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An actin-based Brownian Ratchet enables branched actin networks to generate pushing forces, while a capping protein-based Brownian Ratchet provides force feedback that enables these networks to adapt their architecture in response to changing loads.

Yap interacts with Rif1, a major DNA replication timing factor, and functions as a brake to control the DNA replication program in Xenopus early embryos and post-embryonic stem cells.

Experiments using purified proteins reveal how the network of filaments that underlie cell movement becomes denser when pushing against a stronger mechanical force.

Transcriptomic and bionergetic analysis shows the importance of HIF-1α activation in enabling tissue-resident alveolar macrophages to perform glycolytic metabolism, which prevents their death and attenuates influenza A virus-induced acute lung injury.

Prokaryotic and eukaryotic flagella follow a common trend in swimming cost-effectiveness, but eukaryotic flagella are too large for cells with prokaryote volumes, yielding insight into flagellar dissimilarity between taxa.

Combining particle tracking in living cells with statistical analysis demonstrates how the oligomeric organization of cell surface receptor influences their function, a necessary step in the development of drugs targeting specific receptor conformation.

Pathogenic mutations in KIF22, which dominantly cause bone dysplasia, improperly activate the motor during anaphase in dividing cells leading to chromosome recongression.

In response to proteotoxic stress, squamous cell carcinoma cells hijack the integrated stress response to promote recovery by bolstering protection of microtubule dynamics.

Discovery of how cells couple addition of membranes with insertion of nuclear pore complexes to form and grow the nucleus.

In the absence of centrioles, components of pericentriolar material can self-organize into a single compact microtubule-organizing center through dynein-mediated transport of pericentrin-containing protein complexes if CAMSAP- and Golgi-mediated pathways of microtubule minus-end stabilization and anchoring are disabled.