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Mice Lacking p21 CIP1/WAF1 undergo normal development, but are defective in G1 checkpoint control
Deng C.2; Zhang P.1; Wade Harper J.1; Elledge S.J.2; Leder P.2
1995-08-25
Source PublicationCell
ISSN00928674
Volume82Issue:4Pages:675-684
Abstract

p21 is a CDK Inhibitor regulated by the tumor suppressor p53 and is hypothesized to mediate G1 arrest. p53 has been suggested to derive anti-oncogenic properties from this relationship. To test these notions, we created mice lacking p21. They develop normally and (unlike p53 mice) have not developed spontaneous malignancies during 7 months of observation. Nonetheless, p21 embryonic fibroblasts are significantly deficient in their ability to arrest in G1 In response to DNA damage and nucleotide pool perturbation. p21 cells also exhibit a significant growth alteration in vitro, achieving a saturation density as high as that observed In p53-/- cells. In contrast, other aspects of p53 function, such as thymocytic apoptosis and the mitotic spindle checkpoint, appear normal. These results establish the role of p21 in the G1 checkpoint, but suggest that the antiapoptotic and the anti-oncogenic effects of p53 are more complex. © 1995.

DOI10.1016/0092-8674(95)90039-X
URLView the original
Indexed BySCI
WOS Research AreaBiochemistry & Molecular Biology ; Cell Biology
WOS SubjectBiochemistry & Molecular Biology ; Cell Biology
WOS IDWOS:A1995RR73400018
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Citation statistics
Document TypeJournal article
CollectionFaculty of Health Sciences
Affiliation1.Baylor College of Medicine
2.Harvard Medical School
Recommended Citation
GB/T 7714
Deng C.,Zhang P.,Wade Harper J.,et al. Mice Lacking p21 CIP1/WAF1 undergo normal development, but are defective in G1 checkpoint control[J]. Cell,1995,82(4):675-684.
APA Deng C.,Zhang P.,Wade Harper J.,Elledge S.J.,&Leder P..(1995).Mice Lacking p21 CIP1/WAF1 undergo normal development, but are defective in G1 checkpoint control.Cell,82(4),675-684.
MLA Deng C.,et al."Mice Lacking p21 CIP1/WAF1 undergo normal development, but are defective in G1 checkpoint control".Cell 82.4(1995):675-684.
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