TNF-α treatment induces phosphorylation and cytoplasmic translocation of the retinoblastoma protein, which regulates cytoskeletal organization in skeletal muscle cells.

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.

An adult stem-cell lineage terminally differentiates via recruitment of the RETINOBLASTOMA-RELATED protein by a lineage specific transcription factor.

CDKG1 is a D-cyclin dependent retinoblastoma related protein kinase whose abundance scales with cell size and controls cell division cycle number during multiple fission.

The SCF-family of ubiquitin ligases regulates the key cancer proliferation node by controlling the degradation of RB-like tumor suppressor RBL2/p130.

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.

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

During tumorigenesis loss of p53 not only abrogates cell cycle arrest and apoptosis, but also suppresses the induction of replication-stress-induced DNA double-stranded breaks.

Tailoring Boolean models to 488 prostate cancer patients and 8 cell lines data allows for the experimentally validated personalisation of drug treatments.