The D647N mutation of FGFR1 induces ligand-independent receptor activation.
ATP
FGFR1
Oncogenic mutation
Tyrosine kinase inhibitor
Journal
Biochimica et biophysica acta. General subjects
ISSN: 1872-8006
Titre abrégé: Biochim Biophys Acta Gen Subj
Pays: Netherlands
ID NLM: 101731726
Informations de publication
Date de publication:
12 2023
12 2023
Historique:
received:
10
07
2023
revised:
11
09
2023
accepted:
28
09
2023
medline:
6
11
2023
pubmed:
2
10
2023
entrez:
1
10
2023
Statut:
ppublish
Résumé
The activation loop (A-loop) of kinases, a key regulatory region, is recurrently mutated in several kinase proteins in cancer resulting in dysregulated kinase activity and response to kinase inhibitors. FGFR1 receptor tyrosine kinase represents an important oncogene and therapeutic target for solid and hematological tumors. Here we investigate the biochemical and molecular effects of D647N mutation lying in the A-loop of FGFR1. When expressed in normal and tumoral in vitro cell models, FGFR1
Identifiants
pubmed: 37778450
pii: S0304-4165(23)00168-X
doi: 10.1016/j.bbagen.2023.130470
pii:
doi:
Substances chimiques
Ligands
0
Receptor, Fibroblast Growth Factor, Type 1
EC 2.7.10.1
FGFR1 protein, human
EC 2.7.10.1
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
130470Informations de copyright
Copyright © 2023 The Authors. Published by Elsevier B.V. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of Competing Interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Mitola Stefania and Michela Corsini reports financial support was provided by Italian Association for Cancer Research. Silvia Codenotti and Elisabetta Grillo reports financial support was provided by Umberto Veronesi Foundation.