Interaction of Leukocyte Elastase Inhibitor/L-DNase II with BCL-2 and BAX

Détails

ID Serval
serval:BIB_4316E056D10B
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Interaction of Leukocyte Elastase Inhibitor/L-DNase II with BCL-2 and BAX
Périodique
Biochimica et Biophysica Acta (BBA) - Molecular Cell Research
Auteur(s)
Jaadane Imène, Nagbou Atf, Behar-Cohen Francine, Torriglia Alicia
ISSN
0167-4889
ISSN-L
1879-2596
Statut éditorial
Publié
Date de publication
12/2014
Peer-reviewed
Oui
Volume
1843
Numéro
12
Pages
2807-2815
Langue
anglais
Notes
Publication types: JOURNAL ARTICLE
Résumé
Leukocyte Elastase Inhibitor (LEI, also called serpin B1) is a protein involved in apoptosis among other physiological processes. We have previously shown that upon cleavage by its cognate protease, LEI is transformed into L-DNase II, a protein with a pro-apoptotic activity. The caspase independent apoptotic pathway, in which L-DNase II is the final effector, interacts with other pro-apoptotic molecules like Poly-ADP-Ribose polymerase (PARP) or Apoptosis Inducing Factor (AIF). The screening of LEI/L-DNase II interactions showed a possible interaction with several members of the BCL-2 family of proteins which are known to have a central role in the regulation of caspase dependent cell death. In this study, we investigated the regulation of LEI/L-DNase II pathway by two members of this family of proteins: BAX and BCL-2, which have opposite effects on cell survival. We show that, in both BHK and HeLa cells, LEI/L-DNase II can interact with BCL-2 and BAX in apoptotic and non-apoptotic conditions. These proteins which are usually thought to be anti-apoptotic and pro-apoptotic respectively, both inhibit the L-DNase II pro-apoptotic activity. These results give further insight in the regulation of caspase-independent pathways and highlight the involvement of the intracellular environment of a given protein in the determinism of its function. They also add a link between caspase-dependent and independent pathways of apoptosis.
Mots-clé
Cell Biology, Molecular Biology
Pubmed
Web of science
Open Access
Oui
Création de la notice
02/09/2014 9:13
Dernière modification de la notice
08/05/2019 17:46
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