Abstract：
:D-type cyclins, in association with the cyclin-dependent kinases Cdk4 or Cdk6, promote progression through the G1 phase of the cell cycle by phosphorylating the retinoblastoma protein (RB). The activities of Cdk4 and Cdk6 are constrained by inhibitors such as p16, the product of the CDKN2 gene on human chromosome 9p21 (refs 12-14). The frequent deletion or mutation of CDKN2 in tumour cells suggests that p16 acts as a tumour suppressor. We show that wild-type p16 arrests normal diploid cells in late G1, whereas a tumour-associated mutant of p16 does not. Significantly, the ability of p16 to induce cell-cycle arrest is lost in cells lacking functional RB, including primary fibroblasts from Rb-/- mouse embryos. Thus, loss of p16, overexpression of D-cyclins and loss of RB have similar effects on G1 progression, and may represent a common pathway to tumorigenesis.
journal_name
Naturejournal_title
Natureauthors
Lukas J,Parry D,Aagaard L,Mann DJ,Bartkova J,Strauss M,Peters G,Bartek Jdoi
10.1038/375503a0subject
Has Abstractpub_date
1995-06-08 00:00:00pages
503-6issue
6531eissn
0028-0836issn
1476-4687journal_volume
375pub_type
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