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Loss of CCAAT/enhancer binding protein delta promotes chromosomal instability

  1. Author:
    Huang, A. M.
    Montagna, C.
    Sharan, S.
    Ni, Y. J.
    Ried, T.
    Sterneck, E.

  2. Author Address

    Sterneck, E, Regulat Cell Growth Lab, POB B, Frederick, MD 21702 USA Regulat Cell Growth Lab, Frederick, MD 21702 USA. NCI, Genet Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
    1. Year: 2004
  2. Journal: Oncogene
    1. 23
    2. 8
    3. Pages: 1549-1557
  4. Type of Article: Article
  1. Abstract:

    The transcription factor CCAAT/enhancer binding protein delta (Cebpd, also known as C/EBPdelta, CRP3, CELF, NF-IL6beta) is implicated in diverse cellular functions such as the acute phase response, adipocyte differentiation, learning and memory, and mammary epithelial cell growth control. Here, we report that lack of Cebpd causes genomic instability and centrosome amplifications in primary embryonic fibroblasts derived from 129S1 mice. Upon spontaneous immortalization, Cebpd-deficient fibroblasts acquire transformed features such as impaired contact inhibition and reduced serum dependence. These data identify a novel role for Cebpd in the maintenance of chromosomal stability and suggest a potential tumor suppressor function in vivo

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External Sources

  1. View record in Web of Science®
  2. WOS: 000189219500008

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