Scinovex
reviewTop 1% cited

Regulation of the Cdk inhibitor p27 and its deregulation in cancer

Journal of Cellular Physiology · 2000 · Vol. 183(1) · pp. 10–17
Joyce M. SlingerlandMichele Pagano

Abstract

p27 is a cell cycle inhibitor whose cellular abundance increases in response to many antimitogenic stimuli. In this review, we summarize the current knowledge on p27 function and its regulation by synthesis and by ubiquitin-mediated degradation. Importantly, p27 degradation is enhanced in many aggressive human tumors. The frequency with which this is observed suggests that loss of p27 may confer a growth advantage to these cancers. From a practical point of view, immunodetection of p27 in tumors may prove to be useful in the assessment of prognosis and may ultimately influence the therapy of this disease.

Cancer-related Molecular PathwaysUbiquitin and proteasome pathwaysCancer Research and TreatmentsCDK inhibitorCyclin-dependent kinaseUbiquitinFunction (biology)CancerCancer researchCell biologyBiologyCell cycleCancer cell

MeSH terms

AnimalsEnzyme InhibitorsHomeostasisHumansMicrotubule-Associated ProteinsNeoplasmsBiomarkers, TumorCell Cycle ProteinsCyclin-Dependent KinasesTumor Suppressor ProteinsCyclin-Dependent Kinase Inhibitor p27

Funding

  • U.S. Department of Defense
  • National Institutes of Health
Citations
672
FWCI
23.53
field-weighted impact
References
109
Percentile
100%
vs. same field & year
Citations per year
Citation Network

How this paper connects to the literature. Drag to explore, click any node to open that paper.