AKT1 E17K Inhibits Cancer Cell Migration by Abrogating β-Catenin Signaling.
Journal
Molecular cancer research : MCR
ISSN: 1557-3125
Titre abrégé: Mol Cancer Res
Pays: United States
ID NLM: 101150042
Informations de publication
Date de publication:
04 2021
04 2021
Historique:
received:
15
07
2020
revised:
09
11
2020
accepted:
04
12
2020
pubmed:
12
12
2020
medline:
13
1
2022
entrez:
11
12
2020
Statut:
ppublish
Résumé
Mutational activation of the PI3K/AKT pathway is among the most common pro-oncogenic events in human cancers. The clinical utility of PI3K and AKT inhibitors has, however, been modest to date. Here, we used CRISPR-mediated gene editing to study the biological consequences of AKT1 E17K mutation by developing an AKT1 E17K-mutant isogenic system in a
Identifiants
pubmed: 33303690
pii: 1541-7786.MCR-20-0623
doi: 10.1158/1541-7786.MCR-20-0623
pmc: PMC8026572
mid: NIHMS1654277
doi:
Substances chimiques
CTNNB1 protein, human
0
beta Catenin
0
AKT1 protein, human
EC 2.7.11.1
Proto-Oncogene Proteins c-akt
EC 2.7.11.1
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
573-584Subventions
Organisme : NCI NIH HHS
ID : R01 CA207244
Pays : United States
Organisme : NCI NIH HHS
ID : P30 CA008748
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA234361
Pays : United States
Organisme : NCI NIH HHS
ID : P50 CA221745
Pays : United States
Organisme : NCI NIH HHS
ID : P01 CA094060
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA204749
Pays : United States
Informations de copyright
©2020 American Association for Cancer Research.
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