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von Gamm, M. ; Schaub, A. ; Jones, A. ; Wolf, C. ; Behrens, G.* ; Lichti, J. ; Essig, K.* ; Macht, A. ; Pircher, J.* ; Ehrlich, A.* ; Davari, K.* ; Chauhan, D.* ; Busch, B.* ; Wurst, W. ; Feederle, R. ; Feuchtinger, A. ; Tschöp, M.H. ; Friedel, C.C.* ; Hauck, S.M. ; Sattler, M. ; Geerlof, A. ; Hornung, V.* ; Heissmeyer, V. ; Schulz, C.* ; Heikenwalder, M.* ; Glasmacher, E.

Immune homeostasis and regulation of the interferon pathway require myeloid-derived Regnase-3.

J. Exp. Med. 216, 1700-1723 (2019)
Verlagsversion DOI PMC
Open Access Hybrid
Creative Commons Lizenzvertrag
The RNase Regnase-1 is a master RNA regulator in macrophages and T cells that degrades cellular and viral RNA upon NF-κB signaling. The roles of its family members, however, remain largely unknown. Here, we analyzed Regnase-3-deficient mice, which develop hypertrophic lymph nodes. We used various mice with immune cell-specific deletions of Regnase-3 to demonstrate that Regnase-3 acts specifically within myeloid cells. Regnase-3 deficiency systemically increased IFN signaling, which increased the proportion of immature B and innate immune cells, and suppressed follicle and germinal center formation. Expression analysis revealed that Regnase-3 and Regnase-1 share protein degradation pathways. Unlike Regnase-1, Regnase-3 expression is high specifically in macrophages and is transcriptionally controlled by IFN signaling. Although direct targets in macrophages remain unknown, Regnase-3 can bind, degrade, and regulate mRNAs, such as Zc3h12a (Regnase-1), in vitro. These data indicate that Regnase-3, like Regnase-1, is an RNase essential for immune homeostasis but has diverged as key regulator in the IFN pathway in macrophages.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Nf-kappa-b; Helper T-cells; Messenger-rna; Gene-expression; Roquin; Family; Inflammation; Macrophages; Microrna; Innate
Sprache englisch
Veröffentlichungsjahr 2019
HGF-Berichtsjahr 2019
ISSN (print) / ISBN 0022-1007
e-ISSN 1540-9538
Zeitschrift Journal of Experimental Medicine
Quellenangaben Band: 216, Heft: 7, Seiten: 1700-1723 Artikelnummer: , Supplement: ,
Verlag Rockefeller University Press
Verlagsort 950 Third Ave, 2nd Flr, New York, Ny 10022 Usa
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Diabetes and Obesity (IDO)
Research Unit Signaling and Translation (SAT)
Institute of Structural Biology (STB)
Institute of Environmental Medicine (IEM)
Institute of Developmental Genetics (IDG)
CF Monoclonal Antibodies (CF-MAB)
CF Pathology & Tissue Analytics (CF-PTA)
CF Metabolomics & Proteomics (CF-MPC)
Research Unit Molecular Immune Regulation (AMIR)
Research Unit Analytical Pathology (AAP)
POF Topic(s) 90000 - German Center for Diabetes Research
30203 - Molecular Targets and Therapies
30202 - Environmental Health
30204 - Cell Programming and Repair
30201 - Metabolic Health
30505 - New Technologies for Biomedical Discoveries
30205 - Bioengineering and Digital Health
Forschungsfeld(er) Helmholtz Diabetes Center
Enabling and Novel Technologies
Allergy
Genetics and Epidemiology
Immune Response and Infection
PSP-Element(e) G-501900-226
G-509800-002
G-503000-001
G-503400-002
G-500500-001
G-502210-001
A-630600-001
G-502200-001
G-505700-001
G-501712-001
A-630700-001
G-500390-001
DOI 10.1084/jem.20181762
WOS ID WOS:000473325900018
Scopus ID 85069266271
PubMed ID 31126966
Erfassungsdatum 2019-06-04
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