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Genetics

H. Kiyokawa, R.D. Kineman, K.O. Manova-Todorova, V.C. Soares, E.S. Hoffman, M. Ono, D. Khanam, A.C. Hayday, L.A. Frohman, and A. Koff. "Enhanced growth of mice lacking the cyclin-dependent kinase inhibitor function of p27Kip1," Cell, 85:721-32, 1996. (Cited in more than 155 papers since publication) Comments by Andrew Koff, associate member of the molecular biology program, Memorial Sloan-Kettering Cancer Center, New York Cyclin-dependent kinase (CDK) inhibitors act as a traffic cop of cell

The Scientist Staff

H. Kiyokawa, R.D. Kineman, K.O. Manova-Todorova, V.C. Soares, E.S. Hoffman, M. Ono, D. Khanam, A.C. Hayday, L.A. Frohman, and A. Koff. "Enhanced growth of mice lacking the cyclin-dependent kinase inhibitor function of p27Kip1," Cell, 85:721-32, 1996. (Cited in more than 155 papers since publication)

Comments by Andrew Koff, associate member of the molecular biology program, Memorial Sloan-Kettering Cancer Center, New York

Cyclin-dependent kinase (CDK) inhibitors act as a traffic cop of cell division. However, the precise signals these proteins issue to direct cells have eluded researchers.

Andrew Koff and colleagues proposed three potential ways these proteins might stop and start cellular proliferation:

  1. as a "restriction point" regulator that controls entry into both differentiation and division

  2. as a "checkpoint" system that stops division in response to genetic damage

  3. as a "holding" function that keeps cells in a nonproliferative state

"The question that then comes up is,...

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