Kurt A. Krummel

TL;DR: It is proposed that the C-terminal modifications believed to be critical for proper P53 regulation are not essential, but contribute to a fine-tuning mechanism of homeostatic control in vivo.

TL;DR: A mouse encoding p53 lacking the proline-rich domain (p53DeltaP) exhibited increased sensitivity to Mdm2-dependent degradation and decreased transactivation capacity, correlating with deficient cell cycle arrest and reduced apoptotic responses.

TL;DR: This work assembled a BAC contig of >1 Mb across the second most active common fragile site, FRA16D (16q23.2), and demonstrated that FRA 16D decondensation/breakage occurs over a region of at least 1 Mb, which is the largest common fragile sites cloned to date.

TL;DR: P53TTAA and p53AXXA are efficient transactivators and potent suppressors of oncogene-induced tumors and Pin1 sites in the PRD may modulate p53 stability but do not significantly affect function, which may explain why the sequence of the p53 PRD is so variable in evolution.

TL;DR: It is shown that fine-tuning the expression levels of the cyclin-dependent kinase inhibitor p21, a p53 target gene, contributes significantly to p53-mediated effects on the hematopoietic system and implications for understanding cell competition in response to stresses involved in stem cell transplantation, recovery from adverse hematologic effects of DNA-damaging cancer therapies, and development of radioprotection strategies.