Dexamethasone induces p21
ATM
Ataxia-Telangiectasia
CDKN1A
Lamin A/C
dexamethasone
p21
Journal
FEBS open bio
ISSN: 2211-5463
Titre abrégé: FEBS Open Bio
Pays: England
ID NLM: 101580716
Informations de publication
Date de publication:
08 2023
08 2023
Historique:
revised:
12
05
2023
received:
13
03
2023
accepted:
21
06
2023
medline:
2
8
2023
pubmed:
22
6
2023
entrez:
22
6
2023
Statut:
ppublish
Résumé
Ataxia-Telangiectasia (A-T) is a very rare autosomal recessive multisystemic disorder which to date is still uncurable. The use of glucocorticoid analogs, such as dexamethasone (dex), can improve neurological symptoms in patients, but the molecular mechanism of action of these analogs remains unclear. Here, we report the effects of dex in regulating the interaction between Lamin A/C and HDAC2 in WT and A-T cells. Upon administration of dex to A-T cells, we first observed that the accumulation of HDAC2 on the CDKN1A promoter did not exert a repressive role on p21
Identifiants
pubmed: 37345209
doi: 10.1002/2211-5463.13663
pmc: PMC10392059
doi:
Substances chimiques
Lamin Type A
0
Cyclin-Dependent Kinase Inhibitor p21
0
Glucocorticoids
0
Dexamethasone
7S5I7G3JQL
HDAC2 protein, human
EC 3.5.1.98
Histone Deacetylase 2
EC 3.5.1.98
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1459-1468Informations de copyright
© 2023 The Authors. FEBS Open Bio published by John Wiley & Sons Ltd on behalf of Federation of European Biochemical Societies.
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