Deletion of Nemo-like Kinase in T Cells Reduces Single-Positive CD8
Animals
CD8-Positive T-Lymphocytes
/ physiology
Cell Differentiation
Cell Survival
Histone Deacetylase 1
/ metabolism
Lymphocyte Activation
Lymphoid Enhancer-Binding Factor 1
/ metabolism
Mice
Mice, Inbred C57BL
Mice, Knockout
Protein Serine-Threonine Kinases
/ genetics
Signal Transduction
T-Lymphocyte Subsets
/ physiology
Thymocytes
/ physiology
Wnt Proteins
/ metabolism
Journal
Journal of immunology (Baltimore, Md. : 1950)
ISSN: 1550-6606
Titre abrégé: J Immunol
Pays: United States
ID NLM: 2985117R
Informations de publication
Date de publication:
01 10 2020
01 10 2020
Historique:
received:
30
01
2020
accepted:
23
07
2020
pubmed:
26
8
2020
medline:
30
3
2021
entrez:
26
8
2020
Statut:
ppublish
Résumé
The β-catenin/Wnt signaling pathway plays an important role in all stages of T cell development. Nemo-like kinase (NLK) is an evolutionary conserved serine/threonine kinase and a negative regulator of the Wnt signaling pathway. NLK can directly phosphorylate histone deacetylase 1 (HDAC1), as well as T cell factor/lymphoid enhancer-binding factor (TCF/LEF), causing subsequent repression of target gene transcription. By engineering mice lacking NLK in early stages of T cell development, we set out to characterize the role NLK plays in T cell development and found that deletion of NLK does not affect mouse health or lymphoid tissue development. Instead, these mice harbored a reduced number of single-positive (SP) CD8
Identifiants
pubmed: 32839237
pii: jimmunol.2000109
doi: 10.4049/jimmunol.2000109
doi:
Substances chimiques
Lef1 protein, mouse
0
Lymphoid Enhancer-Binding Factor 1
0
Wnt Proteins
0
Nlk protein, mouse
EC 2.7.11.1
Protein Serine-Threonine Kinases
EC 2.7.11.1
Hdac1 protein, mouse
EC 3.5.1.98
Histone Deacetylase 1
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
1830-1841Informations de copyright
Copyright © 2020 by The American Association of Immunologists, Inc.