Edited by: Eugene Russo
C. Deng, P. Zhang, J.W. Harper, S.J. Elledge, P. Leder, "Mice lacking p21CIP1/WAF1 undergo normal development, but are defective in G1 checkpoint control," Cell, 82, 675-84, 1995. (Cited in more than 170 papers through June 1997)
Comments by Philip Leder, Harvard Medical School
The gene p21CIP1/WAF1 inhibits the proper functioning of cyclin-dependent kinases (CDKs), molecules that help to control cellular duplication. Although p21CIP1/WAF1 is known to be regulated by the tumor suppressor gene p53, the extent of its participation in p53 function is not fully understood: The gene has some role in the pathway that begins with the disruption of p53 and culminates in tumor growth. In this paper, according to Philip Leder, a professor of genetics at Harvard Medical School and a senior investigator of the Howard Hughes Medical Institute, p21CIP1/WAF1-deficient mice were created by using targeted gene disruption in order to pinpoint the p53 ...
