HDAC3 functions as a positive regulator in Notch signal transduction.
Journal
Nucleic acids research
ISSN: 1362-4962
Titre abrégé: Nucleic Acids Res
Pays: England
ID NLM: 0411011
Informations de publication
Date de publication:
17 04 2020
17 04 2020
Historique:
accepted:
03
02
2020
revised:
29
01
2020
received:
30
04
2019
pubmed:
29
2
2020
medline:
7
7
2020
entrez:
29
2
2020
Statut:
ppublish
Résumé
Aberrant Notch signaling plays a pivotal role in T-cell acute lymphoblastic leukemia (T-ALL) and chronic lymphocytic leukemia (CLL). Amplitude and duration of the Notch response is controlled by ubiquitin-dependent proteasomal degradation of the Notch1 intracellular domain (NICD1), a hallmark of the leukemogenic process. Here, we show that HDAC3 controls NICD1 acetylation levels directly affecting NICD1 protein stability. Either genetic loss-of-function of HDAC3 or nanomolar concentrations of HDAC inhibitor apicidin lead to downregulation of Notch target genes accompanied by a local reduction of histone acetylation. Importantly, an HDAC3-insensitive NICD1 mutant is more stable but biologically less active. Collectively, these data show a new HDAC3- and acetylation-dependent mechanism that may be exploited to treat Notch1-dependent leukemias.
Identifiants
pubmed: 32107550
pii: 5763097
doi: 10.1093/nar/gkaa088
pmc: PMC7144913
doi:
Substances chimiques
Histone Deacetylase Inhibitors
0
NOTCH1 protein, human
0
Notch1 protein, mouse
0
Peptides, Cyclic
0
Receptor, Notch1
0
apicidin
0
Histone Deacetylases
EC 3.5.1.98
histone deacetylase 3
EC 3.5.1.98
Lysine
K3Z4F929H6
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
3496-3512Informations de copyright
© The Author(s) 2020. Published by Oxford University Press on behalf of Nucleic Acids Research.
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