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a b s t r a c t p53 gene expresses several protein isoforms modulating p53-mediated responses through regulation of gene expression. Here, we identify a novel p53 isoform, D160p53, lacking the first 159 residues. By knockdown experiments and site-directed mutagenesis, we show that D160p53 is encoded by D133p53 transcript using ATG160 as translational initiation site. This hypothesis is supported by endogenous expression of D160p53 in U2OS, T47D and K562 cells, the latter ones carrying a premature stop codon that impairs p53 and D133p53 protein expression but not the one of D160p53. Overall, these results show that the D133p53 transcript generates two different p53 isoforms, D133p53 and D160p53.

Interleukin-1 receptor antagonist (IL-1ra) has been shown to play a crucial role in the prevention of various inflammatory diseases. There is also convincing evidence that IL-1ra is able to counteract inflammatory effects of IL-1 members implicated in insulin resistance and diabetes. However, the use of knock-out animal models provides evidence to the contrary and the role of IL-1ra in obesity-linked anomalies remains controversial.This minireview gets an insight into recent findings on the implication of IL-1ra and its gene polymorphism in diabetes and obesity, discusses the potential dual effects of IL-1ra observed in different models, and comments on future directions.

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