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INK4α的重叠编码框架编码产生出两个不同的蛋白p16INK4α和p19ARF。p19ARF在最近的研究中表明有细胞周期阻滞作用，它发挥作用时依赖于P53。其机制是通过与MDMZ结合并加速其降解，减少了后者对p53的下调，从而引起p53的积聚。p19ARF－MDM2－p53通路的发现对INK4α基因座的功能是个很好的补充。同时也提示INK4α基因突变或缺失可能同时损害p16INK4α－CDK4N6－RB和p19ARF－MDM2－p53这两条通路。一些肿瘤细胞中也发现确实存在p19ARF基因的失活。
The overlapping coding framework of INK4α encodes two different proteins, p16INK4α and p19ARF. P19 ARF has been shown in recent studies to have a cell cycle arrest that is dependent on P53. Its mechanism is to reduce the latter’s down-regulation of p53 by binding to MDMZ and accelerating its degradation, thereby causing the accumulation of p53. The discovery of the p19ARF-MDM2-p53 pathway is a good complement to the function of the INK4α locus. It also suggests that the mutation or deletion of INK4α may also damage both p16INK4α-CDK4N6-RB and p19ARF-MDM2-p53. The inactivation of the p19ARF gene was also found in some tumor cells.