The antiviral and genomic DNA deaminase APOBEC3B is repressed in normal cells by PRC1.6/E2F6 and DREAM/E2F4 complexes and deregulation of this axis provides a unifying mechanism for overexpression in cancer.

The E2F/Dp transcription factors, which are key cell cycle regulators, can also mediate the regulation of carbohydrate metabolism in larva by controlling both systemic trehalose homeostasis and fat storage.

Cell imaging and mathematical modelling show reciprocal cross-regulation between inflammatory signalling and cell cycle timing, which is mediated through functional interactions between NF-B and E2F proteins.

Chronic fat overload triggers the conversion of quiescent biliary epithelial cells into proliferative progenitors through an E2F-dependent mechanism.

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

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

The MYC transcription factor network member MGA is a subunit of a non-canonical Polycomb complex, which, when inactivated, accelerates tumorigenesis in mouse models of cancer and proliferation in colon organoids.

Mutual suppression of ETV1 by Capicua (CIC) and ETS2 repressor factor (ERF) limits prostate cancer progression.

An ECF-type transporter serves as broad-spectrum heme iron scavenger and allows an opportunistic pathogen to use multiple eukaryotic hemoproteins to overcome nutritional iron-limitation.

In glioblastoma stem cells, oncogenes on extrachromosomal DNA do not cluster at distances in keeping with coordinated transcription, with amplified gene expression driven by copy number rather increased transcriptional efficiency.