Micromanipulation experiments demonstrate that HP1α strengthens interphase and mitotic chromosome mechanics and maintains nuclear shape by chromatin crosslinking, separate from histone methylation.

Characterization of an extra-membrane site in I_Ks formed by KCNQ1 S1, Pore and S6 domains and the near extracellular region of KCNE1, which forms a binding pocket for channel activators.

Pair bond induced transcriptional changes in the nucleus accumbens erode after long-term partner separation.

Deep mutational scanning of homologous proteins shows conservation in allosteric mechanisms but differences in molecular details within the protein family.

Rapid depletion of dynein from oocytes yielded new insights into acentrosomal pole organization and also led to the first evidence that the kinesin-5 motor BMK-1 plays a role in microtubule organization during C. elegans meiosis.

Enzyme evolution is reversible on a structural and functional (phenotypic) level, but through a different mutational pathway that leads to genotypic incompatibility with the ancestor.

The generation of phosphoinositide 3,4,5-trisphosphate causes an increase in the number of TRPV1 ion channels and insulin receptors in the plasma membrane.

Structural promiscuity in PURA protein, induced by patient mutations, impacts nucleic acid binding, unwinding, and subcellular localization, indicating why so many patients display the full disease spectrum of PURA syndrome.

Lactate in pancreatic cancer micro-environment can lead to TET enzyme activation and loss of DNA methylation seen in cancer associated fibroblasts.

Real-time imaging of neural activity in behaving mice reveals that the two canonical types of neurons in the olfactory tubercle carry distinct information about learned odor cues, with D1 neurons representing stimulus valence and D2 neurons mainly representing stimulus identity.