Absence of ATM leads to altered NK cell function in mice.
ATM kinase
Ataxia-telangiectasia
Cytotoxicity
H60
MULT1
NKG2D
Natural killer cells
RAE-1
TNF-α
Journal
Clinical immunology (Orlando, Fla.)
ISSN: 1521-7035
Titre abrégé: Clin Immunol
Pays: United States
ID NLM: 100883537
Informations de publication
Date de publication:
30 Apr 2024
30 Apr 2024
Historique:
received:
25
01
2024
revised:
28
03
2024
accepted:
29
04
2024
medline:
3
5
2024
pubmed:
3
5
2024
entrez:
2
5
2024
Statut:
aheadofprint
Résumé
Ataxia-telangiectasia (A-T) is a rare disorder caused by genetic defects of A-T mutated (ATM) kinase, a key regulator of stress response, and characterized by neurodegeneration, immunodeficiency, and high incidence of cancer. Here we investigated NK cells in a mouse model of A-T (Atm
Identifiants
pubmed: 38697554
pii: S1521-6616(24)00342-5
doi: 10.1016/j.clim.2024.110233
pii:
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
110233Informations de copyright
Copyright © 2024. Published by Elsevier Inc.
Déclaration de conflit d'intérêts
Declaration of competing interest All authors declare no conflicts of interest.