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JNK activation mediates the apoptosis of xCT-deficient cells
System X c − is an anionic amino acid transport system highly specific for cystine and glutamate. The underlying mechanism of cell death of cultured cells from the subtle gray ( sut) mouse which contains an xCT null mutation remains elucidated. Our results show that the death of sut cells is likely...
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| Published in: | Biochemical and biophysical research communications 2008-06, Vol.370 (4), p.584-588 |
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| Main Authors: | , , , , , , , |
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| Language: | English |
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| cited_by | cdi_FETCH-LOGICAL-c451t-a1f1dbfc759ceb99b92693254095540102806886805e5c5bb1530ebc9ff11ee53 |
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| cites | cdi_FETCH-LOGICAL-c451t-a1f1dbfc759ceb99b92693254095540102806886805e5c5bb1530ebc9ff11ee53 |
| container_end_page | 588 |
| container_issue | 4 |
| container_start_page | 584 |
| container_title | Biochemical and biophysical research communications |
| container_volume | 370 |
| creator | Qiao, Hai-Xuan Hao, Chan-Juan Li, Yan He, Xin Chen, Ri-Sheng Cui, Jie Xu, Zhi-Heng Li, Wei |
| description | System X
c
− is an anionic amino acid transport system highly specific for cystine and glutamate. The underlying mechanism of cell death of cultured cells from the subtle gray (
sut) mouse which contains an xCT null mutation remains elucidated. Our results show that the death of
sut cells is likely caused by apoptosis mediated by c-Jun N-terminal kinase (JNK). The JNK activation triggers both a caspase-dependent (caspases-9 and -3) and an ER stress-mediated (eIF2 and CHOP) pathway to induce apoptosis. These findings suggest the possible pathways involved in the cell death of xCT-deficient cells. |
| doi_str_mv | 10.1016/j.bbrc.2008.03.134 |
| format | article |
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− is an anionic amino acid transport system highly specific for cystine and glutamate. The underlying mechanism of cell death of cultured cells from the subtle gray (
sut) mouse which contains an xCT null mutation remains elucidated. Our results show that the death of
sut cells is likely caused by apoptosis mediated by c-Jun N-terminal kinase (JNK). The JNK activation triggers both a caspase-dependent (caspases-9 and -3) and an ER stress-mediated (eIF2 and CHOP) pathway to induce apoptosis. These findings suggest the possible pathways involved in the cell death of xCT-deficient cells.</description><identifier>ISSN: 0006-291X</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1016/j.bbrc.2008.03.134</identifier><identifier>PMID: 18395005</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Amino Acid Transport System y+ - genetics ; Animals ; Apoptosis ; Apoptosis - genetics ; Caspase 3 - metabolism ; Caspase 9 - metabolism ; Cell Line ; Cystine/glutamate transporter ; Endoplasmic Reticulum - metabolism ; ER stress ; Eukaryotic Initiation Factor-2 - metabolism ; JNK ; JNK Mitogen-Activated Protein Kinases - metabolism ; Melanocytes - metabolism ; Melanocytes - physiology ; Mice ; Mice, Mutant Strains ; Oxidative stress ; Transcription Factor CHOP - metabolism</subject><ispartof>Biochemical and biophysical research communications, 2008-06, Vol.370 (4), p.584-588</ispartof><rights>2008 Elsevier Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c451t-a1f1dbfc759ceb99b92693254095540102806886805e5c5bb1530ebc9ff11ee53</citedby><cites>FETCH-LOGICAL-c451t-a1f1dbfc759ceb99b92693254095540102806886805e5c5bb1530ebc9ff11ee53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18395005$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Qiao, Hai-Xuan</creatorcontrib><creatorcontrib>Hao, Chan-Juan</creatorcontrib><creatorcontrib>Li, Yan</creatorcontrib><creatorcontrib>He, Xin</creatorcontrib><creatorcontrib>Chen, Ri-Sheng</creatorcontrib><creatorcontrib>Cui, Jie</creatorcontrib><creatorcontrib>Xu, Zhi-Heng</creatorcontrib><creatorcontrib>Li, Wei</creatorcontrib><title>JNK activation mediates the apoptosis of xCT-deficient cells</title><title>Biochemical and biophysical research communications</title><addtitle>Biochem Biophys Res Commun</addtitle><description>System X
c
− is an anionic amino acid transport system highly specific for cystine and glutamate. The underlying mechanism of cell death of cultured cells from the subtle gray (
sut) mouse which contains an xCT null mutation remains elucidated. Our results show that the death of
sut cells is likely caused by apoptosis mediated by c-Jun N-terminal kinase (JNK). The JNK activation triggers both a caspase-dependent (caspases-9 and -3) and an ER stress-mediated (eIF2 and CHOP) pathway to induce apoptosis. These findings suggest the possible pathways involved in the cell death of xCT-deficient cells.</description><subject>Amino Acid Transport System y+ - genetics</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - genetics</subject><subject>Caspase 3 - metabolism</subject><subject>Caspase 9 - metabolism</subject><subject>Cell Line</subject><subject>Cystine/glutamate transporter</subject><subject>Endoplasmic Reticulum - metabolism</subject><subject>ER stress</subject><subject>Eukaryotic Initiation Factor-2 - metabolism</subject><subject>JNK</subject><subject>JNK Mitogen-Activated Protein Kinases - metabolism</subject><subject>Melanocytes - metabolism</subject><subject>Melanocytes - physiology</subject><subject>Mice</subject><subject>Mice, Mutant Strains</subject><subject>Oxidative stress</subject><subject>Transcription Factor CHOP - metabolism</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><recordid>eNqF0D1PwzAQBmALgWgp_AEGlIkt4c6Jk1hiQRXfFSxFYrNi5yxctU2I3Qr-PYlaiQ2Wu-W9V6eHsXOEBAHzq0WidWcSDlAmkCaYZgdsjCAh5gjZIRsDQB5zie8jduL9AgAxy-UxG2GZSgEgxuz66eU5qkxw2yq4Zh2tqHZVIB-FD4qqtmlD452PGht9TedxTdYZR-sQGVou_Sk7stXS09l-T9jb3e18-hDPXu8fpzez2GQCQ1yhxVpbUwhpSEupJc9lykUGUvQDgZeQl2VegiBhhNYoUiBtpLWIRCKdsMtdb9s1nxvyQa2cHz6o1tRsvMolFpkU_N8gh6IokUMf5Lug6RrvO7Kq7dyq6r4Vghpw1UINuGrAVZCqHrc_uti3b3Tv9Huy1-wD17sA9RhbR53yg5bpTTsyQdWN-6v_B_8LiQw</recordid><startdate>20080613</startdate><enddate>20080613</enddate><creator>Qiao, Hai-Xuan</creator><creator>Hao, Chan-Juan</creator><creator>Li, Yan</creator><creator>He, Xin</creator><creator>Chen, Ri-Sheng</creator><creator>Cui, Jie</creator><creator>Xu, Zhi-Heng</creator><creator>Li, Wei</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>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20080613</creationdate><title>JNK activation mediates the apoptosis of xCT-deficient cells</title><author>Qiao, Hai-Xuan ; 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c
− is an anionic amino acid transport system highly specific for cystine and glutamate. The underlying mechanism of cell death of cultured cells from the subtle gray (
sut) mouse which contains an xCT null mutation remains elucidated. Our results show that the death of
sut cells is likely caused by apoptosis mediated by c-Jun N-terminal kinase (JNK). The JNK activation triggers both a caspase-dependent (caspases-9 and -3) and an ER stress-mediated (eIF2 and CHOP) pathway to induce apoptosis. These findings suggest the possible pathways involved in the cell death of xCT-deficient cells.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>18395005</pmid><doi>10.1016/j.bbrc.2008.03.134</doi><tpages>5</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0006-291X |
| ispartof | Biochemical and biophysical research communications, 2008-06, Vol.370 (4), p.584-588 |
| issn | 0006-291X 1090-2104 |
| language | eng |
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| source | ScienceDirect Freedom Collection 2022-2024 |
| subjects | Amino Acid Transport System y+ - genetics Animals Apoptosis Apoptosis - genetics Caspase 3 - metabolism Caspase 9 - metabolism Cell Line Cystine/glutamate transporter Endoplasmic Reticulum - metabolism ER stress Eukaryotic Initiation Factor-2 - metabolism JNK JNK Mitogen-Activated Protein Kinases - metabolism Melanocytes - metabolism Melanocytes - physiology Mice Mice, Mutant Strains Oxidative stress Transcription Factor CHOP - metabolism |
| title | JNK activation mediates the apoptosis of xCT-deficient cells |
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