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

doi:10.1016/j.febslet.2007.05.005

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

Department of Biomedical Sciences

Research output: Contribution to journal › Article › peer-review

16 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 language	English
Pages (from-to)	2625-2632
Number of pages	8
Journal	FEBS Letters
Volume	581
Issue number	14
DOIs	https://doi.org/10.1016/j.febslet.2007.05.005
Publication status	Published - 2007 Jun 12

Keywords

ATRX
Apoptosis
Drosophila
JNK
XNP
dXNP

ASJC Scopus subject areas

Biophysics
Structural Biology
Biochemistry
Molecular Biology
Genetics
Cell Biology

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10.1016/j.febslet.2007.05.005

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

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.",

keywords = "ATRX, Apoptosis, Drosophila, JNK, XNP, dXNP",

author = "Lee, {Nam Gon} and Hong, {Yoon Ki} and Yu, {Si Young} and Han, {Seung Yeop} and Dongho Geum and Cho, {Kyoung Sang}",

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. ",

year = "2007",

month = jun,

day = "12",

doi = "10.1016/j.febslet.2007.05.005",

language = "English",

volume = "581",

pages = "2625--2632",

journal = "FEBS Letters",

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TY - JOUR

T1 - dXNP, a Drosophila homolog of XNP/ATRX, induces apoptosis via Jun-N-terminal kinase activation

AU - Lee, Nam Gon

AU - Hong, Yoon Ki

AU - Yu, Si Young

AU - Han, Seung Yeop

AU - Geum, Dongho

AU - Cho, Kyoung Sang

N1 - 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.

PY - 2007/6/12

Y1 - 2007/6/12

N2 - 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.

AB - 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.

KW - ATRX

KW - Apoptosis

KW - Drosophila

KW - JNK

KW - XNP

KW - dXNP

UR - http://www.scopus.com/inward/record.url?scp=34249678000&partnerID=8YFLogxK

U2 - 10.1016/j.febslet.2007.05.005

DO - 10.1016/j.febslet.2007.05.005

M3 - Article

C2 - 17531976

AN - SCOPUS:34249678000

SN - 0014-5793

VL - 581

SP - 2625

EP - 2632

JO - FEBS Letters

JF - FEBS Letters

IS - 14

ER -

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

Abstract

Keywords

ASJC Scopus subject areas

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