دورية أكاديمية

The carboxyl-terminal sequence of bim enables bax activation and killing of unprimed cells

التفاصيل البيبلوغرافية
العنوان: The carboxyl-terminal sequence of bim enables bax activation and killing of unprimed cells
المؤلفون: Xiaoke Chi, Dang Nguyen, James M Pemberton, Elizabeth J Osterlund, Qian Liu, Hetal Brahmbhatt, Zhi Zhang, Jialing Lin, Brian Leber, David W Andrews
المصدر: eLife, Vol 9 (2020)
بيانات النشر: eLife Sciences Publications Ltd, 2020.
سنة النشر: 2020
المجموعة: LCC:Medicine
LCC:Science
LCC:Biology (General)
مصطلحات موضوعية: primary murine neurons, MEF cells, BMK cells, apoptosis, Bcl-2 family proteins, mitochondrial outer membrane permeabilization, Medicine, Science, Biology (General), QH301-705.5
الوصف: The Bcl-2 family BH3 protein Bim promotes apoptosis at mitochondria by activating the pore-forming proteins Bax and Bak and by inhibiting the anti-apoptotic proteins Bcl-XL, Bcl-2 and Mcl-1. Bim binds to these proteins via its BH3 domain and to the mitochondrial membrane by a carboxyl-terminal sequence (CTS). In cells killed by Bim, the expression of a Bim mutant in which the CTS was deleted (BimL-dCTS) triggered apoptosis that correlated with inhibition of anti-apoptotic proteins being sufficient to permeabilize mitochondria isolated from the same cells. Detailed analysis of the molecular mechanism demonstrated that BimL-dCTS inhibited Bcl-XL but did not activate Bax. Examination of additional point mutants unexpectedly revealed that the CTS of Bim directly interacts with Bax, is required for physiological concentrations of Bim to activate Bax and that different residues in the CTS enable Bax activation and binding to membranes.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 2050-084X
العلاقة: https://elifesciences.org/articles/44525Test; https://doaj.org/toc/2050-084XTest
DOI: 10.7554/eLife.44525
الوصول الحر: https://doaj.org/article/3930186c3fd04ad4a33907088e2464c2Test
رقم الانضمام: edsdoj.3930186c3fd04ad4a33907088e2464c2
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:2050084X
DOI:10.7554/eLife.44525