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.

Notch signaling controls the collective migration of parapineal cells through its capacity to restrict FGF pathway activation to a few leading cells.

Digital NF-κB signaling achieves orthogonal control over the probability of activation (percentage of activated cells) and dynamic response heterogeneity in the population via the area and shape of the input profile.

Mutational inactivation of the JNK signaling pathway causes genomic instability and breast cancer development.

ERK activation during induction of long-term synaptic plasticity is enhanced by synergistic interactions among signaling pathways mediated by the synaptically located GTPase-activating protein, and each pathway contributes to different ERK temporal dynamics.

Imaging of single cells within a cell population shows the correlation between subcellular accumulation of β-catenin and the transcriptional activation of a target gene.

Hedgehog-pathway activation in adjacent epithelial and stromal cells, but not in epithelial or stromal cells alone, enables the generation of functional de novo hair follicles in unwounded adult mouse skin.

Neuronal reactivation during dopamine modulation induces input-specific LTP at previously primed hippocampal synapses, suggesting a possible solution to the credit assignment problem and a mechanism for memory linking.

Interleukin 4 signaling co-opts the Akt-mTORC1-Acly pathway to couple metabolic input to the control of energetically demanding processes during macrophage M2 activation.

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.