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

16 Citations (Scopus)


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
Issue number14
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.


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

ASJC Scopus subject areas

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


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