The paracaspase MALT1: biological function and potential for therapeutic inhibition.

Détails

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Etat: Public
Version: Final published version
ID Serval
serval:BIB_B68EA67B0DAA
Type
Article: article d'un périodique ou d'un magazine.
Sous-type
Synthèse (review): revue aussi complète que possible des connaissances sur un sujet, rédigée à partir de l'analyse exhaustive des travaux publiés.
Collection
Publications
Institution
Titre
The paracaspase MALT1: biological function and potential for therapeutic inhibition.
Périodique
Cellular and Molecular Life Sciences
Auteur(s)
Jaworski M., Thome M.
ISSN
1420-9071 (Electronic)
ISSN-L
1420-682X
Statut éditorial
Publié
Date de publication
2016
Volume
73
Numéro
3
Pages
459-473
Langue
anglais
Résumé
The paracaspase MALT1 has a central role in the activation of lymphocytes and other immune cells including myeloid cells, mast cells and NK cells. MALT1 activity is required not only for the immune response, but also for the development of natural Treg cells that keep the immune response in check. Exaggerated MALT1 activity has been associated with the development of lymphoid malignancies, and recently developed MALT1 inhibitors show promising anti-tumor effects in xenograft models of diffuse large B cell lymphoma. In this review, we provide an overview of the present understanding of MALT1's function, and discuss possibilities for its therapeutic targeting based on recently developed inhibitors and animal models.
Mots-clé
Amino Acid Motifs, Animals, B-Lymphocytes/metabolism, B-Lymphocytes/physiology, Caspases/metabolism, Caspases/physiology, Humans, Immunomodulation/genetics, Killer Cells, Natural/metabolism, Killer Cells, Natural/physiology, Lymphoma, Large B-Cell, Diffuse/genetics, Models, Molecular, NF-kappa B/metabolism, NF-kappa B/physiology, Neoplasm Proteins/antagonists & inhibitors, Neoplasm Proteins/metabolism, RNA Stability, RNA, Messenger/metabolism, Transcription Factor AP-1/metabolism, Transcription Factor AP-1/physiology
Pubmed
Web of science
Open Access
Oui
Création de la notice
02/02/2016 13:35
Dernière modification de la notice
20/08/2019 15:24
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