The ribosomal protein, Rps27l, plays an oncogenic role by promoting p53 degradation via stabilizing the Mdm2-Mdm4 complex, but a tumor suppressor role by preventing the aneuploidy and loss of p53 heterozygosity.

Functional and mechanistic analyses of cancer cells containing homozygous deletion of TP53 and FXR2 reveal that inhibition of FXR1 blocks cell proliferation in a collateral lethality manner, opening an avenue to develop therapies targeting such cancers.

Mannose phosphate isomerase is a metabolic enzyme regulating cell survival in both embryonic and cancer cells.

The endogenous 3′UTR does not regulate TP53 mRNA or protein level and the 3′UTR is repressive when used alone in reporters, but addition of the coding region has a dominant repressive effect.

Deletion of the ATM cofactor ATMIN reduces PDGFRA expression and strongly suppresses tumorigenesis in a TP53-deficient mouse model of glioblastoma.

The structural maintenance of chromosomes complex, SMC5/6, is crucial for brain development and function as it ensures proficient DNA replication in neural progenitor cells prior to chromosome segregation.

A fully synthetic library of humanized single domain antibodies yields in vitro high affinity antibodies usable in cell biology and translational projects.

Inhibition of Polo-like kinase that has been shown to exhibit antitumor effect unexpectedly disrupts muscle stem cell function, leading to developmental and regenerative failures.

Loss-of-function screening identified transglutaminase 2 (TGM2) as a putative tumor suppressor in the TP53 pathway and revealed that TGM2-mediated autophagy and CDKN1A-mediated cell cycle arrest are two critical barriers that prevent oncogenic transformation.

The MCM-binding protein (MCMBP) promotes the hexamer assembly of the replicative MCM2–7 helicase by interacting with the nascent MCM3 subunit, playing a key role in achieving high expression levels of the functional MCM2–7 helicase for maintaining genome integrity.