Rao, S <br/><br/>
Lovastatin mediated G1 arrest in normal and tumor breast cells is through inhibition of CDK2 activity and redistribution of p21 and p27, independent of p53.  [electronic resource] 

 -  Oncogene  Nov 1998 
 - 2393-402 p.  digital 
<br/><br/> Publication Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S. 
<br/><br/><label>ISSN: </label>0950-9232 
<br/><br/><label>Standard No.: </label>10.1038/sj.onc.1202322  doi 
<br/><br/><label>Subjects--Topical Terms: </label><br/>Antineoplastic Agents--pharmacology<br/>Breast--metabolism<br/>Breast Neoplasms--metabolism<br/>CDC2-CDC28 Kinases<br/>Cell Cycle Proteins<br/>Cyclin D3<br/>Cyclin-Dependent Kinase 2<br/>Cyclin-Dependent Kinase 4<br/>Cyclin-Dependent Kinase Inhibitor p21<br/>Cyclin-Dependent Kinase Inhibitor p27<br/>Cyclin-Dependent Kinases--metabolism<br/>Cyclins--metabolism<br/>Female<br/>G1 Phase--drug effects<br/>Humans<br/>Lovastatin--pharmacology<br/>Microtubule-Associated Proteins--metabolism<br/>Protein Serine-Threonine Kinases--metabolism<br/>Proto-Oncogene Proteins<br/>Retinoblastoma Protein--metabolism<br/>Tumor Cells, Cultured--drug effects<br/>Tumor Suppressor Protein p53--genetics<br/>Tumor Suppressor Proteins