Induction of BIM, a Proapoptotic BH3-Only BCL-2 Family Member, Is Critical for Neuronal Apoptosis
Sympathetic neuronal death induced by nerve growth factor (NGF) deprivation requires the macromolecular synthesis–dependent translocation of BAX from the cytosol to mitochondria and its subsequent integration into the mitochondrial outer membrane, followed by BAX-mediated cytochrome c (cyt c) releas...
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| Veröffentlicht in: | Neuron (Cambridge, Mass.) Mass.), 2001-03, Vol.29 (3), p.615-628 |
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| creator | Putcha, Girish V Moulder, Krista L Golden, Judith P Bouillet, Philippe Adams, Jerry A Strasser, Andreas Johnson, Eugene M |
| description | Sympathetic neuronal death induced by nerve growth factor (NGF) deprivation requires the macromolecular synthesis–dependent translocation of BAX from the cytosol to mitochondria and its subsequent integration into the mitochondrial outer membrane, followed by BAX-mediated cytochrome c (cyt c) release. The gene products triggering this process remain unknown. Here, we report that BIM, a member of the BH3-only proapoptotic subfamily of the BCL-2 protein family, is one such molecule. NGF withdrawal induced expression of BIM
EL, an integral mitochondrial membrane protein that functions upstream of (or in parallel with) the BAX/BCL-2 and caspase checkpoints.
Bim deletion conferred protection against developmental and induced neuronal apoptosis in both central and peripheral populations, but only transiently, suggesting that BIM—and perhaps other BH3-only proteins—serve partially redundant functions upstream of BAX-mediated cyt c release. |
| doi_str_mv | 10.1016/S0896-6273(01)00238-0 |
| format | Article |
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EL, an integral mitochondrial membrane protein that functions upstream of (or in parallel with) the BAX/BCL-2 and caspase checkpoints.
Bim deletion conferred protection against developmental and induced neuronal apoptosis in both central and peripheral populations, but only transiently, suggesting that BIM—and perhaps other BH3-only proteins—serve partially redundant functions upstream of BAX-mediated cyt c release.</description><identifier>ISSN: 0896-6273</identifier><identifier>EISSN: 1097-4199</identifier><identifier>DOI: 10.1016/S0896-6273(01)00238-0</identifier><identifier>PMID: 11301022</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Alternative Splicing ; Animals ; Animals, Newborn ; Apoptosis - physiology ; Apoptosis Regulatory Proteins ; bcl-2-Associated X Protein ; Bcl-2-Like Protein 11 ; BIM protein ; Carrier Proteins - biosynthesis ; Carrier Proteins - genetics ; Carrier Proteins - physiology ; Caspases - metabolism ; Cells, Cultured ; Cycloheximide - pharmacology ; Cytochrome c Group - metabolism ; Cytosol - metabolism ; Dactinomycin - pharmacology ; Enzyme Activation - drug effects ; Enzyme Inhibitors - pharmacology ; Intracellular Membranes - metabolism ; JNK Mitogen-Activated Protein Kinases ; MAP Kinase Kinase 4 ; Membrane Proteins ; Mice ; Mitochondria - metabolism ; Mitochondria - ultrastructure ; Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors ; Mitogen-Activated Protein Kinase Kinases - physiology ; Mutagenesis ; Nerve Growth Factor - administration & dosage ; Nerve Growth Factor - physiology ; Neurons - physiology ; Neurons - ultrastructure ; Phosphatidylinositol 3-Kinases - antagonists & inhibitors ; Phosphatidylinositol 3-Kinases - physiology ; Proto-Oncogene Proteins - metabolism ; Proto-Oncogene Proteins c-bcl-2 - metabolism ; Proto-Oncogene Proteins c-bcl-2 - physiology ; Rats ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger - analysis</subject><ispartof>Neuron (Cambridge, Mass.), 2001-03, Vol.29 (3), p.615-628</ispartof><rights>2001 Cell Press</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c505t-8badaeb918902cd1340fc227aba01df41af8bdeceee28b42e4124139be8a47563</citedby><cites>FETCH-LOGICAL-c505t-8badaeb918902cd1340fc227aba01df41af8bdeceee28b42e4124139be8a47563</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0896-6273(01)00238-0$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11301022$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Putcha, Girish V</creatorcontrib><creatorcontrib>Moulder, Krista L</creatorcontrib><creatorcontrib>Golden, Judith P</creatorcontrib><creatorcontrib>Bouillet, Philippe</creatorcontrib><creatorcontrib>Adams, Jerry A</creatorcontrib><creatorcontrib>Strasser, Andreas</creatorcontrib><creatorcontrib>Johnson, Eugene M</creatorcontrib><title>Induction of BIM, a Proapoptotic BH3-Only BCL-2 Family Member, Is Critical for Neuronal Apoptosis</title><title>Neuron (Cambridge, Mass.)</title><addtitle>Neuron</addtitle><description>Sympathetic neuronal death induced by nerve growth factor (NGF) deprivation requires the macromolecular synthesis–dependent translocation of BAX from the cytosol to mitochondria and its subsequent integration into the mitochondrial outer membrane, followed by BAX-mediated cytochrome c (cyt c) release. The gene products triggering this process remain unknown. Here, we report that BIM, a member of the BH3-only proapoptotic subfamily of the BCL-2 protein family, is one such molecule. NGF withdrawal induced expression of BIM
EL, an integral mitochondrial membrane protein that functions upstream of (or in parallel with) the BAX/BCL-2 and caspase checkpoints.
Bim deletion conferred protection against developmental and induced neuronal apoptosis in both central and peripheral populations, but only transiently, suggesting that BIM—and perhaps other BH3-only proteins—serve partially redundant functions upstream of BAX-mediated cyt c release.</description><subject>Alternative Splicing</subject><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Apoptosis - physiology</subject><subject>Apoptosis Regulatory Proteins</subject><subject>bcl-2-Associated X Protein</subject><subject>Bcl-2-Like Protein 11</subject><subject>BIM protein</subject><subject>Carrier Proteins - biosynthesis</subject><subject>Carrier Proteins - genetics</subject><subject>Carrier Proteins - physiology</subject><subject>Caspases - metabolism</subject><subject>Cells, Cultured</subject><subject>Cycloheximide - pharmacology</subject><subject>Cytochrome c Group - metabolism</subject><subject>Cytosol - metabolism</subject><subject>Dactinomycin - pharmacology</subject><subject>Enzyme Activation - drug effects</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Intracellular Membranes - metabolism</subject><subject>JNK Mitogen-Activated Protein Kinases</subject><subject>MAP Kinase Kinase 4</subject><subject>Membrane Proteins</subject><subject>Mice</subject><subject>Mitochondria - metabolism</subject><subject>Mitochondria - ultrastructure</subject><subject>Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors</subject><subject>Mitogen-Activated Protein Kinase Kinases - physiology</subject><subject>Mutagenesis</subject><subject>Nerve Growth Factor - administration & dosage</subject><subject>Nerve Growth Factor - physiology</subject><subject>Neurons - physiology</subject><subject>Neurons - ultrastructure</subject><subject>Phosphatidylinositol 3-Kinases - antagonists & inhibitors</subject><subject>Phosphatidylinositol 3-Kinases - physiology</subject><subject>Proto-Oncogene Proteins - metabolism</subject><subject>Proto-Oncogene Proteins c-bcl-2 - metabolism</subject><subject>Proto-Oncogene Proteins c-bcl-2 - physiology</subject><subject>Rats</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - analysis</subject><issn>0896-6273</issn><issn>1097-4199</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkE1Lw0AQhhdRtFZ_grInUTA6s0ma5CS2WC1UK6jnZbOZwEqSrbuJ0H9v-oEePQ0vPDMv8zB2hnCDgKPbN0izUTASSXgJeAUgwjSAPTZAyJIgwizbZ4Nf5Igde_8JgFGc4SE7QgwBQYgBU7Om6HRrbMNtycez52uu-KuzammXrW2N5uOnMFg01YqPJ_NA8KmqTR-eqc7JXfOZ5xNnek5VvLSOv1DnbNOH-80Bb_wJOyhV5el0N4fsY_rwPnkK5ovH2eR-HugY4jZIc1UoyjNMMxC6wDCCUguRqFwBFmWEqkzzgjQRiTSPBEUoIgyznFIVJfEoHLKL7d2ls18d-VbWxmuqKtWQ7bzEJE0wAejBeAtqZ713VMqlM7VyK4kg127lxq1ci5OAcuNWrvfOdwVdXlPxt7WT2QN3W4D6N78NOem1oUZTYRzpVhbW_FPxA9bRh4Q</recordid><startdate>20010301</startdate><enddate>20010301</enddate><creator>Putcha, Girish V</creator><creator>Moulder, Krista L</creator><creator>Golden, Judith P</creator><creator>Bouillet, Philippe</creator><creator>Adams, Jerry A</creator><creator>Strasser, Andreas</creator><creator>Johnson, Eugene M</creator><general>Elsevier Inc</general><scope>6I.</scope><scope>AAFTH</scope><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>7TK</scope></search><sort><creationdate>20010301</creationdate><title>Induction of BIM, a Proapoptotic BH3-Only BCL-2 Family Member, Is Critical for Neuronal Apoptosis</title><author>Putcha, Girish V ; Moulder, Krista L ; Golden, Judith P ; Bouillet, Philippe ; Adams, Jerry A ; Strasser, Andreas ; Johnson, Eugene M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c505t-8badaeb918902cd1340fc227aba01df41af8bdeceee28b42e4124139be8a47563</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Alternative Splicing</topic><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Apoptosis - physiology</topic><topic>Apoptosis Regulatory Proteins</topic><topic>bcl-2-Associated X Protein</topic><topic>Bcl-2-Like Protein 11</topic><topic>BIM protein</topic><topic>Carrier Proteins - biosynthesis</topic><topic>Carrier Proteins - genetics</topic><topic>Carrier Proteins - physiology</topic><topic>Caspases - metabolism</topic><topic>Cells, Cultured</topic><topic>Cycloheximide - pharmacology</topic><topic>Cytochrome c Group - metabolism</topic><topic>Cytosol - metabolism</topic><topic>Dactinomycin - pharmacology</topic><topic>Enzyme Activation - drug effects</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Intracellular Membranes - metabolism</topic><topic>JNK Mitogen-Activated Protein Kinases</topic><topic>MAP Kinase Kinase 4</topic><topic>Membrane Proteins</topic><topic>Mice</topic><topic>Mitochondria - metabolism</topic><topic>Mitochondria - ultrastructure</topic><topic>Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors</topic><topic>Mitogen-Activated Protein Kinase Kinases - physiology</topic><topic>Mutagenesis</topic><topic>Nerve Growth Factor - administration & dosage</topic><topic>Nerve Growth Factor - physiology</topic><topic>Neurons - physiology</topic><topic>Neurons - ultrastructure</topic><topic>Phosphatidylinositol 3-Kinases - antagonists & inhibitors</topic><topic>Phosphatidylinositol 3-Kinases - physiology</topic><topic>Proto-Oncogene Proteins - metabolism</topic><topic>Proto-Oncogene Proteins c-bcl-2 - metabolism</topic><topic>Proto-Oncogene Proteins c-bcl-2 - physiology</topic><topic>Rats</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Messenger - analysis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Putcha, Girish V</creatorcontrib><creatorcontrib>Moulder, Krista L</creatorcontrib><creatorcontrib>Golden, Judith P</creatorcontrib><creatorcontrib>Bouillet, Philippe</creatorcontrib><creatorcontrib>Adams, Jerry A</creatorcontrib><creatorcontrib>Strasser, Andreas</creatorcontrib><creatorcontrib>Johnson, Eugene M</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><jtitle>Neuron (Cambridge, Mass.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Putcha, Girish V</au><au>Moulder, Krista L</au><au>Golden, Judith P</au><au>Bouillet, Philippe</au><au>Adams, Jerry A</au><au>Strasser, Andreas</au><au>Johnson, Eugene M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Induction of BIM, a Proapoptotic BH3-Only BCL-2 Family Member, Is Critical for Neuronal Apoptosis</atitle><jtitle>Neuron (Cambridge, Mass.)</jtitle><addtitle>Neuron</addtitle><date>2001-03-01</date><risdate>2001</risdate><volume>29</volume><issue>3</issue><spage>615</spage><epage>628</epage><pages>615-628</pages><issn>0896-6273</issn><eissn>1097-4199</eissn><abstract>Sympathetic neuronal death induced by nerve growth factor (NGF) deprivation requires the macromolecular synthesis–dependent translocation of BAX from the cytosol to mitochondria and its subsequent integration into the mitochondrial outer membrane, followed by BAX-mediated cytochrome c (cyt c) release. The gene products triggering this process remain unknown. Here, we report that BIM, a member of the BH3-only proapoptotic subfamily of the BCL-2 protein family, is one such molecule. NGF withdrawal induced expression of BIM
EL, an integral mitochondrial membrane protein that functions upstream of (or in parallel with) the BAX/BCL-2 and caspase checkpoints.
Bim deletion conferred protection against developmental and induced neuronal apoptosis in both central and peripheral populations, but only transiently, suggesting that BIM—and perhaps other BH3-only proteins—serve partially redundant functions upstream of BAX-mediated cyt c release.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>11301022</pmid><doi>10.1016/S0896-6273(01)00238-0</doi><tpages>14</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Alternative Splicing Animals Animals, Newborn Apoptosis - physiology Apoptosis Regulatory Proteins bcl-2-Associated X Protein Bcl-2-Like Protein 11 BIM protein Carrier Proteins - biosynthesis Carrier Proteins - genetics Carrier Proteins - physiology Caspases - metabolism Cells, Cultured Cycloheximide - pharmacology Cytochrome c Group - metabolism Cytosol - metabolism Dactinomycin - pharmacology Enzyme Activation - drug effects Enzyme Inhibitors - pharmacology Intracellular Membranes - metabolism JNK Mitogen-Activated Protein Kinases MAP Kinase Kinase 4 Membrane Proteins Mice Mitochondria - metabolism Mitochondria - ultrastructure Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors Mitogen-Activated Protein Kinase Kinases - physiology Mutagenesis Nerve Growth Factor - administration & dosage Nerve Growth Factor - physiology Neurons - physiology Neurons - ultrastructure Phosphatidylinositol 3-Kinases - antagonists & inhibitors Phosphatidylinositol 3-Kinases - physiology Proto-Oncogene Proteins - metabolism Proto-Oncogene Proteins c-bcl-2 - metabolism Proto-Oncogene Proteins c-bcl-2 - physiology Rats Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - analysis |
| title | Induction of BIM, a Proapoptotic BH3-Only BCL-2 Family Member, Is Critical for Neuronal Apoptosis |
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