Rb independent inhibition of cell growth by p15(INK4B).

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  • Author(s): Aytac U;Aytac U; Konishi T; David H; Mendoza S; Miller CW
  • Source:
    Biochemical and biophysical research communications [Biochem Biophys Res Commun] 1999 Aug 27; Vol. 262 (2), pp. 534-8.
  • Publication Type:
    Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • Language:
    English
  • Additional Information
    • Source:
      Publisher: Elsevier Country of Publication: United States NLM ID: 0372516 Publication Model: Print Cited Medium: Print ISSN: 0006-291X (Print) Linking ISSN: 0006291X NLM ISO Abbreviation: Biochem Biophys Res Commun Subsets: MEDLINE
    • Publication Information:
      Publication: <2002- >: San Diego, CA : Elsevier
      Original Publication: New York, Academic Press.
    • Subject Terms:
      Cell Cycle Proteins* ; Cell Transformation, Neoplastic* ; Tumor Suppressor Proteins*; Carrier Proteins/*metabolism ; Cyclin-Dependent Kinases/*antagonists & inhibitors ; Growth Inhibitors/*metabolism ; Retinoblastoma Protein/*metabolism; Carrier Proteins/genetics ; Cell Cycle/physiology ; Cyclin-Dependent Kinase Inhibitor p15 ; Cyclin-Dependent Kinase Inhibitor p16/genetics ; Cyclin-Dependent Kinase Inhibitor p16/metabolism ; Recombinant Fusion Proteins/metabolism ; Retinoblastoma Protein/deficiency ; Retinoblastoma Protein/genetics ; Transfection
    • Abstract:
      The INK4 cyclin dependent kinase inhibitors (CDKI), such as p15(INK4B) and p16(INK4A), block cell cycle progression from G to S phase. This is mediated by inhibition of phosphorylation of proteins, including the retinoblastoma susceptibility protein (Rb), by cyclin dependent kinases. Ectopic over-expression of the p16(INK4A) CDKI can inhibit growth of cell lines depending on Rb status. Cell lines lacking Rb, with few exceptions, are resistant to growth inhibition by p16(INK4A). The effects of ectopic over-expression of p15(INK4B) in cell lines with and without wild type Rb were examined by measuring cell recovery. Proliferation was inhibited in cells lacking Rb as well as in cells with wild type Rb expression. Experiments analyzing the effectiveness of chimeric p15(INK4B)/p16(INK4A) proteins indicated that the Rb independent growth inhibition required N-terminal residues of p15(INK4B). Linker insertion mutation of p15(INK4B) showed that the inhibition was dependent on intact ankyrin structures. Double staining flow cytometry found that the growth inhibition correlated with a decrease in cells in G2/M phases of the cell cycle. These findings are consistent with Rb independent inhibition of the progression from G1 to S caused by overexpression of p15(INK4B).
      (Copyright 1999 Academic Press.)
    • Accession Number:
      0 (Carrier Proteins)
      0 (Cell Cycle Proteins)
      0 (Cyclin-Dependent Kinase Inhibitor p15)
      0 (Cyclin-Dependent Kinase Inhibitor p16)
      0 (Growth Inhibitors)
      0 (Recombinant Fusion Proteins)
      0 (Retinoblastoma Protein)
      0 (Tumor Suppressor Proteins)
      EC 2.7.11.22 (Cyclin-Dependent Kinases)
    • Publication Date:
      Date Created: 19990827 Date Completed: 19991001 Latest Revision: 20091119
    • Publication Date:
      20221213
    • Accession Number:
      10.1006/bbrc.1999.1164
    • Accession Number:
      10462509