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本文引用的文献

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A tumor suppressor function for caspase-2.半胱天冬酶-2的肿瘤抑制功能。
Proc Natl Acad Sci U S A. 2009 Mar 31;106(13):5336-41. doi: 10.1073/pnas.0811928106. Epub 2009 Mar 11.
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The enigma of caspase-2: the laymen's view.半胱天冬酶-2之谜：外行的观点。
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Knockdown of BCL2L12 leads to cisplatin resistance in MDA-MB-231 breast cancer cells.敲低BCL2L12会导致MDA-MB-231乳腺癌细胞对顺铂产生耐药性。
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Bcl2L12-mediated inhibition of effector caspase-3 and caspase-7 via distinct mechanisms in glioblastoma.Bcl2L12通过不同机制介导对胶质母细胞瘤中效应半胱天冬酶-3和半胱天冬酶-7的抑制作用。
Proc Natl Acad Sci U S A. 2008 Aug 5;105(31):10703-8. doi: 10.1073/pnas.0712034105. Epub 2008 Jul 31.
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The IRF family transcription factors in immunity and oncogenesis.免疫与肿瘤发生中的IRF家族转录因子。
Annu Rev Immunol. 2008;26:535-84. doi: 10.1146/annurev.immunol.26.021607.090400.
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A cell-type-specific requirement for IFN regulatory factor 5 (IRF5) in Fas-induced apoptosis.Fas诱导的细胞凋亡中对干扰素调节因子5（IRF5）的细胞类型特异性需求。
Proc Natl Acad Sci U S A. 2008 Feb 19;105(7):2556-61. doi: 10.1073/pnas.0712295105. Epub 2008 Feb 11.
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Caspase-2 is required for cell death induced by cytoskeletal disruption.细胞骨架破坏诱导的细胞死亡需要Caspase-2。
Oncogene. 2008 May 29;27(24):3393-404. doi: 10.1038/sj.onc.1211005. Epub 2008 Jan 14.
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DAI (DLM-1/ZBP1) is a cytosolic DNA sensor and an activator of innate immune response.DAI（DLM-1/ZBP1）是一种胞质DNA传感器，也是先天免疫反应的激活剂。
Nature. 2007 Jul 26;448(7152):501-5. doi: 10.1038/nature06013. Epub 2007 Jul 8.
9
Role of IFN regulatory factor 5 transcription factor in antiviral immunity and tumor suppression.干扰素调节因子5转录因子在抗病毒免疫和肿瘤抑制中的作用。
Proc Natl Acad Sci U S A. 2007 Feb 27;104(9):3402-7. doi: 10.1073/pnas.0611559104. Epub 2007 Feb 20.
10
Bcl2L12 inhibits post-mitochondrial apoptosis signaling in glioblastoma.Bcl2L12抑制胶质母细胞瘤中线粒体后的凋亡信号传导。
Genes Dev. 2007 Jan 1;21(1):98-111. doi: 10.1101/gad.1480007.

与相邻的Irf3基因破坏同时发生的突变揭示了Bcl2L12的细胞类型依赖性促凋亡作用。

Cell type-dependent proapoptotic role of Bcl2L12 revealed by a mutation concomitant with the disruption of the juxtaposed Irf3 gene.

作者信息

Nakajima Akira, Nishimura Keishiro, Nakaima Yukana, Oh Tomohiko, Noguchi Shigeru, Taniguchi Tadatsugu, Tamura Tomohiko

机构信息

Department of Immunology, Graduate School of Medicine and Faculty of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan.

出版信息

Proc Natl Acad Sci U S A. 2009 Jul 28;106(30):12448-52. doi: 10.1073/pnas.0905702106. Epub 2009 Jul 17.

DOI:10.1073/pnas.0905702106
PMID:19617565
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2718395/
Abstract

The generation of mice lacking the expression of the IRF3 transcription factor (Irf3(-/-) mice) has revealed its crucial role in the activation of the type I IFN response. The Bcl2l12 gene, encoding Bcl2L12 protein structurally related to the Bcl-2 family, was found to almost overlap with the Irf3 gene, and the null mutation previously introduced into the Irf3 allele resulted in the functional inactivation of the Bcl2l12 gene; therefore, the mice are correctly termed Irf3(-/-)Bcl2l12(-/-) mice. Embryonic fibroblasts from Irf3(-/-)Bcl2l12(-/-) mice (Irf3(-/-)Bcl2l12(-/-) MEFs) showed resistance to DNA damage-induced apoptosis, accompanied by impaired caspase cleavage. This apoptotic defect in Irf3(-/-)Bcl2l12(-/-) MEFs was rescued by the ectopic expression of Bcl2L12, but not IRF3. The Bcl2L12-mediated apoptotic response depended on the cell type and extracellular stimulus. In contrast, the previously reported defect in the induction of type I IFN genes by nucleic acids in Irf3(-/-)Bcl2l12(-/-) MEFs was rescued by expressing IRF3, but not Bcl2L12. Thus, our present study revealed, on the one hand, a cell type-dependent proapoptotic function of Bcl2L12 and, on the other hand, confirmed the essential role of IRF3 in type I IFN response.

摘要

缺乏IRF3转录因子表达的小鼠（Irf3基因敲除小鼠）的产生揭示了其在I型干扰素反应激活中的关键作用。编码与Bcl-2家族结构相关的Bcl2L12蛋白的Bcl2l12基因，被发现几乎与Irf3基因重叠，先前引入Irf3等位基因的无效突变导致Bcl2l12基因功能失活；因此，这些小鼠被正确地称为Irf3(-/-)Bcl2l12(-/-)小鼠。来自Irf3(-/-)Bcl2l12(-/-)小鼠的胚胎成纤维细胞（Irf3(-/-)Bcl2l12(-/-) MEFs）对DNA损伤诱导的凋亡具有抗性，同时伴有半胱天冬酶切割受损。Irf3(-/-)Bcl2l12(-/-) MEFs中的这种凋亡缺陷通过Bcl2L12的异位表达得以挽救，但IRF3不能。Bcl2L12介导的凋亡反应取决于细胞类型和细胞外刺激。相反，先前报道的Irf3(-/-)Bcl2l12(-/-) MEFs中核酸诱导I型干扰素基因的缺陷通过表达IRF3得以挽救，但Bcl2L12不能。因此，我们目前的研究一方面揭示了Bcl2L12细胞类型依赖性的促凋亡功能，另一方面证实了IRF3在I型干扰素反应中的重要作用。