Critical Requirement of SOS1 for Development of BCR/ABL-Driven Chronic Myelogenous Leukemia.
CML
GEF
RAC
RAS
SOS-KO phenotypes
SOS1
SOS2
myeloproliferative disorders
Journal
Cancers
ISSN: 2072-6694
Titre abrégé: Cancers (Basel)
Pays: Switzerland
ID NLM: 101526829
Informations de publication
Date de publication:
11 Aug 2022
11 Aug 2022
Historique:
received:
19
07
2022
revised:
09
08
2022
accepted:
10
08
2022
entrez:
26
8
2022
pubmed:
27
8
2022
medline:
27
8
2022
Statut:
epublish
Résumé
We showed previously that the ABL-mediated phosphorylation of SOS1 promotes RAC activation and contributes to BCR-ABL leukemogenesis, suggesting the relevant role of SOS1 in the pathogenesis of CML. To try and obtain direct experimental evidence of the specific mechanistic implication of SOS1 in CML development, here, we combined a murine model of CML driven by a p210
Identifiants
pubmed: 36010887
pii: cancers14163893
doi: 10.3390/cancers14163893
pmc: PMC9406065
pii:
doi:
Types de publication
Journal Article
Langues
eng
Subventions
Organisme : Instituto de Salud Carlos III
ID : FIS PI19/00934
Organisme : Junta de Castilla y León
ID : SA264P18-UIC 076
Organisme : Fundación Ramón Areces
ID : CIVP19A5942
Organisme : Solorzano-Barruso Foundation
ID : FS/32-2020
Organisme : Centro de Investigación Biomédica en Red de Cáncer
ID : CB16/12/00352
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