Non Animal Testing Database

tBID can directly trigger cell death

December 2021
University of Cologne, Cologne, Germany
During apoptosis, the BCL-2-family protein tBID promotes mitochondrial permeabilization by activating BAX and BAK and by blocking anti-apoptotic BCL-2 members. Here, the researchers report that tBID can also mediate mitochondrial permeabilization by itself, resulting in the release of cytochrome c and mitochondrial DNA, caspase activation and apoptosis even in absence of BAX and BAK. Importantly, this mechanism is physiologically relevant in the immune response against Shigella infection. Furthermore, it can be exploited to kill leukaemia cells with acquired venetoclax resistance due to the lack of active BAX and BAK. These findings define tBID as an effector of mitochondrial permeabilization in apoptosis and provide a new paradigm for BCL-2 proteins, with implications for anti-bacterial immunity and cancer therapy.
BCL-2-family protein tBID can act as a BAX-like effector of apoptosis
Ana J Garcia-Saez
Added on: 03-16-2022
Back to Top
English German

Warning: Internet Explorer

The IE from MS no longer understands current scripting languages, the latest main version (version 11) is from 2013 and has not been further developed since 2015.

Our recommendation: Use only the latest versions of modern browsers, for example Google Chrome, Mozilla Firefox or Microsofrt Edge, because only this guarantees you sufficient protection against infections and the correct display of websites!