{"@context":{"@vocab":"https://cir.nii.ac.jp/schema/1.0/","rdfs":"http://www.w3.org/2000/01/rdf-schema#","dc":"http://purl.org/dc/elements/1.1/","dcterms":"http://purl.org/dc/terms/","foaf":"http://xmlns.com/foaf/0.1/","prism":"http://prismstandard.org/namespaces/basic/2.0/","cinii":"http://ci.nii.ac.jp/ns/1.0/","datacite":"https://schema.datacite.org/meta/kernel-4/","ndl":"http://ndl.go.jp/dcndl/terms/","jpcoar":"https://github.com/JPCOAR/schema/blob/master/2.0/"},"@id":"https://cir.nii.ac.jp/crid/1361699996473435008.json","@type":"Article","productIdentifier":[{"identifier":{"@type":"DOI","@value":"10.1073/pnas.97.1.466"}},{"identifier":{"@type":"URI","@value":"https://pnas.org/doi/pdf/10.1073/pnas.97.1.466"}},{"identifier":{"@type":"NAID","@value":"30016224382"}}],"dc:title":[{"@value":"Epistatic and independent functions of Caspase-3 and Bcl-X\n            <sub>L</sub>\n            in developmental programmed cell death"}],"description":[{"type":"abstract","notation":[{"@value":"<jats:p>\n            The number of neurons in the mammalian brain is determined by a balance between cell proliferation and programmed cell death. Recent studies indicated that Bcl-X\n            <jats:sub>L</jats:sub>\n            prevents, whereas Caspase-3 mediates, cell death in the developing nervous system, but whether Bcl-X\n            <jats:sub>L</jats:sub>\n            directly blocks the apoptotic function of Caspase-3\n            <jats:italic>in vivo</jats:italic>\n            is not known. To examine this question, we generated\n            <jats:italic>bcl-x</jats:italic>\n            /\n            <jats:italic>caspase-3</jats:italic>\n            double mutants and found that\n            <jats:italic>caspase-3</jats:italic>\n            deficiency abrogated the increased apoptosis of postmitotic neurons but not the increased hematopoietic cell death and embryonic lethality caused by the\n            <jats:italic>bcl-x</jats:italic>\n            mutation. In contrast,\n            <jats:italic>caspase-3</jats:italic>\n            , but not\n            <jats:italic>bcl-x</jats:italic>\n            , deficiency changed the normal incidence of neuronal progenitor cell apoptosis, consistent with the lack of expression of Bcl-X\n            <jats:sub>L</jats:sub>\n            in the proliferative population of the embryonic cortex. Thus, although Caspase-3 is epistatically downstream to Bcl-X\n            <jats:sub>L</jats:sub>\n            in postmitotic neurons, it independently regulates apoptosis of neuronal founder cells. Taken together, these results establish a role of programmed cell death in regulating the size of progenitor population in the central nervous system, a function that is distinct from the classic role of cell death in matching postmitotic neuronal population with postsynaptic targets.\n          </jats:p>"}]}],"creator":[{"@id":"https://cir.nii.ac.jp/crid/1580009751483526400","@type":"Researcher","foaf:name":[{"@value":"K. A. Roth"}],"jpcoar:affiliationName":[{"@value":"Department of Pathology, Washington University School of Medicine, St. Louis, MO 63110; Section of Immunobiology, Howard Hughes Medical Institute, and Section of Neurobiology, Yale University School of Medicine, New Haven, CT 06510; and Vertex Pharmaceuticals, Inc., Cambridge, MA 02139"}]},{"@id":"https://cir.nii.ac.jp/crid/1381699996473435014","@type":"Researcher","foaf:name":[{"@value":"C.-Y. Kuan"}],"jpcoar:affiliationName":[{"@value":"Department of Pathology, Washington University School of Medicine, St. Louis, MO 63110; Section of Immunobiology, Howard Hughes Medical Institute, and Section of Neurobiology, Yale University School of Medicine, New Haven, CT 06510; and Vertex Pharmaceuticals, Inc., Cambridge, MA 02139"}]},{"@id":"https://cir.nii.ac.jp/crid/1381699996473435136","@type":"Researcher","foaf:name":[{"@value":"T. F. Haydar"}],"jpcoar:affiliationName":[{"@value":"Department of Pathology, Washington University School of Medicine, St. Louis, MO 63110; Section of Immunobiology, Howard Hughes Medical Institute, and Section of Neurobiology, Yale University School of Medicine, New Haven, CT 06510; and Vertex Pharmaceuticals, Inc., Cambridge, MA 02139"}]},{"@id":"https://cir.nii.ac.jp/crid/1381699996473435012","@type":"Researcher","foaf:name":[{"@value":"C. D'Sa-Eipper"}],"jpcoar:affiliationName":[{"@value":"Department of Pathology, Washington University School of Medicine, St. Louis, MO 63110; Section of Immunobiology, Howard Hughes Medical Institute, and Section of Neurobiology, Yale University School of Medicine, New Haven, CT 06510; and Vertex Pharmaceuticals, Inc., Cambridge, MA 02139"}]},{"@id":"https://cir.nii.ac.jp/crid/1381699996473435137","@type":"Researcher","foaf:name":[{"@value":"K. S. Shindler"}],"jpcoar:affiliationName":[{"@value":"Department of Pathology, Washington University School of Medicine, St. Louis, MO 63110; Section of Immunobiology, Howard Hughes Medical Institute, and Section of Neurobiology, Yale University School of Medicine, New Haven, CT 06510; and Vertex Pharmaceuticals, Inc., Cambridge, MA 02139"}]},{"@id":"https://cir.nii.ac.jp/crid/1381699996473435013","@type":"Researcher","foaf:name":[{"@value":"T. S. Zheng"}],"jpcoar:affiliationName":[{"@value":"Department of Pathology, Washington University School of Medicine, St. Louis, MO 63110; Section of Immunobiology, Howard Hughes Medical Institute, and Section of Neurobiology, Yale University School of Medicine, New Haven, CT 06510; and Vertex Pharmaceuticals, Inc., Cambridge, MA 02139"}]},{"@id":"https://cir.nii.ac.jp/crid/1381699996473435008","@type":"Researcher","foaf:name":[{"@value":"K. Kuida"}],"jpcoar:affiliationName":[{"@value":"Department of Pathology, Washington University School of Medicine, St. Louis, MO 63110; Section of Immunobiology, Howard Hughes Medical Institute, and Section of Neurobiology, Yale University School of Medicine, New Haven, CT 06510; and Vertex Pharmaceuticals, Inc., Cambridge, MA 02139"}]},{"@id":"https://cir.nii.ac.jp/crid/1381699996473435011","@type":"Researcher","foaf:name":[{"@value":"R. A. Flavell"}],"jpcoar:affiliationName":[{"@value":"Department of Pathology, Washington University School of Medicine, St. Louis, MO 63110; Section of Immunobiology, Howard Hughes Medical Institute, and Section of Neurobiology, Yale University School of Medicine, New Haven, CT 06510; and Vertex Pharmaceuticals, Inc., Cambridge, MA 02139"}]},{"@id":"https://cir.nii.ac.jp/crid/1381699996473435009","@type":"Researcher","foaf:name":[{"@value":"P. Rakic"}],"jpcoar:affiliationName":[{"@value":"Department of Pathology, Washington University School of Medicine, St. Louis, MO 63110; Section of Immunobiology, Howard Hughes Medical Institute, and Section of Neurobiology, Yale University School of Medicine, New Haven, CT 06510; and Vertex Pharmaceuticals, Inc., Cambridge, MA 02139"}]}],"publication":{"publicationIdentifier":[{"@type":"PISSN","@value":"00278424"},{"@type":"EISSN","@value":"10916490"}],"prism:publicationName":[{"@value":"Proceedings of the National Academy of Sciences"}],"dc:publisher":[{"@value":"Proceedings of the National Academy of Sciences"}],"prism:publicationDate":"2000-01-04","prism:volume":"97","prism:number":"1","prism:startingPage":"466","prism:endingPage":"471"},"reviewed":"false","url":[{"@id":"https://pnas.org/doi/pdf/10.1073/pnas.97.1.466"}],"createdAt":"2002-07-26","modifiedAt":"2022-04-13","relatedProduct":[{"@id":"https://cir.nii.ac.jp/crid/1360567180073986560","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Laminin regulates postnatal oligodendrocyte production by promoting oligodendrocyte progenitor survival in the subventricular zone"}]},{"@id":"https://cir.nii.ac.jp/crid/1360584339765310336","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Apoptotic cell death in disease—Current understanding of the NCCD 2023"}]},{"@id":"https://cir.nii.ac.jp/crid/1360846640818526080","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Local Apoptosis Modulates Early Mammalian Brain Development through the Elimination of Morphogen-Producing Cells"}]},{"@id":"https://cir.nii.ac.jp/crid/1390282679673200384","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy","isCitedBy"],"jpcoar:relatedTitle":[{"@language":"en","@value":"The Role of Apaf-1 in Programmed Cell Death: From Worm to Tumor."},{"@language":"ja-Kana","@value":"Role of Apaf 1 in Programmed Cell Death From Worm to Tumor"}]},{"@id":"https://cir.nii.ac.jp/crid/1390282679838820608","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@language":"en","@value":"Apoptosis in the Medaka Embryo in the Early Developmental Stage"}]}],"dataSourceIdentifier":[{"@type":"CROSSREF","@value":"10.1073/pnas.97.1.466"},{"@type":"CIA","@value":"30016224382"},{"@type":"CROSSREF","@value":"10.1002/glia.22365_references_DOI_NdEYKF7arNqtcuIrPOp9M5Yapzo"},{"@type":"CROSSREF","@value":"10.1038/s41418-023-01153-w_references_DOI_NdEYKF7arNqtcuIrPOp9M5Yapzo"},{"@type":"CROSSREF","@value":"10.1267/ahc.06013_references_DOI_NdEYKF7arNqtcuIrPOp9M5Yapzo"},{"@type":"CROSSREF","@value":"10.1016/j.devcel.2013.11.015_references_DOI_NdEYKF7arNqtcuIrPOp9M5Yapzo"},{"@type":"CROSSREF","@value":"10.1247/csf.28.3_references_DOI_NdEYKF7arNqtcuIrPOp9M5Yapzo"}]}