Par-4 overexpression impedes leukemogenesis in the Eµ-TCL1 leukemia model through downregulation of NF-κB signaling.
Journal
Blood advances
ISSN: 2473-9537
Titre abrégé: Blood Adv
Pays: United States
ID NLM: 101698425
Informations de publication
Date de publication:
23 04 2019
23 04 2019
Historique:
received:
13
09
2018
accepted:
23
02
2019
entrez:
17
4
2019
pubmed:
17
4
2019
medline:
15
5
2020
Statut:
ppublish
Résumé
Prostate apoptosis response 4 (Par-4) is a tumor suppressor that prevents proliferation and induces cell death in several solid tumors. However, its role in B-cell malignancies has not been elucidated. To describe the role of Par-4 in chronic lymphocytic leukemia (CLL) pathogenesis, we developed a B-cell-specific human Par-4-overexpressing mouse model of CLL using the TCL1 leukemia model. While Par-4 transgenic mice did not display any obvious defects in B-cell development or function, disease burden as evidenced by abundance of CD19
Identifiants
pubmed: 30987970
pii: bloodadvances.2018025973
doi: 10.1182/bloodadvances.2018025973
pmc: PMC6482354
doi:
Substances chimiques
Apoptosis Regulatory Proteins
0
Proto-Oncogene Proteins
0
TCL1A protein, human
0
Tumor Suppressor Proteins
0
prostate apoptosis response-4 protein
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1255-1266Subventions
Organisme : NCI NIH HHS
ID : R01 CA197844
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA159296
Pays : United States
Organisme : NCI NIH HHS
ID : P30 CA016058
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA165469
Pays : United States
Organisme : NCI NIH HHS
ID : R35 CA197734
Pays : United States
Informations de copyright
© 2019 by The American Society of Hematology.
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