Activation of Notch receptors by ligands in the same cell (cis-activation) is a prevalent and functional mode of signaling in the Notch pathway, and co-exists with trans-activation and cis-inhibition.

Cis and trans activation of the receptor tyrosine kinase RET lead to similar biological outcomes in rapidly adapting mechanoreceptors in vivo.

The timing and outcome of mammalian cell lineage decisions can be controlled by slow, stochastic events on individual regulatory gene loci.

CRISPR knock-outs and functional genomic approaches probe the regulatory mechanism restricting the Hox gene Ubx to butterfly hindwings, explaining color pattern differentiation from forewings.

DNA motifs tuned for low affinity binding of BMP-induced pMad/Medea transcription factors function to restrict gene activation to small subsets of the many Drosophila neurons that exhibit active BMP signaling.

Silencers and enhancers targeted by a common transcription factor in photoreceptors are distinguished by the number and diversity of binding transcription factor binding sites they contain.

Analysis of a variant without lysine in the intracellular domain reveals a ubiquitylation-independent signalling activity of the DSL ligand Delta and novel functions of the Neuralized and Mindbomb1 E3-ligases during Notch signalling.

Differences in the flexible linkers connecting the kinase domain to an oligomeric hub modulate CaMKII activity by changing the balance between activating and inhibitory autophosphorylation.

Notch ligands expressed in the same cell as the Notch receptor are crucial to prevent accidental, ligand-independent Notch activity.

Understanding protein kinase regulation by activation loop autophosphorylation depends on a critical assessment of experimental design, execution, and interpretation.