γ-Catenin-Dependent Signals Maintain BCR-ABL1
Animals
Fusion Proteins, bcr-abl
/ genetics
Gene Expression Regulation, Leukemic
Humans
K562 Cells
Mice, Inbred NOD
Mice, SCID
Mice, Transgenic
Precursor B-Cell Lymphoblastic Leukemia-Lymphoma
/ genetics
Proto-Oncogene Proteins c-myc
/ genetics
Survivin
/ genetics
Wnt Signaling Pathway
beta Catenin
/ genetics
gamma Catenin
/ genetics
B cell acute lymphoblastic leukemia (B-ALL)
BCR-ABL1
BIRC5 (Survivin)
MYC
chronic myeloid leukemia (CML)
junction plakoglobin
β-catenin
γ-catenin
Journal
Cancer cell
ISSN: 1878-3686
Titre abrégé: Cancer Cell
Pays: United States
ID NLM: 101130617
Informations de publication
Date de publication:
15 04 2019
15 04 2019
Historique:
received:
30
10
2015
revised:
29
01
2019
accepted:
14
03
2019
entrez:
17
4
2019
pubmed:
17
4
2019
medline:
6
2
2020
Statut:
ppublish
Résumé
The BCR-ABL1 fusion protein is the cause of chronic myeloid leukemia (CML) and of a significant fraction of adult-onset B cell acute lymphoblastic leukemia (B-ALL) cases. Using mouse models and patient-derived samples, we identified an essential role for γ-catenin in the initiation and maintenance of BCR-ABL1
Identifiants
pubmed: 30991025
pii: S1535-6108(19)30150-3
doi: 10.1016/j.ccell.2019.03.005
pii:
doi:
Substances chimiques
BCR-ABL1 fusion protein, human
0
BIRC5 protein, human
0
Birc5 protein, mouse
0
CTNNB1 protein, human
0
CTNNB1 protein, mouse
0
JUP protein, human
0
Jup protein, mouse
0
MYC protein, human
0
Myc protein, mouse
0
Proto-Oncogene Proteins c-myc
0
Survivin
0
beta Catenin
0
gamma Catenin
0
Fusion Proteins, bcr-abl
EC 2.7.10.2
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
649-663.e10Informations de copyright
Copyright © 2019 Elsevier Inc. All rights reserved.