in mice identify the transcription factor MafB as a potent regulator of specific features of the synapses underlying hearing.

Mutations in CHD7, which cause CHARGE syndrome, cause a reduction in FGF8 signalling and subsequent abnormalities in the cerebellar vermis in both mice and humans.

The ribosomal protein, Rps27l, plays an oncogenic role by promoting p53 degradation via stabilizing the Mdm2-Mdm4 complex, but a tumor suppressor role by preventing the aneuploidy and loss of p53 heterozygosity.

Differentiation-specific maintenance of genome integrity during S-phase is essential for establishing both the structure and function of the cerebral cortex.

Multipotent cardiac precursors within a population of mesoderm are rapidly fated to specific anatomic locations in the developing mouse heart.

Post-phosphoryl modification of α-dystroglycan requires the glucuronyltransferase B4GAT1; this enzyme synthesizes the acceptor glycan that serves as a primer for the glycosyltransferase LARGE to synthesize the laminin-binding glycan.