Chemotherapeutics altering DNA topology evoke RNA polymerase I inhibition, rDNA damage and consequent formation of PNAs that segregate persistent rDNA lesions from the active nucleolus, with implications for rDNA maintenance and design of new cancer treatment strategies targeting rDNA repair.

Aurora A kinase, an anti-cancer drug target, can be activated by two independent mechanisms.

Plasticity arising from autocatalytic receptor activation coexists with robustness in ligand responsiveness only by differential endosomal sorting of spontaneous and ligand-activated EGFR as distinct molecular states.

In potassium-dependent NTPases, insertion of the activating potassium ion into the active site leads to rotation of the gamma-phosphate yielding a near-eclipsed, catalytically productive conformation of the triphosphate chain.

Disruption of epoxide hydrolysis inducing oxidative stress and cellular senescence is a novel mechanism responsible for lipoatrophic monogenic diabetes.

Two cancer related proteins, tyrosine phosphatase PTPRK and ubiquitin ligase ZNRF3, interact to downregulate Wnt receptors, thereby regulating Spemann organizer function during Xenopus development.

Depletion of PHF19 in prostate cancer cells leads to an increase in MTF2 and PRC2 chromatin occupancy causing deregulation of key genes critical for proliferation and metastasis.

Single-cell transcriptomic profiling and systematic analysis of pulmonary neuroendocrine cells identifies over 40 hormones and neuropeptides expressed in myriad combinations, and predicts their targets in mouse and human lung, revealing extraordinary sensory and signaling diversity and potential physiological functions.

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

Transcription factors downstream of Hippo signaling control formation of the Left-Right Organizer by regulating major signaling pathways, expression of transcription factors and regulators of epigenetic programming involved in this process.