The cyclin-dependent kinase inhibitors (CKIs) p27 and p57 are structurally similar, and their biochemical and cellular functions have been thought to be equivalent. However, mice deficient in either p27 or p57 exhibit markedly different phenotypes, suggesting that the in vivo roles of these two proteins might differ. To address this apparent discrepancy, we have generated a knock-in mouse model in which the endogenous p57 gene is replaced by the p27 gene, with p27 thus being expressed instead of p57. This mouse model has provided evidence that p57 functions as a bona fide CKI in vivo and that most of its roles can be performed by p27. Our findings also highlight and provide insight into the question of what determines the distinct cellular responses to abnormal cell cycling induced by the loss of CKIs.
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