• 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

The roles of Bid.

作者信息

Esposti M Degli

机构信息

Cancer Research Campaign Molecular Pharmacology Group, School of Biological Sciences, University of Manchester, Oxford Road, Manchester M13 9PT, UK.

出版信息

Apoptosis. 2002 Oct;7(5):433-40. doi: 10.1023/a:1020035124855.

DOI:10.1023/a:1020035124855
PMID:12207176
Abstract

Bid is an abundant pro-apoptotic protein of the Bcl-2 family that is crucial for death receptor-mediated apoptosis in many cell systems. Bid action has been proposed to involve the mitochondrial re-location of its truncated form, tBid, to facilitate the release of apoptogenic proteins like cytochrome c. However, the precise mechanism of (t)Bid action is unknown. To advance our knowledge, this review evaluates the basic steps of Bid activation--caspase cleavage, dissociation of tBid, and lipid-mediated mitochondrial relocation--and their structure-function aspects. Relevant current information is thoroughly examined to outline the problems that hamper our understanding of the possible roles of Bid in cell life and death, and suggest valuable directions for obtaining a clarification of its pro-apoptotic mechanism.

摘要

相似文献

1
The roles of Bid.
Apoptosis. 2002 Oct;7(5):433-40. doi: 10.1023/a:1020035124855.
2
Bid, a widely expressed proapoptotic protein of the Bcl-2 family, displays lipid transfer activity.Bid是一种广泛表达的Bcl-2家族促凋亡蛋白,具有脂质转移活性。
Mol Cell Biol. 2001 Nov;21(21):7268-76. doi: 10.1128/MCB.21.21.7268-7276.2001.
3
Cleavage of BID during cytotoxic drug and UV radiation-induced apoptosis occurs downstream of the point of Bcl-2 action and is catalysed by caspase-3: a potential feedback loop for amplification of apoptosis-associated mitochondrial cytochrome c release.在细胞毒性药物和紫外线辐射诱导的细胞凋亡过程中,BID的裂解发生在Bcl-2作用点的下游,并由caspase-3催化:这是一个潜在的反馈回路,用于放大与细胞凋亡相关的线粒体细胞色素c释放。
Cell Death Differ. 2000 Jun;7(6):556-65. doi: 10.1038/sj.cdd.4400689.
4
Pro-apoptotic Bid induces membrane perturbation by inserting selected lysolipids into the bilayer.促凋亡蛋白Bid通过将选定的溶血磷脂插入双层膜来诱导膜扰动。
Biochem J. 2005 Apr 1;387(Pt 1):109-18. doi: 10.1042/BJ20041389.
5
Cleavage of BID by caspase 8 mediates the mitochondrial damage in the Fas pathway of apoptosis.半胱天冬酶8对BID的切割介导了凋亡的Fas途径中的线粒体损伤。
Cell. 1998 Aug 21;94(4):491-501. doi: 10.1016/s0092-8674(00)81590-1.
6
Sequence and functional similarities between pro-apoptotic Bid and plant lipid transfer proteins.促凋亡蛋白Bid与植物脂质转移蛋白之间的序列和功能相似性。
Biochim Biophys Acta. 2002 Feb 15;1553(3):331-40. doi: 10.1016/s0005-2728(02)00187-1.
7
The anti-apoptotic effect of leukotriene D4 involves the prevention of caspase 8 activation and Bid cleavage.白三烯D4的抗凋亡作用涉及防止半胱天冬酶8激活和Bid裂解。
Biochem J. 2003 Apr 1;371(Pt 1):115-24. doi: 10.1042/BJ20021669.
8
Direct addition of BimL to mitochondria does not lead to cytochrome c release.将BimL直接添加到线粒体中不会导致细胞色素c的释放。
FEBS Lett. 2002 Jul 3;522(1-3):29-34. doi: 10.1016/s0014-5793(02)02871-5.
9
Cadmium induces apoptotic cell death in WI 38 cells via caspase-dependent Bid cleavage and calpain-mediated mitochondrial Bax cleavage by Bcl-2-independent pathway.镉通过不依赖Bcl-2的途径,经半胱天冬酶依赖性的Bid裂解和钙蛋白酶介导的线粒体Bax裂解,诱导WI 38细胞发生凋亡性细胞死亡。
Biochem Pharmacol. 2004 Nov 1;68(9):1845-55. doi: 10.1016/j.bcp.2004.06.021.
10
Release of cytochrome c and activation of pro-caspase-9 following lysosomal photodamage involves Bid cleavage.溶酶体光损伤后细胞色素c的释放及前半胱天冬酶-9的激活涉及Bid裂解。
Cell Death Differ. 2002 Sep;9(9):934-44. doi: 10.1038/sj.cdd.4401048.

引用本文的文献

1
Bisabolol as a natural anticancer agent: molecular insights and therapeutic potential in oncology.红没药醇作为一种天然抗癌剂:肿瘤学中的分子见解与治疗潜力
Med Oncol. 2025 Sep 20;42(11):485. doi: 10.1007/s12032-025-03005-8.
2
Photoswitchable intein for light control of covalent protein binding and cleavage.用于光控共价蛋白质结合与切割的光开关内含肽
Nat Commun. 2025 Sep 11;16(1):8263. doi: 10.1038/s41467-025-63595-9.
3
Vimentin and p53 Immunoreactivity in Cases of Traumatic Brain Injury.创伤性脑损伤病例中的波形蛋白和p53免疫反应性
J Pers Med. 2025 Mar 31;15(4):135. doi: 10.3390/jpm15040135.
4
Transcriptome Data Combined With Mendelian Randomization Analysis Identifies Key Genes Associated With Mitochondria and Programmed Cell Death in Intervertebral Disc Degeneration.转录组数据结合孟德尔随机化分析确定与椎间盘退变中线粒体和程序性细胞死亡相关的关键基因。
JOR Spine. 2025 Mar 24;8(1):e70057. doi: 10.1002/jsp2.70057. eCollection 2025 Mar.
5
Single cell analysis reveals that SPP1 macrophages enhance tumor progression by triggering fibroblast extracellular vesicles.单细胞分析显示,SPP1巨噬细胞通过触发成纤维细胞外泌体来促进肿瘤进展。
Transl Oncol. 2025 May;55:102347. doi: 10.1016/j.tranon.2025.102347. Epub 2025 Mar 13.
6
Quantitative chemical proteomics reveals that phenethyl isothiocyanate covalently targets BID to promote apoptosis.定量化学蛋白质组学研究表明,苯乙基异硫氰酸酯通过共价靶向BID来促进细胞凋亡。
Cell Death Discov. 2024 Oct 29;10(1):456. doi: 10.1038/s41420-024-02225-7.
7
Activation of p38 and JNK by ROS Contributes to Deoxybouvardin-Mediated Intrinsic Apoptosis in Oxaliplatin-Sensitive and -Resistant Colorectal Cancer Cells.活性氧(ROS)对p38和JNK的激活作用有助于脱氧布瓦西丁介导的奥沙利铂敏感和耐药结直肠癌细胞的内源性凋亡。
Antioxidants (Basel). 2024 Jul 19;13(7):866. doi: 10.3390/antiox13070866.
8
The Spectrum of CAR Cellular Effectors: Modes of Action in Anti-Tumor Immunity.嵌合抗原受体(CAR)细胞效应器的谱系:抗肿瘤免疫中的作用模式
Cancers (Basel). 2024 Jul 22;16(14):2608. doi: 10.3390/cancers16142608.
9
Highly expressed of BID indicates poor prognosis and mediates different tumor microenvironment characteristics in clear cell renal cell carcinoma.BID的高表达预示着透明细胞肾细胞癌的预后不良,并介导不同的肿瘤微环境特征。
Discov Oncol. 2024 May 20;15(1):176. doi: 10.1007/s12672-024-01035-8.
10
Upregulated ECM genes and increased synaptic activity in Parkinson's human DA neurons with PINK1/ PRKN mutations.帕金森病中携带PINK1/PRKN突变的人类多巴胺能神经元中细胞外基质基因上调及突触活动增加。
NPJ Parkinsons Dis. 2024 May 18;10(1):103. doi: 10.1038/s41531-024-00715-0.