PuSH - Publication Server of Helmholtz Zentrum München

Export: TXT Text RIS Endnote (RIS) BIB BibTeX
Höckendorf, U.* ; Yabal, M.* ; Herold, T.* ; Munkhbaatar, E.* ; Rott, S.* ; Jilg, S.* ; Kauschinger, J.* ; Magnani, G.* ; Reisinger, F. ; Heuser, M.* ; Kreipe, H.* ; Sotlar, K.* ; Engleitner, T.* ; Rad, R.* ; Weichert, W.* ; Peschel, C.* ; Ruland, J.* ; Heikenwälder, M. ; Spiekermann, K.* ; Slotta-Huspenina, J.* ; Groß, O.* ; Jost, P.J.*

RIPK3 restricts myeloid leukemogenesis by promoting cell death and differentiation of leukemia initiating cells.

Cancer Cell 30, 75-91 (2016)
Publ. Version/Full Text DOI PMC
Closed
Open Access Green as soon as Postprint is submitted to ZB.
Since acute myeloid leukemia (AML) is characterized by the blockade of hematopoietic differentiation and cell death, we interrogated RIPK3 signaling in AML development. Genetic loss of Ripk3 converted murine FLT3-ITD-driven myeloproliferation into an overt AML by enhancing the accumulation of leukemia-initiating cells (LIC). Failed inflammasome activation and cell death mediated by tumor necrosis factor receptor caused this accumulation of LIC exemplified by accelerated leukemia onset in Il1r1(-/-), Pycard(-/-), and Tnfr1/2(-/-) mice. RIPK3 signaling was partly mediated by mixed lineage kinase domain-like. This link between suppression of RIPK3, failed interleukin-1β release, and blocked cell death was supported by significantly reduced RIPK3 in primary AML patient cohorts. Our data identify RIPK3 and the inflammasome as key tumor suppressors in AML.
Impact Factor
Scopus SNIP
Web of Science
Times Cited
Scopus
Cited By
Altmetric
23.214
4.665
69
82
Tags
Annotations
Special Publikation
Hide on homepage

Edit extra information
Edit own tags
Private
Edit own annotation
Private
Hide on publication lists
on hompage
Mark as special
publikation
Publication type Article: Journal article
Document type Scientific Article
Keywords Nlrp3 Inflammasome Activation; Hematopoietic Stem; Progenitor Cells; In-vitro; Necrosis; Mice; Mlkl; Aml; Necroptosis; Mutations
Language english
Publication Year 2016
HGF-reported in Year 2016
ISSN (print) / ISBN 1535-6108
e-ISSN 1878-3686
Journal Cancer Cell
Quellenangaben Volume: 30, Issue: 1, Pages: 75-91 Article Number: , Supplement: ,
Publisher Cell Press
Publishing Place Cambridge, Mass.
Reviewing status Peer reviewed
Institute(s) Institute of Virology (VIRO)
POF-Topic(s) 30504 - Mechanisms of Genetic and Environmental Influences on Health and Disease
Research field(s) Immune Response and Infection
PSP Element(s) G-551600-001
DOI 10.1016/j.ccell.2016.06.002
WOS ID WOS:000380077100013
Scopus ID 84979732790
PubMed ID 27411587
Erfassungsdatum 2016-07-26
[➜Report correction]