dXNP, a Drosophila homolog of XNP/ATRX, induces apoptosis via Jun-N-terminal kinase activation

Nam Gon Lee, Yoon Ki Hong, Si Young Yu, Seung Yeop Han, Dongho Geum, Kyoung Sang Cho

    Research output: Contribution to journalArticlepeer-review

    17 Citations (Scopus)

    Abstract

    XNP/ATRX, a causative gene of X-linked α-thalassemia/mental retardation syndrome, encodes an SNF2 family ATPase/helicase protein. To better understand the role of XNP/ATRX in development, we isolated and characterized a Drosophila XNP/ATRX homolog, dXNP, which contains highly conserved SNF2 and helicase domains. Ectopically expressed dXNP induced strong apoptosis in the developing eye and wing, but did not affect cell cycle progression or the expression of wingless and engrailed, essential regulators of development. The dXNP-induced apoptosis was strongly suppressed by DJNKK/hemipterous mutation, and dXNP increased JNK activity. Taken together, these results suggest that dXNP regulates apoptosis via JNK activation.

    Original languageEnglish
    Pages (from-to)2625-2632
    Number of pages8
    JournalFEBS Letters
    Volume581
    Issue number14
    DOIs
    Publication statusPublished - 2007 Jun 12

    Bibliographical note

    Funding Information:
    This work was supported by the faculty research fund of Konkuk University in 2005. We thank Jeehye Park (KAIST, Korea) for critical reading of this manuscript.

    Keywords

    • ATRX
    • Apoptosis
    • Drosophila
    • JNK
    • XNP
    • dXNP

    ASJC Scopus subject areas

    • Biophysics
    • Structural Biology
    • Biochemistry
    • Molecular Biology
    • Genetics
    • Cell Biology

    Fingerprint

    Dive into the research topics of 'dXNP, a Drosophila homolog of XNP/ATRX, induces apoptosis via Jun-N-terminal kinase activation'. Together they form a unique fingerprint.

    Cite this