• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

Bcl-2家族蛋白与线粒体

Bcl-2 family proteins and mitochondria.

作者信息

Reed J C, Jurgensmeier J M, Matsuyama S

机构信息

The Burnham Institute, Program on Apoptosis and Cell Death Research, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA.

出版信息

Biochim Biophys Acta. 1998 Aug 10;1366(1-2):127-37. doi: 10.1016/s0005-2728(98)00108-x.

DOI:10.1016/s0005-2728(98)00108-x
PMID:9714773
Abstract

The Bcl-2 family of proteins plays a pivotal role in regulating cell life and death. Many of these proteins reside in the outer mitochondrial membrane, oriented towards the cytosol. Cytoprotective Bcl-2 family proteins such as Bcl-2 and Bcl-XL prevent mitochondrial permeability transition pore opening and release of apoptogenic proteins from mitochondria under many circumstances that would otherwise result in either apoptosis or necrosis. In contrast, some pro-apoptotic members of this family such as Bax can induce these destructive changes in mitochondria in both mammalian cells and when expressed exogenously in yeast. The mechanisms by which Bcl-2 family proteins control cell life and death remain elusive, but may include both the ability to form ion channels or pores in membranes and physical interactions with a variety of proteins implicated in apoptosis regulation.

摘要

Bcl-2蛋白家族在调节细胞生死过程中起着关键作用。这些蛋白中的许多定位于线粒体外膜,面向细胞质。在许多情况下,诸如Bcl-2和Bcl-XL等具有细胞保护作用的Bcl-2家族蛋白可防止线粒体通透性转换孔开放及凋亡蛋白从线粒体释放,否则这些情况会导致凋亡或坏死。相反,该家族的一些促凋亡成员,如Bax,在哺乳动物细胞中以及在酵母中外源表达时,均可诱导线粒体发生这些破坏性变化。Bcl-2家族蛋白控制细胞生死的机制仍然不明,但可能包括在膜中形成离子通道或孔的能力以及与多种参与凋亡调节的蛋白的物理相互作用。

相似文献

1
Bcl-2 family proteins and mitochondria.Bcl-2家族蛋白与线粒体
Biochim Biophys Acta. 1998 Aug 10;1366(1-2):127-37. doi: 10.1016/s0005-2728(98)00108-x.
2
Bcl-2 family proteins regulate the release of apoptogenic cytochrome c by the mitochondrial channel VDAC.Bcl-2家族蛋白通过线粒体通道VDAC调节凋亡诱导因子细胞色素c的释放。
Nature. 1999 Jun 3;399(6735):483-7. doi: 10.1038/20959.
3
Investigation of bax-induced release of cytochrome c from yeast mitochondria permeability of mitochondrial membranes, role of VDAC and ATP requirement.对bax诱导酵母线粒体释放细胞色素c的研究:线粒体膜通透性、电压依赖性阴离子通道的作用及ATP需求
Eur J Biochem. 1999 Mar;260(3):684-91. doi: 10.1046/j.1432-1327.1999.00198.x.
4
Regulation of apoptosis by BH3 domains in a cell-free system.细胞游离体系中BH3结构域对细胞凋亡的调控
Curr Biol. 1997 Dec 1;7(12):913-20. doi: 10.1016/s0960-9822(06)00410-6.
5
Mechanisms of cytochrome c release by proapoptotic BCL-2 family members.促凋亡BCL-2家族成员释放细胞色素c的机制。
Biochem Biophys Res Commun. 2003 May 9;304(3):437-44. doi: 10.1016/s0006-291x(03)00615-6.
6
The voltage-dependent anion channel: an essential player in apoptosis.电压依赖性阴离子通道:细胞凋亡中的关键角色。
Biochimie. 2002 Feb-Mar;84(2-3):187-93. doi: 10.1016/s0300-9084(02)01370-6.
7
Bax and Bcl-xL independently regulate apoptotic changes of yeast mitochondria that require VDAC but not adenine nucleotide translocator.Bax和Bcl-xL独立调节酵母线粒体的凋亡变化,这种变化需要电压依赖性阴离子通道(VDAC),但不需要腺嘌呤核苷酸转位酶。
Oncogene. 2000 Sep 7;19(38):4309-18. doi: 10.1038/sj.onc.1203788.
8
Bax and other pro-apoptotic Bcl-2 family "killer-proteins" and their victim the mitochondrion.Bax及其他促凋亡的Bcl-2家族“杀手蛋白”与其受害者线粒体。
Cell Tissue Res. 2001 Dec;306(3):347-61. doi: 10.1007/s00441-001-0472-0. Epub 2001 Oct 30.
9
Control of mitochondrial permeability by Bcl-2 family members.Bcl-2家族成员对线粒体通透性的调控。
Biochim Biophys Acta. 2004 Mar 1;1644(2-3):107-13. doi: 10.1016/j.bbamcr.2003.10.016.
10
Essential role of voltage-dependent anion channel in various forms of apoptosis in mammalian cells.电压依赖性阴离子通道在哺乳动物细胞各种形式凋亡中的重要作用。
J Cell Biol. 2001 Jan 22;152(2):237-50. doi: 10.1083/jcb.152.2.237.

引用本文的文献

1
Chronic mild stress disrupts mitophagy and mitochondrial status in rat frontal cortex.慢性轻度应激会破坏大鼠前额叶皮质中的线粒体自噬和线粒体状态。
J Transl Med. 2025 May 23;23(1):580. doi: 10.1186/s12967-025-06604-1.
2
Two spurge species, Euphorbia resinifera O. Berg and Euphorbia officinarum subsp. echinus (Hook.f. & Coss.) Vindt inhibit colon cancer.两种大戟属植物,乳浆大戟和飞扬草,抑制结肠癌。
BMC Complement Med Ther. 2024 Jul 10;24(1):261. doi: 10.1186/s12906-024-04566-3.
3
Anti-Colorectal Cancer Effects of Fucoidan Complex-Based Functional Beverage Through Retarding Proliferation, Cell Cycle and Epithelial-Mesenchymal Transition Signaling Pathways.
褐藻糖胶复合功能性饮品通过抑制增殖、细胞周期和上皮-间充质转化信号通路抑制结直肠癌的作用。
Integr Cancer Ther. 2023 Jan-Dec;22:15347354231213613. doi: 10.1177/15347354231213613.
4
Novel -Arylmethyl-aniline/chalcone hybrids as potential VEGFR inhibitors: synthesis, biological evaluations, and molecular dynamic simulations.新型芳基甲基苯胺/查尔酮杂合体作为潜在的 VEGFR 抑制剂:合成、生物评价和分子动力学模拟。
J Enzyme Inhib Med Chem. 2023 Dec;38(1):2278022. doi: 10.1080/14756366.2023.2278022. Epub 2023 Nov 20.
5
RAGE Inhibitors for Targeted Therapy of Cancer: A Comprehensive Review.RAGE 抑制剂在癌症靶向治疗中的应用:全面综述。
Int J Mol Sci. 2022 Dec 23;24(1):266. doi: 10.3390/ijms24010266.
6
Cancer and Apoptosis.癌症与细胞凋亡。
Methods Mol Biol. 2022;2543:191-210. doi: 10.1007/978-1-0716-2553-8_16.
7
Mitochondrial Medicine: A Promising Therapeutic Option Against Various Neurodegenerative Disorders.线粒体医学:对抗多种神经退行性疾病的有前途的治疗选择。
Curr Neuropharmacol. 2023;21(5):1165-1183. doi: 10.2174/1570159X20666220830112408.
8
Ameliorates Non-Alcoholic Fatty Liver Disease by Inhibiting Oxidative Stress-Mediated Steatosis and Apoptosis through NRF2-ARE Activation.通过激活NRF2-ARE抑制氧化应激介导的脂肪变性和细胞凋亡来改善非酒精性脂肪性肝病。
Antioxidants (Basel). 2021 Jul 29;10(8):1226. doi: 10.3390/antiox10081226.
9
Anticancer Properties of Fluorinated Aminophenylhydrazines on A549 Lung Carcinoma Cell Line.氟化氨基苯肼对A549肺癌细胞系的抗癌特性
Iran J Public Health. 2021 Mar;50(3):550-556. doi: 10.18502/ijph.v50i3.5596.
10
Effects of imperatorin on apoptosis and synaptic plasticity in vascular dementia rats.欧前胡素对血管性痴呆大鼠细胞凋亡及突触可塑性的影响。
Sci Rep. 2021 Apr 21;11(1):8590. doi: 10.1038/s41598-021-88206-7.