TP53 codon 72 Arg/Arg polymorphism is associated with a higher risk for inflammatory bowel disease development

Table 1 Summary of biological and biochemical differences between ⁷²Arg and ⁷²Pro TP53 isoforms

Property	72Arg vs72Pro TP53
Electrophoretic mobility	72Arg migrates slightly faster on SDS[16,19,20]
Subcellular localization	72Arg is cytoplasmic/mitochondrial possibly through interaction with CD2AP/Cin85 adaptor protein family[21] or with mitochondrial (mt) polymerase gamma, which may also promote mtDNA repair[22,23] 72Pro is predominantly nuclear[21,24]
Apoptosis induction	72Arg is a stronger apoptosis inducer[24], with faster kinetics of cell death[16] possibly through more efficient inhibition of 72Pro by iASPP[25] or preferential localization of 72Arg to mitochondria and induction of apoptosis through a transcriptionally independent pathway[24]
Suppression of transformed cell growth	72Arg is two times more active in suppressing colony formation[16]
Susceptibility to HPV E6 degradation	72Arg is more susceptible to degradation[26,27]
Transcription activation	72Arg associates and inactivates p73 more efficiently[20], thus inhibiting apoptosis72Pro is a stronger inducer of transcription and it has more affinity to TAFII32 and TAFII70[16]
Leukemia inhibitory factor transactivation	72Arg is more active towards this function[28,29], which may be advantageous in cold climates due to increased fertility[18]