Cell cycle arrest requires the interaction of GAS41 with p53, but the loss-of-functional mutation of p53 breaks down the suppressive machinery of cell cycle, which is partially responsible for aberrant cellular proliferation. I will introduce the important papers.
1. GAS41 is required for repression of the p53 tumor suppressor pathway during normal cellular proliferation. GAS41 is prebound to the promoters of two p53 tumor suppressor pathway genes (p21 and p14ARF) in normal unstressed cells but is dissociated from both promoters in response to stress signals that activate p53. (doi: 10.1128/MCB.02185-05Mol. Cell. Biol. June 2006vol. 26 no. 11 4006-4016)
2. The newly identified complex GAS41-PP2Cβ, and not PP2Cβ alone, is specifically required for dephosphorylation of serine 366 on p53. Ectopic expression of GAS41 and PP2Cβ reduces UV radiation-induced p53 up-regulation, thereby increasing the cell survival upon genotoxic DNA damage. (doi:10.1074/jbc.C110.210211April 1, 2011 The Journal of Biological Chemistry,286, 10911-10917.)
Do you mean transcriptional repressors or anything that blocks p53? Because hdm2 is probably the most famous p53 repressor, it and several other E3 ubiquitin ligases regulate p53 degradation. Here's a good place to start: PMID: 25128494