The involvement of SETD2 in an important DNA repair pathway could explain the high frequency of SETD2 mutations in several cancers and may provide an alternative mechanism to evade the p53-mediated checkpoint.

Tumor Protein p53 Binding Protein 1 and Ubiquitin Specific Peptidase 28 engage p53 to promote mitotic efficiency.

ATR/Chk1 contribute to G2 arrest in developing tracheoblasts, and arrest in G2 facilitates cellular and hypertrophic organ growth.

Mutation of Glycine 34 to Arginine within the N-terminal tail of histone H3 alters post-translational modifications on Lysine 36 and is associated with a delay in replication restart, defective homologous recombination and an increase in genomic instability.

Arabidopsis deploys the core signalling module that perceives distinct stress signals, such as DNA damage and heat stresses, and represses G2/M-specific genes, thereby causing cell cycle arrest.

SPIN1, a nucleolar protein, plays an oncogenic role by suppressing the tumor suppressor p53's function via regulation of the uL18-MDM2-p53 pathway.

Disruption of TFEB and TFE3 results in diminished p53 signaling capacity and altered cell cycle regulation under genotoxic stress conditions.

The protein p53 negatively impacts the ability of a CRISPR screen to discriminate between essential and non-essential genes, hence, p53 status should be considered in these screens.

The initiation of human genome replication requires the six-subunit origin recognition complex (ORC) and CDC6, with ORC playing additional roles during mitosis and in organization of the cell nucleus.

Selective APC/C-mediated proteolysis of cyclin B drives progression through the metaphase-anaphase transition whilst wide-spread waves of dephosphorylation co-ordinate the subsequent events of mitotic exit.