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dXNP/DATRX increases apoptosis via the JNK and dFOXO pathway in Drosophila neurons
Mutation of the XNP/ATRX gene, which encodes an SNF2 family ATPase/helicase protein, leads to ATR-X syndrome and several other X-linked mental retardation syndromes. Although XNP/ATRX is a chromatin remodeler, the molecular mechanism by which mental retardation occurs in patients with ATR-X has yet...
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| Published in: | Biochemical and biophysical research communications 2009-06, Vol.384 (2), p.160-166 |
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| cites | cdi_FETCH-LOGICAL-c385t-37209e3d4af89536b1fa2630acb36c0599198a5180e7cd451f94ab6a3c5b81073 |
| container_end_page | 166 |
| container_issue | 2 |
| container_start_page | 160 |
| container_title | Biochemical and biophysical research communications |
| container_volume | 384 |
| creator | Hong, Yoon Ki Lee, Nam Gon Lee, Min Jung Park, Min Soo Choi, Gahee Suh, Yoon Seak Han, Seung Yeop Hwang, Soojin Jeong, Gilsang Cho, Kyoung Sang |
| description | Mutation of the
XNP/ATRX gene, which encodes an SNF2 family ATPase/helicase protein, leads to ATR-X syndrome and several other X-linked mental retardation syndromes. Although XNP/ATRX is a chromatin remodeler, the molecular mechanism by which mental retardation occurs in patients with ATR-X has yet to be determined. To better understand the role of XNP/ATRX in neuronal development, we expressed
Drosophila XNP (
dXNP/DATRX) ectopically in
Drosophila neurons. Neuronal expression of
dXNP/DATRX resulted in various developmental defects and induced strong apoptosis. These defects and apoptosis were suppressed by
Drosophila inhibitor of apoptosis protein 1. Expression of
dXNP/DATRX also increased JNK activity and the levels of
reaper and
hid transcripts, which are pro-apoptotic factors that activate caspase. Furthermore,
dXNP/DATRX-induced rough eye phenotype and apoptosis were suppressed by
dFOXO deficiency. These results suggest that dXNP/DATRX is involved in caspase-dependent apoptosis in
Drosophila neurons
via regulation of the JNK and
dFOXO pathway. |
| doi_str_mv | 10.1016/j.bbrc.2009.04.112 |
| format | article |
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XNP/ATRX gene, which encodes an SNF2 family ATPase/helicase protein, leads to ATR-X syndrome and several other X-linked mental retardation syndromes. Although XNP/ATRX is a chromatin remodeler, the molecular mechanism by which mental retardation occurs in patients with ATR-X has yet to be determined. To better understand the role of XNP/ATRX in neuronal development, we expressed
Drosophila XNP (
dXNP/DATRX) ectopically in
Drosophila neurons. Neuronal expression of
dXNP/DATRX resulted in various developmental defects and induced strong apoptosis. These defects and apoptosis were suppressed by
Drosophila inhibitor of apoptosis protein 1. Expression of
dXNP/DATRX also increased JNK activity and the levels of
reaper and
hid transcripts, which are pro-apoptotic factors that activate caspase. Furthermore,
dXNP/DATRX-induced rough eye phenotype and apoptosis were suppressed by
dFOXO deficiency. These results suggest that dXNP/DATRX is involved in caspase-dependent apoptosis in
Drosophila neurons
via regulation of the JNK and
dFOXO pathway.</description><identifier>ISSN: 0006-291X</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1016/j.bbrc.2009.04.112</identifier><identifier>PMID: 19406101</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Apoptosis ; ATRX ; Caspases - metabolism ; dFOXO ; DNA Helicases ; DNA-Binding Proteins - genetics ; DNA-Binding Proteins - metabolism ; Drosophila ; Drosophila melanogaster - cytology ; Drosophila melanogaster - genetics ; Drosophila melanogaster - growth & development ; Drosophila Proteins - genetics ; Drosophila Proteins - metabolism ; dXNP ; Forkhead Transcription Factors - metabolism ; JNK ; JNK Mitogen-Activated Protein Kinases - metabolism ; Neurogenesis - genetics ; Neuronal development ; Neurons - enzymology ; Neurons - physiology ; Neuropeptides - genetics ; Transcription, Genetic</subject><ispartof>Biochemical and biophysical research communications, 2009-06, Vol.384 (2), p.160-166</ispartof><rights>2009 Elsevier Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c385t-37209e3d4af89536b1fa2630acb36c0599198a5180e7cd451f94ab6a3c5b81073</citedby><cites>FETCH-LOGICAL-c385t-37209e3d4af89536b1fa2630acb36c0599198a5180e7cd451f94ab6a3c5b81073</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19406101$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hong, Yoon Ki</creatorcontrib><creatorcontrib>Lee, Nam Gon</creatorcontrib><creatorcontrib>Lee, Min Jung</creatorcontrib><creatorcontrib>Park, Min Soo</creatorcontrib><creatorcontrib>Choi, Gahee</creatorcontrib><creatorcontrib>Suh, Yoon Seak</creatorcontrib><creatorcontrib>Han, Seung Yeop</creatorcontrib><creatorcontrib>Hwang, Soojin</creatorcontrib><creatorcontrib>Jeong, Gilsang</creatorcontrib><creatorcontrib>Cho, Kyoung Sang</creatorcontrib><title>dXNP/DATRX increases apoptosis via the JNK and dFOXO pathway in Drosophila neurons</title><title>Biochemical and biophysical research communications</title><addtitle>Biochem Biophys Res Commun</addtitle><description>Mutation of the
XNP/ATRX gene, which encodes an SNF2 family ATPase/helicase protein, leads to ATR-X syndrome and several other X-linked mental retardation syndromes. Although XNP/ATRX is a chromatin remodeler, the molecular mechanism by which mental retardation occurs in patients with ATR-X has yet to be determined. To better understand the role of XNP/ATRX in neuronal development, we expressed
Drosophila XNP (
dXNP/DATRX) ectopically in
Drosophila neurons. Neuronal expression of
dXNP/DATRX resulted in various developmental defects and induced strong apoptosis. These defects and apoptosis were suppressed by
Drosophila inhibitor of apoptosis protein 1. Expression of
dXNP/DATRX also increased JNK activity and the levels of
reaper and
hid transcripts, which are pro-apoptotic factors that activate caspase. Furthermore,
dXNP/DATRX-induced rough eye phenotype and apoptosis were suppressed by
dFOXO deficiency. These results suggest that dXNP/DATRX is involved in caspase-dependent apoptosis in
Drosophila neurons
via regulation of the JNK and
dFOXO pathway.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>ATRX</subject><subject>Caspases - metabolism</subject><subject>dFOXO</subject><subject>DNA Helicases</subject><subject>DNA-Binding Proteins - genetics</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>Drosophila</subject><subject>Drosophila melanogaster - cytology</subject><subject>Drosophila melanogaster - genetics</subject><subject>Drosophila melanogaster - growth & development</subject><subject>Drosophila Proteins - genetics</subject><subject>Drosophila Proteins - metabolism</subject><subject>dXNP</subject><subject>Forkhead Transcription Factors - metabolism</subject><subject>JNK</subject><subject>JNK Mitogen-Activated Protein Kinases - metabolism</subject><subject>Neurogenesis - genetics</subject><subject>Neuronal development</subject><subject>Neurons - enzymology</subject><subject>Neurons - physiology</subject><subject>Neuropeptides - genetics</subject><subject>Transcription, Genetic</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><recordid>eNqFkEtv1DAURi0EokPhD7BAXrFLeq9jO7HEpuqDV9VBVZFmZznOjcajmSTYmaL-ezyakdjBypvznSsfxt4jlAioLzZl20ZfCgBTgiwRxQu2QDBQCAT5ki0AQBfC4OqMvUlpA4AotXnNztBI0NmxYA_d6v7HxfXl48OKh8FHcokSd9M4zWMKiT8Fx-c18W_337kbOt7dLldLPrl5_ds95wW_jmMap3XYOj7QPo5Deste9W6b6N3pPWc_b28er74Ud8vPX68u7wpfNWouqlqAoaqTrm-MqnSLvRO6AufbSntQxqBpnMIGqPadVNgb6VrtKq_aBqGuztnHo3eK4689pdnuQvK03bqBxn2yuhZSNUr8FxT5mKq1zKA4gj5_KkXq7RTDzsVni2APye3GHpLbQ3IL0ubkefThZN-3O-r-Tk6NM_DpCFCO8RQo2uQDDZ66EMnPthvDv_x_AHOGkA4</recordid><startdate>20090626</startdate><enddate>20090626</enddate><creator>Hong, Yoon Ki</creator><creator>Lee, Nam Gon</creator><creator>Lee, Min Jung</creator><creator>Park, Min Soo</creator><creator>Choi, Gahee</creator><creator>Suh, Yoon Seak</creator><creator>Han, Seung Yeop</creator><creator>Hwang, Soojin</creator><creator>Jeong, Gilsang</creator><creator>Cho, Kyoung Sang</creator><general>Elsevier Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7SS</scope><scope>7TK</scope><scope>7X8</scope></search><sort><creationdate>20090626</creationdate><title>dXNP/DATRX increases apoptosis via the JNK and dFOXO pathway in Drosophila neurons</title><author>Hong, Yoon Ki ; Lee, Nam Gon ; Lee, Min Jung ; Park, Min Soo ; Choi, Gahee ; Suh, Yoon Seak ; Han, Seung Yeop ; Hwang, Soojin ; Jeong, Gilsang ; Cho, Kyoung Sang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c385t-37209e3d4af89536b1fa2630acb36c0599198a5180e7cd451f94ab6a3c5b81073</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>ATRX</topic><topic>Caspases - metabolism</topic><topic>dFOXO</topic><topic>DNA Helicases</topic><topic>DNA-Binding Proteins - genetics</topic><topic>DNA-Binding Proteins - metabolism</topic><topic>Drosophila</topic><topic>Drosophila melanogaster - cytology</topic><topic>Drosophila melanogaster - genetics</topic><topic>Drosophila melanogaster - growth & development</topic><topic>Drosophila Proteins - genetics</topic><topic>Drosophila Proteins - metabolism</topic><topic>dXNP</topic><topic>Forkhead Transcription Factors - metabolism</topic><topic>JNK</topic><topic>JNK Mitogen-Activated Protein Kinases - metabolism</topic><topic>Neurogenesis - genetics</topic><topic>Neuronal development</topic><topic>Neurons - enzymology</topic><topic>Neurons - physiology</topic><topic>Neuropeptides - genetics</topic><topic>Transcription, Genetic</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hong, Yoon Ki</creatorcontrib><creatorcontrib>Lee, Nam Gon</creatorcontrib><creatorcontrib>Lee, Min Jung</creatorcontrib><creatorcontrib>Park, Min Soo</creatorcontrib><creatorcontrib>Choi, Gahee</creatorcontrib><creatorcontrib>Suh, Yoon Seak</creatorcontrib><creatorcontrib>Han, Seung Yeop</creatorcontrib><creatorcontrib>Hwang, Soojin</creatorcontrib><creatorcontrib>Jeong, Gilsang</creatorcontrib><creatorcontrib>Cho, Kyoung Sang</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Biochemical and biophysical research communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hong, Yoon Ki</au><au>Lee, Nam Gon</au><au>Lee, Min Jung</au><au>Park, Min Soo</au><au>Choi, Gahee</au><au>Suh, Yoon Seak</au><au>Han, Seung Yeop</au><au>Hwang, Soojin</au><au>Jeong, Gilsang</au><au>Cho, Kyoung Sang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>dXNP/DATRX increases apoptosis via the JNK and dFOXO pathway in Drosophila neurons</atitle><jtitle>Biochemical and biophysical research communications</jtitle><addtitle>Biochem Biophys Res Commun</addtitle><date>2009-06-26</date><risdate>2009</risdate><volume>384</volume><issue>2</issue><spage>160</spage><epage>166</epage><pages>160-166</pages><issn>0006-291X</issn><eissn>1090-2104</eissn><abstract>Mutation of the
XNP/ATRX gene, which encodes an SNF2 family ATPase/helicase protein, leads to ATR-X syndrome and several other X-linked mental retardation syndromes. Although XNP/ATRX is a chromatin remodeler, the molecular mechanism by which mental retardation occurs in patients with ATR-X has yet to be determined. To better understand the role of XNP/ATRX in neuronal development, we expressed
Drosophila XNP (
dXNP/DATRX) ectopically in
Drosophila neurons. Neuronal expression of
dXNP/DATRX resulted in various developmental defects and induced strong apoptosis. These defects and apoptosis were suppressed by
Drosophila inhibitor of apoptosis protein 1. Expression of
dXNP/DATRX also increased JNK activity and the levels of
reaper and
hid transcripts, which are pro-apoptotic factors that activate caspase. Furthermore,
dXNP/DATRX-induced rough eye phenotype and apoptosis were suppressed by
dFOXO deficiency. These results suggest that dXNP/DATRX is involved in caspase-dependent apoptosis in
Drosophila neurons
via regulation of the JNK and
dFOXO pathway.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>19406101</pmid><doi>10.1016/j.bbrc.2009.04.112</doi><tpages>7</tpages></addata></record> |
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| ispartof | Biochemical and biophysical research communications, 2009-06, Vol.384 (2), p.160-166 |
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| language | eng |
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| source | Elsevier |
| subjects | Animals Apoptosis ATRX Caspases - metabolism dFOXO DNA Helicases DNA-Binding Proteins - genetics DNA-Binding Proteins - metabolism Drosophila Drosophila melanogaster - cytology Drosophila melanogaster - genetics Drosophila melanogaster - growth & development Drosophila Proteins - genetics Drosophila Proteins - metabolism dXNP Forkhead Transcription Factors - metabolism JNK JNK Mitogen-Activated Protein Kinases - metabolism Neurogenesis - genetics Neuronal development Neurons - enzymology Neurons - physiology Neuropeptides - genetics Transcription, Genetic |
| title | dXNP/DATRX increases apoptosis via the JNK and dFOXO pathway in Drosophila neurons |
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