Cyclin D1 protein stability is regulated by ubiquitin-proteasome mechanism mediated by multiple E3 ligases, including newly identified Keap1, DDB2, and WSB2.

Imaging of single cells within a cell population shows the correlation between subcellular accumulation of β-catenin and the transcriptional activation of a target gene.

A c-Myc-transcribed long noncoding RNA namely LAST (LncRNA-assisted stabilization of transcripts) collaborates with a cellular factor CNBP to promote the stability of CCND1/cyclin D1 mRNA post-transcriptionally, ensuring the proper G1/Sphase transition of the cell cycle.

Mucins, long associated with cancer aggression, remodel the cancer glycocalyx in a way that promotes proliferation in the metastatic site by enhancing integrin-mediated adhesion and thus driving cell cycle progression.

The LIM-homedomain transcription factor Lhx2 confers competence to retinal progenitor cells to activate and maintain Sonic Hedgeghog signaling at physiological levels during a key phase of tissue growth and cell type generation.

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.

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.