RUNX1 is required in granulocyte-monocyte progenitors to attenuate inflammatory cytokine production by neutrophils.
RUNX1
hematopoiesis
inflammation
retroelements
transposable elements
Journal
Genes & development
ISSN: 1549-5477
Titre abrégé: Genes Dev
Pays: United States
ID NLM: 8711660
Informations de publication
Date de publication:
01 07 2023
01 07 2023
Historique:
received:
09
01
2023
accepted:
07
07
2023
pmc-release:
01
01
2024
medline:
21
8
2023
pubmed:
4
8
2023
entrez:
3
8
2023
Statut:
ppublish
Résumé
The transcription factor RUNX1 is mutated in familial platelet disorder with associated myeloid malignancy (FPDMM) and in sporadic myelodysplastic syndrome and leukemia. RUNX1 was shown to regulate inflammation in multiple cell types. Here we show that RUNX1 is required in granulocyte-monocyte progenitors (GMPs) to epigenetically repress two inflammatory signaling pathways in neutrophils: Toll-like receptor 4 (TLR4) and type I interferon (IFN) signaling. RUNX1 loss in GMPs augments neutrophils' inflammatory response to the TLR4 ligand lipopolysaccharide through increased expression of the TLR4 coreceptor CD14. RUNX1 binds
Identifiants
pubmed: 37536952
pii: gad.350418.123
doi: 10.1101/gad.350418.123
pmc: PMC10499021
doi:
Substances chimiques
Toll-Like Receptor 4
0
Core Binding Factor Alpha 2 Subunit
0
guanosine 5'-monophosphorothioate
76310-16-2
Cytokines
0
Chromatin
0
STAT1 Transcription Factor
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, N.I.H., Intramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
605-620Subventions
Organisme : NHLBI NIH HHS
ID : U01 HL100405
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL091724
Pays : United States
Organisme : NIDDK NIH HHS
ID : F30 DK128926
Pays : United States
Organisme : NICHD NIH HHS
ID : T32 HD083185
Pays : United States
Organisme : NHLBI NIH HHS
ID : F31 HL150952
Pays : United States
Organisme : NHLBI NIH HHS
ID : T32 HL007439
Pays : United States
Commentaires et corrections
Type : UpdateOf
Informations de copyright
© 2023 Zezulin et al.; Published by Cold Spring Harbor Laboratory Press.
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