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Asymmetrical expression dictates functional dominance of one STAT5 paralog at cellular and tissue levels despite redundancy at molecular and genomic levels.

The loss of p53 in bone cells activates critical signaling pathways; these are also essential in bone cancer.

Skeletal muscle cells constantly monitor their own activity and that of their partner neuron at synapses, enabling them to provide the neuron with feedback regarding neurotransmitter release.

p63 uses an intricate network of domain-domain interactions to control its function in long-term quality maintenance of resting oocytes.

Excess expression of the Gadd45 mRNA accounts for lethality when nonsense-mediated decay is lost in Drosophila and mammalian cells, revealing that this pathway is a critical gene regulatory mechanism.

Mouse models in which hypoxia can be genetically triggered in retinal pigmented epithelial cells show that hypoxia-induced metabolic stress alone can lead to photoreceptor atrophy/dysfunction.

Heterotrimeric G proteins are coupled to and regulate plant receptor signaling, which allows optimum immune activation and enhances the production of reactive oxygen species.

The completion of neural tube closure requires small GTPase-regulated membrane protrusions from non-neural ectoderm cells at the tips of the neural folds.

The ZNRF2 enzyme helps the mTOR protein complex to sense amino acid levels and regulate mammalian cell growth.