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A role for mixed lineage kinases in regulating transcription factor CCAAT/enhancer-binding protein-beta-dependent gene expression in response to interferon-gamma

  1. Author:
    Roy, S. K.
    Shuman, J. D.
    Platanias, L. C.
    Shapiro, P. S.
    Reddy, S. P. M.
    Johnson, P. F.
    Kalvakolanu, D. V.

  2. Author Address

    Univ Maryland, Sch Med, Greenebaum Canc Ctr, Dept Microbiol & Immunol, Baltimore, MD 21201 USA. Univ Maryland, Sch Med, Mol & Cellular Biol Program, Baltimore, MD 21201 USA. Univ Maryland, Sch Pharm, Baltimore, MD 21201 USA. NCI, Lab Prot Dynam & Signaling, NIH, Frederick, MD 21702 USA. Northwestern Univ, Sch Med, Robert Lurie Canc Ctr, Chicago, IL 60611 USA. Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Environm Hlth Sci, Baltimore, MD 21205 USA Kalvakolanu, DV, Univ Maryland, Sch Med, Greenebaum Canc Ctr, Dept Microbiol & Immunol, 665 W Baltimore St,9th Floor, Baltimore, MD 21201 USA
    1. Year: 2005
    2. Date: JUL 1
  2. Journal: Journal of Biological Chemistry
    1. 280
    2. 26
    3. Pages: 24462-24471
  4. Type of Article: Article
  1. Abstract:

    Transcription factor CCAAT/enhancer-binding protein-beta(C/EBP-beta) regulates a variety of cellular functions in response to exogenous stimuli. We have reported earlier that C/EBP-beta induces gene transcription through a novel interferon (IFN)- response element called gamma-IFN-activated transcriptional element. We show here that IFN-gamma-induced, C/EBP-beta/gamma-IFN-activated transcriptional element-dependent gene expression is regulated by mixed lineage kinases (MLKs), members of the mitogen-activated protein kinase kinase kinase family. MLK3 appears to activate C/EBP-beta in response to IFN-gamma by a mechanism involving decreased phosphorylation of a specific phosphoacceptor residue, Ser(64), within the transactivation domain. Decreased phosphorylation of Ser64 was independent of IFN-gamma-stimulated ERK1/2 activation and did not require the ERK phosphorylation site Thr(189) located in regulatory domain 2 of C/EBP-beta. Together these studies provide the first evidence that MLK3 is involved in IFN-gamma signaling and identify a novel mechanism of transcriptional activation by IFN-gamma

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External Sources

  1. View record in Web of Science®
  2. WOS: 000230114000022

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