The retinoblastoma tumor suppressor regulates cell cycle progression when it's in 14 mono-phosphorylated isoforms.

Two related DNA replication initiation proteins contribute to the decision of whether to enter a new round of the cell division cycle or enter into a period of proliferative quiescence.

PHF13 interacts with transcriptional complexes containing RNA polymerase II to recruit/stabilize them at H3K4me2/3 containing active or bivalent promoters.

Lin37 is essential for cell-cycle gene repression by the DREAM complex in cellular quiescence and a combined loss of Lin37 and Rb prevents cell-cycle exit in response to growth-limiting signals.

Biochemical and cell biological data suggest a model of nascent integrin adhesion complex formation based on synergistic phase separation of pathways surrounding the focal adhesion kinase (FAK) and the adaptor protein p130Cas.

Molecular, cellular, and computational analyses reveal key insights into PP2A/B55α's mechanisms of substrate recruitment and active site engagement, and facilitate identification/validation of new substrates, a step towards understanding PP2A/B55α's role in multiple cellular processes.

Isotope tracing, mathematical modeling, and single-cell ATP analysis reveal changes in blood cell metabolism under various conditions, showing stressed hematopoietic stem cells support hematopoiesis through glycolytic ATP production via PFKFB3.

Endogenous laminins are necessary to build a functional acinus via generating NO, activating p53, HOXD10 and other positive players, but tumor cells neither make laminin nor generate NO, unless they are reverted to an organized structure.

NHE1-CaM complexes of multiple stoichiometries regulate cellular Ca²⁺-dependent NHE1 activity and can contribute to NHE1 dimerization, the latter shown by the NMR structure of CaM linking two NHE1 cytosolic tails.